MDL Docket No. 1203, C.A. NO. 99-20593, MDL NO. 03-20220 (E.D. Pa. Feb. 12, 2004)

From Casetext: Smarter Legal Research

In re Diet Drugs Products Liability Litigation

United States District Court, E.D. Pennsylvania

Feb 12, 2004

MDL Docket No. 1203, C.A. NO. 99-20593, MDL NO. 03-20220 (E.D. Pa. Feb. 12, 2004)

Opinion

MDL Docket No. 1203, C.A. NO. 99-20593, MDL NO. 03-20220

February 12, 2004

Peter L. Zimroth, ARNOLD PORTER LLP, New York, NY, for Defendant Wyeth

Robert D. Rosenbaum, Helene B. Madonick, Geoffrey J. Michael, ARNOLD PORTER LLP, Washington, D.C., for Defendant Wyeth

William M. Gage, BUTLER, SNOW, O'MARA, STEVENS CANNADA, PLLC, Jackson, MS, for Defendant Wyeth

Michael T. Scott, Paul B. Kerrigan, REED SMITH LLP, Philadelphia, PA for Defendant Wyeth

Nancy Guy Armstrong, Armstrong Guy, LLC, McComb, MS, for plaintiffs

J. Robert Ramsay, Amanda Clearman Waddell, Bryant, Clark, Dukes, Blakeslee, Ramsay Hammond, P.L.L.C., Hattiesburg, Mississippi, for JERRY ILES, M.D.

Whitman B. Johnson, III, Juliette V. Wilson, Currie Johnson Griffin Gaines Myers, P.A., Jackson, MS, for KATHERINE HENSLEIGH, M.D.

DECLARATION OF TERI R. RICHARDSON

HARVEY BARTLE, III, District Judge

1. I am an attorney licensed to practice law in the state of California and am associated with the law firm of Arnold Porter. As such, I have acted as counsel for defendant Wyeth and its affiliated entities (collectively "Wyeth") in the case of LaPlant v. American Home Products Corp., et al., Civ. No. 99-20593.

2. After many months of attempting to obtain it, in August 2003, Arnold and Porter received a MO disk with the full tracings and hemodynamic data from Gail LaPlant's April 2003 right heart catheterization from the University of California San Diego ("UCSD"). A representative from UCSD told my legal assistant, Edward McCarthy, that specialized equipment was needed to read the MO disk. After investigation, I learned that Dr. Shook had such equipment.

3. On February 6, 2004, I spoke with Michael Woerner, one of Gail LaPlant's attorneys, about plaintiff's requests for an extension of time to respond to Wyeth's motion to dismiss and to depose Dr. Shook, as set forth in their opposition. I told Mr. Woerner that Wyeth was willing to provide plaintiff with her requested 60-day extension to obtain a declaration from Dr. Channick. I also told him that Wyeth was willing to make Dr. Shook available for a deposition concerning the subject matter of his declaration, in exchange for plaintiff's willingness to make any expert declarant that she might use in her opposition available for deposition. Mr. Woerner asked for time to confer with his co-counsel on Wyeth's offer, which I accepted.

4. On February 9, 2004, I again spoke with Mr. Woerner regarding Wyeth's proposed offer to provide plaintiff with additional time for responding to Wyeth's motion and to make Dr. Shook available for deposition. Mr. Woerner declined Wyeth's offer pending a decision by the MDL Court regarding whether Wyeth would be allowed to use Dr. Shook's declaration to support its motion.

I declare under penalty of perjury under the laws of the United States that the foregoing is true and correct. Executed in Los Angeles, California, on this 11th day of February.

WYETH'S MOTION PURSUANT TO PRETRIAL ORDER NO. 2383 TOCOMPEL PRODUCTION OF COMPLETE MEDICAL EVIDENCE ANDCERTIFICATION FROM CLASS MEMBER REBECCA MEADES ANDMOTION TO COMPEL PLAINTIFF FOR DEPOSITION

On February 26, 2002, this Court entered Pretrial Order No. 2383 ("PTO 2383"), which sets forth procedures for resolving motions to enforce paragraph 7 of Pretrial Order No. 1415 ("PTO 1415") against Class Members who assert claims for primary pulmonary hypertension ("PPH"), as that term and medical condition are described in the Nationwide Class Action Settlement Agreement with American Home Products Corporation ("Settlement Agreement").

Paragraph 2 of PTO 2383 states that Class Members filing suits based on claims for PPH are required, within 30 days of receipt of the written request of Wyeth or any other Released Party, to provide Wyeth or such Released Party with "all medical evidence, including medical records and tests, that relate to a diagnosis that the Class member has PPH" and a "certification stating that the information being produced to the requesting party is a complete set of medical evidence upon which the Class Member is relying to establish PPH." Class Member Rebecca Meades has failed to produce complete medical evidence and also failed to provide Wyeth with the required certification. Class Member Rebecca Meades has also ignored repeated requests that she make herself available for deposition.

Wyeth therefore moves this Court pursuant to Paragraph 4 of PTO 2383 to compel Ms. Meades to produce "all medical evidence, including medical records and tests, that relate to a diagnosis that [she] has PPH" and to certify that the production is a "complete set of medical evidence upon which [she] is relying to establish PPH," as required by Paragraph 2 of PTO 2383. Wyeth also moves for this Court to compel Ms. Meades to produce herself for deposition.

Wyeth respectfully submits the enclosed Memorandum in support of this motion and has provided the Court with a proposed form of Order.

WYETH'S MEMORANDUM IN SUPPORT OF ITS MOTION PURSUANTTO PRETRIAL ORDER NO. 2383 TO COMPEL PRODUCTION OF COMPLETEMEDICAL EVIDENCE AND CERTIFICATION FROM CLASS MEMBER REBECCAMEADES AND MOTION TO COMPEL PLAINTIFF FOR DEPOSITION

This case, initially comprised of three plaintiffs, began as one of those not uncommon cases in Mississippi state court in which several plaintiffs file suit alleging PPH as defined by the Settlement Agreement, yet have no basis for such a suit. Two of the original plaintiffs in this case have already dismissed their claims, agreeing that their claims (if any) are for heart valve regurgitation and not PPH. The third (and sole remaining) plaintiff, Rebecca Meades, appeared to have settled her claims in a prior suit, but later was discovered to have dismissed those claims without prejudice for failure to present any evidence that she even used diet drugs. In other words, this case is a do-over. After Wyeth notified plaintiffs' counsel, they dismissed two out of the three plaintiffs. As to Ms. Meades, who had been dismissed from her prior suit in 2001, plaintif's counsel has recast as a PPH plaintiff and procured — for the first time in the four years since her original claim was filed — affidavits from her, her spouse, and her friend, vividly recalling Ms. Meades being prescribed Pondimin and ingesting it almost eight years ago. The doctor defendant has filed a separate motion for summary judgment on the ground that the plaintiff did not prescribe diet drugs, which Wyeth will join in. In the meantime, although we believe the case should be dismissed, Wyeth has been attempting, unsuccessfully, to obtain discovery, which it is clearly entitled to pursuant to paragraph 2 of Pretrial Order No. 2383. In particular, because we have been unable to procure plaintiffs cooperation, we seek an order from the Court requiring plaintiff to produce a complete set of medical records relating to her purported diagnosis of PPH and to present herself for a deposition forthwith.

FACTUAL BACKGROUND

I. ENTRY OF PTO 2383

On August 28, 2000, the Court entered Pretrial Order No. 1415 ("PTO 1415"), enjoining Class Members who had not timely and properly exercised opt-out rights from asserting and/or continuing to prosecute Settled Claims against Wyeth or other Released Parties. Claims based on PPH are not "Settled Claims" under the Settlement Agreement and therefore such claims are not barred by this Court's injunction. See PTO 1415 ¶ Settlement Agreement §§ I.46 I. 53. The Court has explained that a "determination of whether a putative PPH plaintiff has been diagnosed with PPH . . . is a threshold question that determines the eligibility of that Class Member to assert such a claim. Under the Settlement Agreement, AHP and any other Released Party should not be required to litigate a claim allegedly based on PPH that is initiated by a person whose medical condition does not meet the criteria of Section 1.46 [of the Settlement Agreement]." PTO 2383 at Recital D.

PTO 2383 sets forth the procedures for determining whether a plaintiff may proceed with a claim for PPH. Specifically, it provides that Class Members filing suits allegedly based on PPH are required, within 30 days of receipt of Wyeth's written request, to provide Wyeth with "all medical evidence, including medical records and tests, that relate to a diagnosis that the Class Member has PPH." PTO 2383 at ¶ 2. The order further requires that the produced evidence "must be accompanied by a certification stating that the information being produced to the requesting party is a complete set of medical evidence upon which the Class Member is relying to establish PPH." Id. PTO 2383 also authorizes Wyeth to file motions with this Court to compel the production of medical evidence and certification in the event that a Class Member fails to provide them. Id. at ¶ 4.

II. WYETH'S REPEATED REQUESTS FOR MEDICAL EVIDENCE FROM MS. MEADES

On March 11, 2003, plaintiffs Katie Murray, Rebecca Meades, and Janet Thrash served Wyeth with a complaint filed in Adams County, Mississippi, alleging that they had developed PPH as defined by the National Settlement agreement as a result of their ingestion of diet drugs. On April 9, 2003, Wyeth removed the case to the United States District Court for the Southern District of Mississippi.

All parties except plaintiff Meades, Wyeth and defendant Professional Weight Loss Center ("PWLC") are to be dismissed from this case by agreement of the parties. See Pretrial Order No. 3168 (Dec. 8, 2003). All remaining parties are diverse from one another and this Court has jurisdiction under 28 U.S.C. § 1332.

After transfer, this case received a discovery initiation date ("DID") of July 1, 2003. On July 8, 2003, Wyeth requested that plaintiff produce medical evidence and certification pursuant to PTO 2383. In that same letter, Wyeth informed plaintiff that the Circuit Court of Jefferson County, Mississippi, had dismissed her claims with prejudice in a prior diet drug lawsuit entitled Diane Jefferson, et al. v. American Home Products Corporation, et al., and requested that she sign a stipulation for dismissal of this suit. Plaintiff ignored both requests.

See Letter from Stephanie M. Rippee to Nancy Guy Armstrong (July 8, 2003), Exhibit A.

On September 5, 2003, Wyeth wrote plaintiff again requesting 2383 records and again requesting that Ms. Meades sign a stipulation for dismissal of her claims based on the Diane Jefferson dismissal with prejudice. Plaintiff responded by stating that she had no record of receiving the July 8, 2003, letter, but that if Wyeth would resend the July 2003 letter she would provide certification and records within twenty days of receipt. Plaintiff also produced an order dismissing Ms. Meades without prejudice in the Diane Jefferson case. The next day, Wyeth resent its 2383 request to plaintiff, noting that plaintiffs' 2383 records and certification would be due on October 2, 2003, by agreement of the parties.

See Letter from Geoffrey J. Michael to Nancy Guy Armstrong (Sept. 5, 2003), Exhibit B.

See Letter from Michael J. Miller to Geoffrey J. Michael (Sept. 15, 2003), Exhibit C.

See Letter from Geoffrey J. Michael to Michael J. Miller (Sept. 16, 2003), Exhibit D.

Plaintiffs failed to meet the agreed belated October 2, 2003, deadline for production of 2383 records. Coincidentally, plaintiff missed the deadline for the filing of her case-specific expert reports on October 1, 2003. Wyeth informed plaintiffs of both deficiencies on October 9, 2003. However, Wyeth gave the plaintiff the benefit of the doubt due to alleged confusion relating to a lost letter and conflicting orders of dismissal, and thus suggested resetting the DID to the date when plaintiff did provide 2383 records.

See Letter from Geoffrey J. Michael to Michael J. Miller (Oct. 9, 2003), Exhibit E.

On October 20, 2003, plaintiff finally produced some of Ms. Meades' medical records, but did not provide certification, as plaintiff's counsel stated, "I need to verify that all other possible causes of PPH as to Rebecca Meades have been excluded pursuant to PTO 2383." To date, plaintiff's counsel has provided no such certification. Moreover, the records produced by plaintiff were woefully incomplete. After reviewing the medical records that were provided by plaintiff counsel, Wyeth. on December 31, 2003, requested the plaintiff provide records that were clearly missing from the face of the records, including:

See Letter from Kenneth W. Smith to Geoffrey J. Michael (Oct. 20, 2003), Exhibit F

• Records and tapes relating to echocardiograms performed on 5/12/03, 9/10/02, 5/27/01 and 4/2/00;

• Records relating to and the actual tracings of heart catheterizations performed on 5/12/03 (RHC), 9/9/02 (LHC) and 9/10/02 (RHC);

• Records relating to a sleep study, if any;

• Records relating to a V-Q scan, if any;

• Records relating to the exclusion of conditions known to cause pulmonary hypertension by a Board Certified Cardiologist or Pulmonologist;

• Any other medical records relating to Ms. Murray [sic]'s purported diagnosis of PPH.

To date, plaintiff has not produced the requested records, except for the 2001 echocardiogram videotape.

III. WYETH'S REPEATED REQUEST FOR MS. MEADES' DEPOSITION

Despite the inadequacy of plaintiff's production of medical records and certification, Wyeth. in an attempt to move discovery forward, requested that plaintiff provide dates from Ms. Meades' deposition on November 19, 2003. Plaintiff ignored this request. On December 16, 2003, Wyeth again requested a date for plaintiff's deposition. On December 21, 2003, one of Plaintiffs counsel, Mr. Miller, responded that another plaintiff's counsel, Mr. Guy, would provide deposition dates. To date, none of plaintiff's counsel have provided dates for Ms. Meades' deposition, despite Wyeth sending a third letter requesting deposition dates to both Mr. Miller and Mr. Guy on December 31, 2003.

See Letter from Geoffrey J. Michael to Kenneth Smith (Nov. 19, 2003), Exhibit G.

See Letter from Geoffrey J. Michael to Kenneth Smith (Dec. 16, 2003, mistakenly labeled Nov. 19, 2003), Exhibit H.

See Letter from Michael J. Miller to Geoffrey J. Michael (Dec. 21, 2003), Exhibit I.

See Letter from Geoffrey J. Michael to Michael Miller and Paul Guy (Dec. 31, 2003), Exhibit J.

ARGUMENT

Ms. Meades is clearly violating PTO 2383 by failing to provide to Wyeth "all medical evidence" relevant to Ms. Meades' purported PPH diagnosis. See PTO 2383 ¶ 2 (emphasis added). Ms. Meades has failed to provide the obviously relevant medical evidence that exists despite repeated requests by Wyeth and repeated extensions being granted by Wyeth. It is now six months since Wyeth first requested 2383 records from plaintiff, and five months after PTO 2383 required plaintiff to produce the medical evidence and certification; plaintiff still has produced insufficient medical records and no certification. The list of records that Wyeth believes exist from the face of the limited amount of records that were produced, include the following:

• Records and tapes relating to echocardiograms performed on 5/12/03, 9/10/02, and 4/2/00;

• Records relating to and the actual tracings of heart catheterizations performed on 5/12/03 (RHC), 9/9/02 (LHC) and 9/10/02 (RHC);

• Records relating to a sleep study, if any;

• Records relating to a V-Q scan, if any;

• Records relating to the exclusion of conditions known to cause pulmonary hypertension by a Board Certified Cardiologist or Pulmonologist; and

• Any other medical records relating to Ms. Murray [sic]'s purported diagnosis of PPH.

Plaintiff has compounded her 2383 deficiency by refusing to produce herself for deposition, despite Wyeth making three written requests for deposition dates over the past two and a half months. Thus, Wyeth has not only been unable to utilize full PTO 2383 records to examine what this Court has called the "threshold" question of plaintiff's eligibility to proceed as a PPH plaintiff under the Settlement Agreement but also unable to proceed with any meaningful discovery as to the merits of Ms. Meades' claims.

Because plaintiff has failed to comply with the requirements of PTO 2383, Wyeth requests that this Court enter an order requiring Plaintiff to produce, within ten days, (a) all medical evidence, including medical records and tests, that relates to a diagnosis that Ms. Meades has PPH, and (b) a certification that the materials produced represent a complete set of medical evidence upon which Ms. Meades is relying to establish that she has PPH.

Because plaintiff has repeatedly failed to provide dates for her own deposition, Wyeth requests that this Court enter an order requiring Plaintiff to provide, within ten days, two dates during which she is available for deposition within the two calendar weeks.

CONCLUSION

For the foregoing reasons, Wyeth respectfully requests that the Court grant its motion to compel.

PRETRIAL ORDER NO. _____

WHEREAS, Class Member Rebecca Meades has filed a complaint against American Home Products Corporation, now known as Wyeth. alleging claims based on primary pulmonary hypertension ("PPH"); and

WHEREAS, this Court has established procedures, in Pretrial Order No. 2383 ("PTO 2383") for resolving motions to enforce Pretrial Order No. 1415 against Class Members who assert claims allegedly based on PPH; and

WHEREAS, Wyeth has made written requests of Ms. Meades, pursuant to Paragraph 2 of PTO 2383, that said Class Member provide Wyeth with all medical evidence, including medical records and tests, that relate to a diagnosis that Ms. Meades has PPH, and that such evidence be accompanied by a certification stating that the information being provided to Wyeth is a complete set of medical evidence upon which Ms. Meades is relying to establish PPH as defined by Section I.46 of the Settlement Agreement; and

WHEREAS, Ms. Meades has not produced all such medical evidence and certification to Wyeth pursuant to the requirements of PTO 2383; and

WHEREAS, Wyeth has made several written requests over several months for Ms. Meades to make herself available for deposition; and

WHEREAS, Ms. Meades has not provided dates upon which she may be deposed; IT IS THEREFORE ORDERED AS FOLLOWS:

(1) Class Member Rebecca Meades is hereby ordered and directed within 10 days to produce to Wyeth "all medical evidence, including medical records and tests, that the Class Member has PPH" and a certification signed by plaintiffs counsel that the records produced constitute a "complete set of medical evidence upon which the Class Member is relying to establish PPH" as required by Paragraph 2 of PTO 2383; and

(2) Class Member Rebecca Meades is hereby ordered and directed within 10 days to provide to Wyeth two dates during which she is available for deposition within the following two calendar weeks.

EXHIBIT A

BUTUER, SNOW, O'MARA, STEVENS CANNADA, PLLCATTORNEYS AT LAW POST OFFICE BOX 22567 JACKSON, MISSISSIPPI 39225-2567 STEPHANIE M. RIPPEE (601) 985-4569 AMSOUIH PLAZA 17TH FLOOR July 8, 2003 210 EAST CAPITOL STREET JACKSON, MISSISSIPPI 39201 TELEPHONE: (601) 948-5711 FACSIMILE: (601) 985-500 E-Mail:stephanie.rippee@budersnow.com www.budersnow.com Nancy Guy Armstrong Armstrong Guy Law Firm, L.L.C. P.O. Box 1343 McComb, MS 39649

Re: Katie R. Murray, et al. v. Wyeth Corporation, et al. Cause No. 02-KV-0227-J In the Circuit Court of Adams County

Dear Ms. Armstrong:

On behalf of Wyeth. I am writing to address the status of the plaintiffs in the above-referenced case, with respect to the terms of the Nationwide Class Action Settlement with American Home Products Corporation (the "Settlement"), approved by the United States District Court for the Eastern District of Pennsylvania in In re Diet Drugs (Phentermine/Fenfluramine/ Dexfenfluramine) Products Liability Litigation (Sheila Brown et al. v. American Home Products Corporation), MDL Docket No. 1203, Civ. No. 99-20593.

Our records reflect that plaintiffs Katie Murry and Janet Murray did not timely and properly submit an Opt-Out from the Settlement. Further, as you are aware, the MDL Court has entered an injunction prohibiting any class member who has not timely and properly exercised an opt-out from the Settlement from asserting any Settled Claims against Wyeth. See Pretrial Order No. ("PTO") 1415, ¶ 7.

A person who has Primary Pulmonary Hypertension ("PPH") may assert claims against Wyeth based upon that condition, but only persons with PPH as specifically defined in the Nationwide Class Action Settlement Agreement (the "Settlement Agreement") are eligible for this PPH exclusion. See Settlement Agreement § 1.46. The Settlement Agreement definition of PPH requires specific findings and medical records demonstrating by particular results that certain medical conditions have been excluded. Id. at § 1.46.a(1) and (2). Further, the Settlement Agreement definition of PPH requires that a Board-Certified Cardiologist or Board-Certified Pulmonologist have ruled out alternative conditions known to cause PPH. Id. at § 1.46.a(3).

Pursuant to PTO 2383, the MDL Court has ordered that class members, who are filing suits allegedly based upon PPH, are required:

upon written request of Wyeth . . . to provide Wyeth . . . with all medical evidence, including medical records and tests, that relate to a diagnosis that the Class Member has PPH as defined by the criteria set forth in Sections 1.46 and 1.53 of the Settlement Agreement. Such medical evidence shall be disclosed within thirty (30) days of a written request and must be accompanied by a certification stating that the information being produced to the requesting party is a complete set of medical evidence upon which theClass Member is relying to establish PPH as defined by Sections 1.46 and 1.53 of the Settlement Agreement.

See PTO 2383, ¶ 2 (emphasis added)

Accordingly, within thirty (30) days of this letter, please submit to this office the required medical evidence and accompanying certification for plaintiffs.

Further, plaintiff Rebecca Meades dismissed her claims with prejudice in a previously filed diet drug lawsuit captioned "Dianne F. Jefferson, et al. v. American Home Products Corporation, et al." A copy of the Jefferson dismissal is enclosed for your convenience. I have also enclosed a Stipulation for dismissal of the claims raised by Rebecca Meades in this lawsuit, which I ask that you please sign and return to me.

Sincerely, BUTLER, SNOW, O'MARA, STEVENS CANNADA, PLLC Stephanie M. Rippee

STIPULATION AND PRETRIAL ORDER NO.

AND NOW, this __ day of _________, 2003, it is hereby STIPULATED, ORDERED, ADJUDGED and DECREED, pursuant to Federal Rule of Civil Procedure 41(a)(1)(ii), that the claim of Plaintiff Rebecca Meades in the above-captioned case is hereby dismissed with prejudice as to all named defendants, with each party to bear its own costs and counsel fees.

APPROVED AND SO ORDERED.

DIANNE F. JEFFERSON, et al. PLAINTIFFS v. AMERICAN HOME PRODUCTS CORPORATION, et al. DEFENDANTS CIVIL ACTION NO. 2000-66 Circuit Court of Jeferson Country June 6, 2001

Douic Brow Jawbs, for American Home Products Corporation

Bobby Gill III, for plaintiffs

AGREED ORDER OF DISMISSAL WITH PREPUPICE

THIS MATTER came before the Court upon the joint motion ore tenus of the plaintiffs and the defendant American Home Products Corporation for entry of an order of dismissal with prejudice. The Court, being advised that all parties to this action agree that said motion should be granted and being otherwise fully advised in the premises, finds the motion well taken so that it should be GRANTED.

IT IS, THEREFORE, ORDERED, ADJUDGED AND DECREED that the claims of the following plaintiffs against any and all defendants in this civil action shall be, and hereby are, DISMISSED WITH PREJUDICE:

1. DIANNE F.JEFFERSON

2. SHIRLEY ANN ADDISON

3. BRENDA M. AINSWORTH

4. KATHRYN W. ALEXANDER

5. AMY ALLEN

6. MARTHA ALLEN

7. PAULETTE ANDERSON

8. ARETHA LYNN ANDERSON-PEGUES

9. BARBER JANE ANDREWS

10. TIFFANY P. ANDREWS

11. CAROL LYNN AZLIN

12. PEGGBE SUE BAGGETT

13. CAROLYN BAGWELL

14. DRUSSELL BAILEY

15. JEFFERY W. BAILEY

16. MARVIE LOUISE BALL

17. SHEILA BALLARD

18. DEAN W. BARBER

19. NANCY GALE BARKSDALE

20. PAMELA BARNETT

21. LINDA GAEL BDSTG

22. BARBARA J. BISHOP

23. KAREN BISHOP

24. BOBBIE REEBOBO

25. SHELBY JEAN BOLLS

26. CATHERINE BOUDREAUX

27. CAROLYN KENNEDY BOWEN

28. SHELLY BOWEN

29. DARRELLBOYD

30. THERESA BRANDON

31. KAYTY SUSAN BRETT

32. CAROLYN A. BRIDGES

33. DANNY J. BRISTOW

34. DEBBIE BRITT

35. GLENDABROTHERTON

36. SHEILA BRISCOE BROWNLEE

37. GLORIA BRYANT

38. KATHERINE BRYANT

39. JOYCE BURCHAM

40. COLLEEN M. BURGES

41. MITCHELL K. BURLESON

42. SHELIARENIA BURLESON

43. MARVILOU BURNS

44. TERESA BURNS

45. EULA BURROUGHS

46. ELIZABETH BYRD

47. MARILYN CAMPBELL

48. LISACARADINE

49. JULIEHARLOW CARRUTH

50. SONYA RENEE CASE

51. CAROLYN JEAN CAUTHEN

52. DEWAJNE GAIL CAUTHEN

53. RHONDA CAYSON

54. DIANNA MARSHALL CHANDLER

55. LISA ANN CHISM

56. BRENDA K. CHRISTIAN

57. DEBBIE LYNN CLANTON

58. ROBERTA M. CLAPHAM

59. GLORIA CLAY

60. LISA CAROL CLAYTON

61. GLORIA JEAN COBB

62. ANGELA G. COGGINS

63. CONNIE COKER

64. LILLIECONLEY

65. JENNIFER ESTESS COOPER

66. ARIANAE B. COPELAND

67. JUDITH A. CORNELL

68. LAWRENCE COULTER, JR.

69. JOAN COX

70. DORIE KELLY CROUCH

71. SALLY ANN CROWELL

72. CAROL RENA CUMMMGS

73. PAMELA K. DAHLEM

74. JANICEDABBS DAVENPORT

75. CAROL J. DAVIS

76. CHRISTOPHER SHANE DAVIS

77. DANA DAVIS

78. MICHAEL AUSTIN DAVIS

79. SONYAGAYLE DAVIS

80. STACY DILLARD DAVIS

81. GLENN L. DAWSON

82. NELLIE DELASHMIT

83. CYNTHIA DARLENE DEMPSEY

84. JANICE DENNIS

85. ALANA DeVAUGHN

86. JANICE L. DOTSON

87. RUBEN THOMAS DOTY, SR.

88. JOYCE T. DOZIER

89. KARYDUNCAN

90. HEDDI M. DUNN

91. DACIA S. DURR

92. CONNIE BROCK EATON

93. CHRISTINE ECKFORD

94. PAMELA ANN EDLIN

95. DEBRA ANN EDMONSON

96. MILDRED MAY EDMONSON

97. CAROL EDWARDS

98. EMILY C. EDWARDS

99. VIRGINIA ELLIOTT

100. MELISSAELLIS

101. SUSAN M. ERICKSON

102. CLYDE VERNONESTRIDGE

103. ANGELIA FUTATO EVERETT

104. KITZI MEADOR FABRE

105. LAUREB ANN FARMS

106. JANET M. FBLGO

107. MILDRED W. FITZPATRICK

108. VINCENT T. FLESHER, JR.

109. AVIE E. FLOYD

110. LINDA S. FLOYD

111. DANA R. FORTINBERRY

112. SHIRLEY ANN FOSTER

113. KAREN TANT FRANCIS

114. LANA MURPHY FRANKS

115. DE YAMPERT BRAME GARNER

116. ERNEST LEVI GARNER, III

117. MARY CHARLENE GARRETT

118. KAREN LYNN GARRISON

119. GAIL RUTLAND GENO

120. PAMELA JEAN GENTRY

121. VICKI M. GENTRY

122. ETTA ELIZABETH GILL

123. PAIGEE.GILL

124. WENDY G. GELLESPIE

125. PAM A. GIPSON

126. KIM GOLDEN

127. ELIZABETH MARIE GRAHAM

128. JANET GRAHAM

129. GLENDA SUE GRAY

130. THERESA C. GRAY

131. BRENDA J. GREAR

132. TANYA M. GRIFFIN

133. HAZEL GRISHAM

134. JEAN GUNTHARD

135. JENNIFER KL HALE

136. MELINDAHALLMAN

137. JENNIFER HAMM

138. MISTY D. HAMPTON

139. DEBORAH RENE HANKINS

140. MARTHA ALICE HANKMS

141. CHRISTY MICHELLE HARGETT

142. MARGARET SUSAN HARLOW

143. ELLA W. HARMON

144. AMELIA ELIZABETH HARRIS

145. DEBORAH HATHCOCK

146. LORI ANN HAYES

147. SUSAN HEARD

148. ELIZABETH HEAJRN

149. TAMMY DeANGELO HELENIAK

150. MYRNA HENDERSON

151. MELINDA S. HENDRICK

152. LOIS ANN HERRON

153. CHARLOTTE A. HESTER

154. PEGGY HESTER

155. KEN HIGGINBOTHAM

156. BENNY R. HILL

157. DAVID CLAYTON HILL

158. KRISTYHILLMER

159. NELLIE HELLMBR

160. PATRICIA HOGUE

161. CYNTHIA HOLLEY

162. ELIZABETH HOLLOWAY

163. JANICEL YNNHOLT

164. SUSAN HOLT

165. FRANCES R. HOOPER

166. DEBBIEHUEY

167. DAWN JOHNSON HUGHES

168. PATRICIA HUGHES

169. GLENDA JEAN HUMPHREY

170. DENA ANN HYATT

171. SUSAN DIANNEIRVING

172. DIANNE JACKSON

173. BILLY GENE JOHNSON

174. DORRIS F. JOHNSON

175. SANDRA D. JOHNSTON

176. CHRISTINE S. JOLLY

177. DANNY GENE JONES

178. DEBRA L. JONES

179. MARGIE R. JONES

180. NANCY D.JONES

181. SHERRY JONES

182. STACI KARAM

183. DEBRA M. KEETON

184. TERRI KEITH

185. SHAUNNARENE KENNEDY

186. JERRY DAYMONKEOWN

187. CHARLIE MAE KILPATRICK, INDIVIDUALLY AND AS REPRESENTATIVE OF THE HEIRS AT LAW OF WILLIAM KILPATRICK

188. AMY RACHEL KMBLE

189. SONYA KIMBLE

190. AMANDA L. KMBROUGH

191. BARBARA C. KING

192. KRISTIK.KING

193. PATRICIA D. KING

194. SARAH LACAZE

195. REBECCA JO LADNER

196. ROSE LAMBERT

197. GINGER MICHELLE LANGLEY

198. TERRY J. LARABEE

199. DELORIS LATHAM

200. JUDITH ANN LATHAM

201. SUZANNES.LEE

202. BRANDY LEOPARD

203. JACQUELINE LEOPARD

204. NELL A. LEWIS

205. PATRICIA ANN LEWIS

206. DONNA HOPE LINDSEY

207. DOROTHY J. LINEBERRY

208. DEBBIE LINZELL

209. ABBEY H. LISHMAN

210. CYNTHIA LLOYD

211. SHERRY LOCKHART

212. ANNIE M. LOVE

213. PAMELA L. MacKENZIE

214. BRENDAMANLEY

215. SUSAN GAIL MARSHALL

216. TERESA MARSHALL

217. LESLIE BETH MART

218. MARY MASK

219. SHIRLEY MATTHEWS

220. JEAN MAULDIN

221. CANDICE L. MAXWELL-EDWARDS

222. VELVEETALARSHAYMAY

223. WILLIAM N. McARTHUR

224. PAMELA D. McCALEB

225. RITA R. McCLAIN

226. KIMBERLY McCRELESS

227. SANDRA DANIEL McCULLOUGH

228. ANGIE L. McDONALD

229. VICKI FOWLER McDONALD

230. ANNIE BEE McFARLAND

231. DOROTHY JEAN McGEE

232. VIRGINIA McKEE

233. DONNA CONN McMAHON

234. JOSEPHINE McMLLIAN

235. JENNIFER LEIGH McMINN

236. LISA OWEN McNABB

237. REBECCA MEADES

238. WAYNE ALAN MGACZ

239. BETSY LINDLEY MILLER

240. DEMETRIA MILLER

241. SUSANNE MILLER

242. BESSIE MILLS

243. MARY JONES MONTGOMERY

244. MCHELLE MORRIS

245. SYBIL L. MUIRHEAD

246. LISA MURPHREE

247. DORIS NAIL

248. JOHN D. NAIL

249. GERTIE NEWMAN

250. JULIE NIBLETT

251. DEBRA KAY NICHOLS

252. JEREMIAH DeWAYNE NICHOLS

253. SHELIA NICHOLS

254. VICKEYLAMBNORRIS

255. KRISTYLYNNNUGENT

256. VERONICA RACHELLE OSBEY

257. MARY S. PACE

258. PAULA RENA PAGE

259. LETITIA PAYNE

260. DOROTHY PETERS

261. CHARLOTTE PETTY

262. TRELUY PETTY

263. JANE PHELPS

264. JOYCE PHILLIPS

265. JUDY SHOEMAKER PHILLIPS

266. JUNE A. PHILLIPS

267. PAM PHILLIPS

268. KRISTI PITCOCK PIERCE

269. KATHY PIPKINS

270. REGMA D. POE

271. ELIZABETH SUE PORTER

272. MCHELLE LUCILLE POWELL

273. DARRELL RAKESTRAW

274. DANA P. RAMEY

275. BRENDASHARON RANDOLPH

276. JULIE C. RATH

277. JOSSIE REDMOND

278. MICHELLE CAROL REEDY

279. W. REX REESE

280. ANGELA Y. RICE

281. LYLE RICHARDSON

282. MAUDIE RICHARDSON

283. JILL RILEY

284. SHERRY L. RILEY

285. DEMETRIA ROBBINS

286. MARGARET ANN ROBBINS

287. SASHEKA LYNAE ROBBINS

288. CYNTHIA R. ROBERTS

289. WANDA ROBERTS

290. PEGGIE JONES ROBINSON

291. JANNIE ROBY

292. MARINDAROBY

293. TRACYROBY

294. ARTERIARODRIGUEZ

295. LaVONNE ROGERS

296. LORA GLENN ROGERS

297. PAMELA ROGERS

298. TONIA R. ROGERS

299. BARRONMACKROTENBERRY

300. NELLIE MARIE RUSHING

301. TAMMIE LEIGHANNE RUTLEDGE

302. MORANDA SAMPLE

303. SHELIA ANN SANCILLO

304. TONY ANDREW SANCILLO

305. JOANN SANDERS

306. AMANDA SAVAGE

307. LERONDA SAVAGE

308. NENA SCOTT

309. CYNTHIA SELF

310. BETTYE JO SEXTON

311. CARLAS ANN SEXTON

312. LLOYD DAVID SEXTON

313. EVELYN SHUMPERT

314. MARY SIMPSON

315. DANNY L. SMITH

316. KENNETH SMITH

317. PEGGY SMITH

318. PATSY SPARKS

319. KMBERLY SPENCER

320. CYNTHIA T. STALLINGS

321. MARSHA P. STEPP

322. RHONDA STEVANS

323. RHODORA STEWART

324. JOSEPH Y. STINGLEY

325. ELAINE STRAUGHTER

326. STACY N. STREET

327. DOROTHY STRICKLAND

328. MARY KATHLEEN STROUD

329. CHERYLANNSULLINS

330. MARY KATE SWINDLE

331. MICHAEL R. SWORDS

332. SUZANNETACKER

333. DANA LEIGH TACKETT

334. SONIA LaBETH TACKITT

335. TAMMY WADE TADLOCK

336. ANGELA DORIAN TAYLOR

337. CAROL THOMAS

338. CHARLOTTE THOMAS

339. LOIS THOMAS, INDIVIDUALLY AND AS THE WRONGFUL DEATH BENEFICIARY OF WANDA E. HURSSEY, DECEASED

340. LUCINDA THOMAS

341. PATRICIA RENEE THOMAS

342. EARLINE T. THOMPSON

343. SHARRONNICOLE THOMPSON

344. TRACEY LYNN THOMPSON

345. VERA V. THURMAN

346. LISA J. TIMMONS

347. BARBARA LYNN TODD

348. ELIZABETH TURNER

349. CAROLYN TUTOR

350. MARTHA KAYTYNES

351. ROGER D. VANLANDINGHAM

352. JANET FARISH VEAZEY

353. DAWN VENTURA

354. MARYF.VINTRINI

355. MINNIE SUE WADE

356. VICKI CHAMBLEE WALKER

357. FRANKIE WALLACE

358. EARLENE WALTON

359. LINDA ANN WARREN

360. YULONDA WASHINGTON

361. DEBORAH ANNA WATERMAN

362. FRANKIE MARIE WATSON

363. JANE WATSON

364. ROBERT L. WATTS

365. LEE FLORA WAYNE

366. JUDY G. WEAVER

367. STEVEN WEEKS

368. ANNIE WELCH

369. CHARLOTTE A. WELCH

370. NINA WELCH

371. CHRISTI WHALEY

372. JESSIE D. WHIRLEY

373. SHANA WHISE

374. ARLESIA WHITE

375. KIMBERLY WHTTE

376. NELLIE WHITE

377. DORIS ANN WHTTFBBLD

378. DEBORAH A. WHITTINGTON

379. TAMMY H. WILEY

380. TAMMIE COOK WILKERSON

381. GEORGIA WILLIAMS

382. GERALD W. WILLIAMS

383. BRENDA WILSON

384. MARY QUANA WINDERS

385. PAUL H. WINDHAM

386. JANICE WOOD

387. BMMLY M. WOOTEN

388. JANICE WRIGHT

SO ORDERED.

AGREED AND APPROVED. EXHIBIT B

ARNOLD PORTER Geoffrey J. Michael Geoffrey_Michael@aporter.com

202,942,6592 202,942,5999 Fax 555 Twelfth Street, NW Washington, DC 20004-1206

September 5, 2003

VIA FEDERAL EXPRESS

Nancy Guy Armstrong, Esquire Armstrong Guy Law Firm, L.L.C. 626 Delaware Avenue McComb, MS 39648

Re: Katie R. Murray, et al. v. Wyeth Corp., et al., MDL Case No. 03-20220

Dear Ms. Armstrong:

I am in receipt of the fact sheets you served in the above-referenced case. As you know, the complaint in this case alleges that Katie Murray, Rebecca Meades, and Janet Thrash meet the National Settlement's definition of primary pulmonary hypertension ("PPH"). In a letter dated July 8, 2003, pursuant to PTO 2383, Wyeth requested that you produce within thirty days a complete set of medical evidence upon which Ms. Murray and Ms. Thrash rely to establish PPH as defined by the Settlement Agreement. In that letter, we also informed you that Ms. Meades had previously dismissed her claims against Wyeth with prejudice in the Diane Jefferson case and provided you with a copy of that dismissal.

To date, you have responded to neither our 2383 request for medical evidence nor our request that you stipulate to the dismissal of Rebecca Meades. Nevertheless, the fact sheets that you have provided make it clear that neither Ms. Murray nor Ms. Thrash meet the Settlement definition of PPH. Ms. Murray and Ms. Thrash each clearly state on page 17 of their respective fact sheets that they have moderate mitral regurgitation. As such, they each fail part 2(a) of the definition of PPH, which requires ruling out the existence of "valvular disease (other than . . . trivial, clinically insignificant left-sided valvular regurgitation)." See Report and Recommendation No, 6 of the Special Master (5/9/03) (enclosed).

Therefore, I am enclosing an agreed order dismissing the claims of Rebecca Meades with prejudice and another dismissing the claims of Katie Murray and Janet Thrash without prejudice that I ask you to sign and return to me. Please call me if you have any questions.

Sincerely,

Geffrey J. Michael

STIPULATION AND PRETRIAL ORDER NO.

AND NOW, this __ day of _______, 2003, it is hereby STIPULATED, ORDERED, ADJUDGED, and DECREED, pursuant to Federal Rule of Civil Procedure 41(a)(1)(ii), that the claims of Plaintiff Rebecca Meades in the above-captioned case are hereby dismissed with prejudice as to all named defendants, with each party to bear its own costs and counsel fees.

STIPULATION AND PRETRIAL ORDER NO.

AND NOW, this __ day of _______, 2003, it is hereby STIPULATED, ORDERED, ADJUDGED, and DECREED, pursuant to Federal Rule of Civil Procedure 41(a)(1)(ii), that the claims of Plaintiffs Katie Murray and Janet Thrash in the above-captioned case are hereby dismissed without prejudice as to all named defendants, with each party to bear its own costs and counsel fees.

IN RE: DIET DRUGS (PHENTERMINE/FENFLURAMINE/DBXFBNPLURAMINS) PRODUCTS LIABILITY LITIGATION, THIS DOCUMENT RELATES TO: SHEILA BROWN, ET AL. v. AMERICAN HOME PRODUCTS CORPORATION MDL DOCKET NO. 1203, CIVIL ACTION NO. 99-20593 United States District Court, E.D. Pennsylvania May 9, 2003

REPORT MID RECOMMENDATION NO. 6 OF SPECIAL MASTER(AS TO MOTION TO ENFORCE PARAGRAPH 7 OF PRETRIAL ORDERNO. 1415 ABAIHST CAROL ANNETTE BRADY)

I. INTRODUCTION

On May 9, 2002, Wyeth filed a Motion to Enforce Pretrial Order No. 1415 Against class Member Carol Annette Brady ("Wyeth's Motion"), and an accompanying Memorandum ("Wyeth's Memorandum"), seeking an Order from the Court requiring Ms. Brady ("Plaintiff") to dismiss her Primary Pulmonary Hypertension ("PPH") claim and barring her from reasserting such a claim until she demonstrates that she has PPH as defined in Sections 1.46 and 1.53 of the Nationwide Class Action Settlement Agreement with American Home Products Corporation ("Settlement Agreement"). Pursuant to Paragraph 1 of Pretrial Order No. 2383, Wyeth's Motion was referred to me. See Pretrial Order No. 2383, ¶ 1.

Upon consideration of Wyeth's Motion and Plaintiff's Response, I recommend that Plaintiff be barred and enjoined from asserting her claim against Wyeth or any other Released Party because it is a Settled Claim. I also recommend that the Court enter an Order requiring Plaintiff to dismiss her current action against Wyeth.[1] Finally, I recommend denial of Wyeth's request that Plaintiff be barred from reasserting her PPH claim unless she first demonstrates that she is qualified to do so under the Settlement Agreement.[2]

II. BACKGROUND

A. Settlement Agreement

On August 28, 2000, the Honorable Louis C. Bechtle entered Pretrial Order No. 1415, certifying a nationwide class and approving the Settlement Agreement pursuant to Federal Rule of. Civil Procedure 23.See Pretrial Order No. 1415. Pursuant to Pretrial Order No. 1415, Class Members who have not timely and properly exercised opt-out rights are barred and enjoined from assarting and prosecuting "Settled Claims" against Wyeth or any other Released Party. See Pretrial Order No. 1415, 17. The term "Settled Claims" is defined as:

any and all claims, including assigned claims, whether known or unknown, asserted or unasserted, regardless of the legal theory, existing now or arising in the future by any or all members of the Settlement Class arising out of or relating to the purchase, use, manufacture, sale, dispensing, distribution, promotion, marketing, clinical investigation, administration, regulatory approval, prescription, ingestion, and labeling of Pondimin® and/or Redux™, alone or in combination with any other substance, including, without limitation, any other drug, dietary supplement, herb, or botanical.

See settlement Agreement, § 1.53, at 12.[3] Settled Claims, however, do not include those claims based on diagnoses of PPH:

Notwithstanding the foregoing, Settled Claims do not include claims based on PPH, including claims for compensatory, punitive, exemplary or multiple damages based on PPH; provided, however, that if a Class Member receives settlement benefits from Fund B, he/she may not bring a lawsuit based upon a claim for PPH, unless the Class Member was diagnosed with PPH before the Class Member had left-sided heart valve abnormalities (other than those which produce trivial, clinically insignificant left-sided regurgitation) or Endocardial Fibrosis. . . . Settlement Agreement, § 1.53, at 13

(emphasis added). The Settlement Agreement defines PPH, in pertinent part, as follows:

B. For a diagnosis based on examinations and clinical findings prior to death:

(1)(a) Mean pulmonary artery pressure by cardiac catheterization of 225 mm Hg at rest or

30 mm Hg with exercise with a normal pulmonary artery wedge pressure 15 mm Hg; or

(b) A peak systolic pulmonary artery pressure of 60 mm Hg at rest measured by Doppler echocardiogram utilizing standard procedures; or

(c) Administration of Flolan to the patient based on a diagnosis of PPH with cardiac catheterization. not done due to increased risk in the face of severe right heart dysfunction, and

(2) Medical records which demonstrate that the following conditions have been excluded by the following results:

(a) Echocardiogram demonstrating no primary cardiac disease including, but not limited to, shunts, valvular disease (other than tricuspid or pulmonary valvular insufficiency as a result of PPH or trivial, clinically insignificant left-sided valvular regurgitation), and congenital heart disease (other than patent foramen ovale); and

(b) Left ventricular dysfunction defined as LVEF 40% defined by MUGA, Echocardiogram or cardiac catheterization; and

(c) Pulmonary function tests demonstrating the absence of obstructive lung disease (FEV/FVC 50% of predicted) and the absence of greater than mild restrictive lung disease (total lung capacity 60% or predicted at rest); and

(d) Perfusion lung scan ruling out pulmonary embolism; and

(e) If, but only if, the lung scan is indeterminate or high probability, a pulmonary angiogram or a high resolution angio computed tomography scan demonstrating absence of thromboembolic disease; and

(3) Conditions known to cause pulmonary hypertension including connective ti0sua disease known to be causally related to pulmonary hypertension, toxin induced lung disease known to be causally related to pulmonary hypertension, portal hypertension, significant obstructive sleep apnea, interstitial fibrosis (such as silicosis, asbestosis, and granulomatous disease) defined as greater than mild patchy interstitial lung disease, and familial causes, have been ruled out by a Board-Certified Cardiologist or Board-Certified Pulmonologist as the cause of the person's pulmonary hypertension.

See Settlement Agreement, § 1.46, at 8-9 (citations omitted). Pursuant to this definition, plaintiffs may assert PPH claims against Wyeth or any other Released Party only if their diagnoses meet these specific criteria.[4]

B. The Parties' Arguments

In this matter, Wyeth seeks the enforcement of Paragraph 7 of Pretrial Order No. 1415, which bars and enjoins Class Members who do not exercise their opt-out rights from pursuing Settled Claims. See Pretrial Order No. 1415, ¶ 7. Wyeth contends that Plaintiff's PPH claim is a Settled Claim because her medical condition does not meet the definition of PPH in Section 1.46.a. of the Settlement Agreement. Specifically, Wyeth argues that although Plaintiff appears to satisfy Parts I and III of the PPH definition, she fails to satisfy Part II due to a June 23, 2001 echocardiogram report, signed by A. Razzak Tai, M.D. See Wyeth's Memorandum at 4-5, Exhibit D; see also Settlement Agreement, § 1.46.a. (2)(a), at 9. This-report shows that Plaintiff was diagnosed as having moderate mitral regurgitation and moderate aortic insufficiency, which must be excluded. See id.

Wyeth also argues that Plaintiff is attempting to rely upon one echocardiogram to satisfy Part I (b) of the PPH definition and another echocardiogram to satisfy Part II(a) of the PPH definition. see Wyeth's Memorandum at 4-5. According to Wyeth, Plaintiff must rely upon the results of only one echocardiogram. see id. That is, Plaintiff cannot mix and match echocardiogram reports to meet Parts I and II of the PPH definition. See id. Thus, Wyeth argues that Plaintiff has not produced the requisite objective medical evidence to demonstrate that no primary cardiac disease has been excluded, as required by Part II(a) of the PPH definition. See id. at 4.

In response, Plaintiff argues that her medical condition satisfies all parts of the PPH definition, [6] including Part II(a), because she has "produced an echocardiogram demonstrating no primary cardiac disease . . . including valvular disease. . . ." See Plaintiff's Response and Memorandum in Opposition to Defendant Wyeth's Motion to Enforce Pretrial Order No. 1415 Against Class Member Carol Annette Brady ("Plaintiff's Response") at 2, 4.[7] An echocardiogram performed on July 16, 2001 by Naresh K. Parikh, M.D., a Board-Certified Cardiologist, indicates that Plaintiff had "[n]ormal aortic and mitral valves." See id., at 4-5.

Further, Plaintiff contends that the June 23, 2001 echocardiogram report signed by A, Razzak Tai, M.D., a Board-Certified Cardiologist, also meets Part II(a) of the PPH definition because diagnoses of moderate mitral regurgitation and moderate aortic insufficiency do not qualify as "primary" cardiac disease. See id. at 5-6. In support, Plaintiff argues, among other things, that Steven Stogner, M.D., a Board-Certified Pulmonologist, determined that "[t]he [June 23, 2001] echo report . . . noted no primary cardiac disease including intracardiac shunts or valvular disease other than insignificant mitral regurgitation and aortic insufficiency." See id. at 6-7. Finally, Plaintiff argues that any question regarding the interpretation of her echocardiograms is a question that should be decided by a jury, See id. at 9-10.

On June 4, 2002, Wyeth filed a Reply, stating that Plaintiff does not meet the PPH definition "because the very echocardiogram describing her as having the requisite pulmonary artery systolic pressure under Part 1 of the definition also described her as having significant valvular regurgitation, which disqualifies her under Part 2." See Reply of Wyeth to Plaintiff's Response and Memorandum in Opposition to Defendant Wyeth's Motion ("Wyeth's Reply") at 1. In support, Wyeth explains that while Plaintiff's June 23, 2001 echocardiogram report satisfies Part I(b) of the PPH definition, it does not satisfy Part II (a) of the definition, see id. at 2-5. Wyeth further explains that while Plaintiff's July 16, 2001 echocardiogram report satisfies Part II(a) of the PPH definition, it does not record the peak systolic pulmonary artery pressure needed to satisfy Part Kb) of the PPH definition, See id. Wyeth argues that Plaintiff cannot "cut and paste together a qualifying echocardiogram report" to satisfy the PPH definition, as ic "manipulates the Settlement Agreement to find PPH where it doesn't exist." See id. at 2.

Additionally, Wyeth argues that moderate mitral regurgitation and moderate aortic insufficiency are not "clinically insignificant" by definition and, therefore, Plaintiff's June 23, 2001 echocardiogram cannot satisfy Part II (a) of the PPH definition. See id. at 6-11. Finally, Wyeth contends that Part II of the PPH definition calls for the production of specific medical evidence based on certain medical tests to exclude particular conditions. See id. Unlike Part III of the PPH definition. Part II does not permit an interpretation of medical evidence to substitute for actual medical evidence. See id.

On July 22, 2002, I heard oral arguments. See Tr. of Teleconference Dated July 22, 2002. During the teleconference, I directed counsel for Plaintiff to submit information about the qualifications of the doctors who interpreted the echocardiograms at issue, see id. at 18. I also directed counsel for Plaintiff and Wyeth to submit supplemental briefs regarding the burden associated with substantiating Wyeth's entitlement to injunctive relief. See id. at 6, 19.

As requested, on July 31, 2002, the parties submitted supplemental briefs. See Letter Dated July 31, 2002, from Daniel W. Sigelman, Esquire to Special Master Gregory P. Miller, Esquire; Wyeth's Supplemental Memorandum in Support of Its Motion to Enforce PTO 1415 Against Class Member Carol Annette Brady ("Wyeth's Supplemental Memorandum). According to Plaintiff, Drs. Tai and Parikh are Board-Certified Cardiologists. Additionally, Plaintiff argues that Wyeth should bear the burden of persuasion in overcoming the legal presumption that Plaintiff is entitled to proceed in her state court action unencumbered by the injunction in Pretrial Order 1415. See id. at 1-4. Wyeth contends that, while it bears the burden of persuasion "to convince the Court to enter an enforcement order in a particular case[,]" Plaintiff bears the burden of production "to produce evidence that she in fact meets the Settlement definition of PPH." See Wyeth's Supplemental Memorandum at 2. Wyeth also contends that the ultimate issue in Plaintiff's case is one of contract interpretation, which should be decided as a matter of law. See id. at 3-4.

On February 11, 2003, I heard additional oral arguments from the parties about the interpretation of the PPH definition and the use of more than one echocardiogram report to satisfy Parts I and II of the PPH definition. See Tr. of Feb. 11, 2003 Teleconference. Michael D. Pishbein, Esquire, Class Counsel to the Settlement Class, participated in the teleconference.[8] In addressing the issue of reliance on multiple echocardiograms to satisfy the PPH definition, Mr. Pishbein stated that, as a matter of contract interpretation, it would be inappropriate to permit the combination of the results of multiple echocardiograms to satisfy Parts I (b) and II (a) of the PPH definition. See id. at 14-15. Specifically, Mr. Fishbein explained that when there is no cardiac catheterization to determine pulmonary artery pressure, an echocardiogram should be read to diagnose both the right-side of the heart (per Part I (b) of the PPH definition) and the left-side of the heart (per Part II (a) of the PPH definition) in concert. See id.

III. DISCUSSION

Under Pretrial Order No. 2383, 1 must determine whether a putative PPH plaintiff's medical condition meets the PPH definition in the Settlement Agreement. See Pretrial Order No. 2383, ¶ D. In most oases, this requires only a comparison of a plaintiff's medical evidence to the PPH definition or the checklist attached as an exhibit to Pretrial Order No. 2383. See id. at ¶ 12. The instant case, however, requires the interpretation of the PPH definition regarding whether a plaintiff may rely on certain parts of two separate echocardiogram reports co establish a diagnosis of PPH. I also must determine whether a Board-Certified Pulmonologist's opinion that diagnoses of moderate mitral regurgitation and moderate aortic insufficiency are "insignificant" meets Part II (a) of the PPH definition.

As stated by the Third Circuit Court of Appeals in In re Cendant Corporation Prides Litigation, 233 P.3d 188 (3d Cir. 2000), basic contract principles apply to settlement agreements. See id. at 193. See also Plymouth Mut. Life, Ins. Co. V. Illinois Mid-Continent Life Ins. Co. of Chicago, Illinois, 378 F.2d 389, 391 (3d Cir. 1967) (applying basic contract principles in construing settlement agreement); MCI Teleeommunications Corp. v. Performance Fifty Corp., CIV. A. No. 88-9181, 1989 WL 86217, at *1 (E.D.Pa. July 31, 1989) ("A settlement: agreement is a contract and therefore subject to the rules of contract interpretation."). Chief among the principles of contract law is effectuation of the parties' intent, See Constitution Bank v. Kalinowski, 38 F. Supp.2d 384, 385 (E.D.Pa. 1999). Where the terms of a contract are clear, the plain language of the settlement agreement controls and the intent of the parties is determined by the settlement agreement alone. See Plymouth Mut., 378 F.2d at 391;Constitution Bank, 38 F. Supp.2d at 385-86.

"A contract is to be enforced so as to give effect to the reasonable expectations created by the parties in entering into the bargain."Walther Cie v. U.S. Fidelity Guaranty Co., 397 F. Supp. 937, 941 (M.D.Pa. 1975). Proper interpretation of a settlement agreement "requires consideration of 'the situation of the parties, the attendant circumstances and the ends they sought to achieve.'" see Constitution Bank, 38 F. Supp.2d at 386 (citation omitted). See also Chadwick v. Capital Advisors, Inc., Civ.A. No. 89-0144, 1992 WL 121616, at *5 (E.D.Pa. May 26, 1992) ("In construing a contract, the intention of the parties is paramount[,] and the court will adopt an interpretation which under all the circumstances ascribes the most reasonable, probable and natural conduct of the parties, bearing in mind the objects manifestly to be accomplished.").

In interpreting the PPH definition, I have concluded that a putative PPH plaintiff cannot rely on pieces of che results of more than one echocardiogram to satisfy Parts 1(b) and 11(a) of the PPH definition. In reaching this conclusion, I considered the plain terms of the Settlement Agreement as well as the positions of Wyeth and Class Counsel regarding the application of the PPH definition. Although the PPH definition is silent regarding whether a plaintiff may rely on more than one echocardiogram report to establish PPH, Wyeth and Class Counsel, through Mr. Fishbein, agree that one complete echocardiogram report is required to satisfy Parts I (b) and II (a). Moreover, Wyeth and Class Counsel agree that this interpretation is consistent with the medical components of a PPH diagnosis. See Tr. of Feb. 11, 2003 Teleconference, at 14-17. Thus, I have concluded that requiring one source of proof to meet Parts I (b) and II (a) effectuates the reasonable expectations and intent of the parties. To conclude otherwise would permit plaintiffs to circumvent the terms of the Settlement Agreement and pursue causes of actions based on Settled Claims.[9]

Plaintiff's action is pending in the Second Judicial District of the Circuit Court of Jones County, Mississippi.

I do not find that this case warrants my recommendation of additional remedies as permitted under Paragraph 9 of Pretrial Order No. 2383. See Pretrial Order No. 2383.

All of the definitions and terms of the Settlement Agreement were adopted by the Court in Pretrial Order No. 1415. See Pretrial Order No. 1415, ¶ 1.

On January 4, 2002, the Court entered Pretrial Order No. 2337, which solicited comments and/or objections to a proposed Pretrial Order for resolving Motions to Enforce Pretrial Order No. 1415. See Pretrial Order No. 2337. Various parties submitted objections to the proposed Pretrial Order. The Objectors challenged, among other things: (1) the jurisdiction and authority of the Court to enforce Paragraph 7 of Pretrial Order No. 1415; (2) the definition of PPH, as outlined in the Settlement Agreement; (3) the time limitations in enforcing Paragraph 7 of Pretrial Order Ho. 3.415; (4) the burden of proof or persuasion in enforcing Paragraph 7 of Pretrial Order Ho. 1415; and (5) the imposition of sanctions on parties. On January 28, 2002, Wyeth responded to the objections.

On January 30, 2002, the Court heard oral arguments from counsel for Wyeth. Class Counsel to the Settlement Class, and various Objectors. Thereafter, on February 26, 2002, the Court entered Pretrial Order No. 2383, which established the procedure for resolving Motions to Enforce Paragraph 7 of Pretrial Order No. 14 IS against Class Members asserting alleged PPH claims against Wyeth or any other Released Party, See Pretrial Order No. 2383.

I am forwarding for the Court's convenience copies of the parties' submissions and the transcripts of the July 22, 2002 and February 11, 2003 Teleconferences.

Plaintiff points out that "Wyeth concedes that Plaintiff Brady meets Parts (1) and (3) of the PPH definition in the Settlement Agreement,"See Plaintiff's Response and Memorandum in Opposition to Defendant Wyeth's Motion to Enforce Pretrial Order No. 1415 Against Class Member Carol Annette Brady at 3.

Plaintiff's echocardiograms include: U) March 31, 2000 echocardiogram interpreted by Dr. Lawrence J. Leader; (2) June 23, 2001 echocardiogram interpreted by Dr. A. Razzak Tai; and (3) July 16, 2001 echocardiogram interpreted by Dr. Naresh K. Parikh. Plaintiff relies on the results of her June 23, 2001 echocardiogram to satisfy Part I(b) of the PPH definition and the results of her June 23, 2001 and/or July 16, 2001 echocardiograms to satisfy Part II(a). See Plaintiff's Response at 3-9. Plaintiff also points out that Dr. Leader diagnosed her with "borderline pulmonary hypertension." See id. at 2, n. 2.

Wyeth and Class Counsel are signatories to the Settlement Agreement.

Recently, the Court entered Pretrial Order No. 2793, which addresses a similar issue. See Memorandum and Pretrial Order Ho. 2793. Therein, the Court ruled that a plaintiff could not mix and match cardiac catheterization results to satisfy the pulmonary artery pressure and pulmonary artery wedge pressure requirements of Part I(a) of the PPH definition, see id. at 4-5. The Court found that a reasonable interpretation of the PPH definition would not permit a plaintiff to mix and match pressure readings that "could be obtained weeks, months, or even years apart." See id.

Plaintiff has failed to establish that her medical condition meets Part II(a) of the PPH definition. First, Plaintiff has not produced one echocardiogram report that meets both Part Kb) and Part II(a) of the PPH definition. While Plaintiff's June 23, 2001 echocardiogram report establishes that she meets Part I (b) of the PPH definition, it also shows that Plaintiff was diagnosed as having, among other things, "moderate mitral regurgitation" and "moderate aortic insufficiency." Thus, the results of this echocardiogram fail to meet Part II (a) of the PPH definition. Likewise, despite the fact that Plaintiff's July 16, 2001 echocardiogram report demonstrates "no primary cardiac disease," as required by Part II(a) of the PPH definition, Plaintiff's peak systolic pulmonary artery pressure was not recorded. Thus, Plaintiff's July 16, 2001 echocardiogram results do not satisfy Part I(b) of the PPH definition.

Second, Plaintiff's argument that "moderate mitral regurgitation" and "moderate aortic insufficiency" are clinically insignificant is unpersuasive. Part II(a) of the PPH definition requires, by echocardiogram, the exclusion of primary cardiac disease, including "valvular disease (other than . . . trivial, clinically insignificant left-sided valvular regurgitation)." See § 1.46.a.1., at 9. The plain meaning of the phrase "trivial, clinically insignificant left-sided valvular regurgitation" does not include diagnoses of moderate mitral regurgitation and moderate aortic insufficiency. In other words, "moderate" does not mean "trivial" or "clinically insignificant." Additionally, Part II(a) of the PPH definition expressly requires a putative PPH plaintiff to produce medical records demonstrating that primary cardiac disease has been excluded. See id. Thus, Plaintiff cannot rely on the opinion of her Board-Certified Pulmonologist to supplant her June 23, 2001 echocardiogram report, which states that she was diagnosed with moderate mitral regurgitation and moderate aortic insufficiency.

IV. RECOMMENDATION

Plaintiff has not demonstrated that her claim against Wyeth is a non-Settled Claim. Accordingly, I recommend that Plaintiff be: (1) barred and enjoined from pursuing her current PPH claim against Wyeth; and (2) required to dismiss her pending action.

V. CONCLUSION

Any party wishing to appeal this Report and Recommendation No. 6 must file such an appeal with the Court within eleven (11) days of receipt, as permitted by Paragraph 10 of Pretrial Order No. 2383.

SO RECOMMENDED.

**EXHIBIT CMILLER ASSOCIATES*TRIAL ATTORNEYS***

Michael J. Miller — VA, MD, DC 809 CAMRON Street Patricia M. Spioer — VA, MD, NY, DC Alexandria, Virginia 23314 J. Christopher Ide — VA, MD, DC Marvis DePalmo Swarts, R.N., M.F.S. Kenneth Warren Smith — VA, DC, FL, MS Kathleen Overton, R.N., N.M.C.C., C.M.C.N. Sandra M. Rohrstaff — VA Marla J. Burt, R.N., B.S.N. Christopher A. Gomez — PA, VA Marla J. Burt, R.N., B.S.N. Christopher A.Godard — VA, MD, DC Website doctoratlaw.com Gary A. Godard — VA, MD, DC Telephone: 703,519,8080 Marian L. Beckett — VA 1,800,882,2525 Michele A. DiMartino — PA, N.J. Facsimile: 703,519,8084 Denialle L. Bridgeforth — VA Of Counsel Edward A. Williamson, MS September 15, 2003

Geoffrey Michael, Esquire Arnold Porter 555 Twelfth Street, NW Washington, DC 20004-1206

Re: Katie R. Murray, @t al v. Wyeth Corp., at al, MDL Case No. 03-20220

Dear Geoff:

Thank you for taking my phone call the other day. I received a copy of your letter to Nancy Armstrong dated September 5, 2003. In your letter you make reference to a "PTO 2383" Setter dated July 8, 2003. I am sure when you tell us your sent the letter that it was absolutely sent. However, unfortunately Ms. Armstrong's office does not have any evidence of receipt of that letter nor does our office. Pursuant to our telephone conversation of September 9, 2003, if you will kindly send me your PTO 2383 letter again, we will respond within twenty days with a certification response, (I received that letter of July 8, 2003 on Thursday after our call.)

We believe you are incorrect in your assertion that Ms. Meades case was dismissed with prejudice in the Diane Jefferson case. It is our position that the Rebecca Meades case was dismissed without prejudice in that case. In support of our position, please find enclosed a copy of the order entered June 6, 2001 by the Honorable Lemar Pickard dismissing inter alia Rebecca Meade without prejudice. Accordingly, we will not agree to dismiss Ms. Meade's case.

While we completely disagree that the Murray or Thrash case are in any way governed by the Carl Brady opinion, we nevertheless agree to dismiss those two claims without prejudice and re-file them as left-sided valve cases. If you will prepare the appropriate order for such dismissal it will be endorsed by plaintiffs' counsel.

Very truly yours,

MILLER ASSOCIATES

Michael J. Miller

ORDER

IT IS ORDERED, ADJUDGED, AND DECREED that following Adcion Nancy Gale Barksdale Gloria Bryant Dorris F. Johnson, Nancy D. Jones, Rebecca Mendes, Lora Glem Rogers, Cynthia T. Stallings, Lee Flora Wayne, Georgia Williams, Emmly M. Wooten, Complaints filed herein are dismissed without prejudice against all Defendants with each party to hear their own costs.

SO ORDERED.

EXHIBIT D

ARNOLD PORTER Geoffrey J. Michael Geoffrey_Michael@aporter.com 202.942.6592 202.942.5999 Fax 555 Twelfth Street, NW Washington, DC 20004-1206

September 16, 2003

VIA FEDERAL EXPRESS

Michael J. Miller, Esquire Miller Associates 809 Cameron Street Alexandria, VA 22314

Re: Katie R. Murray, et al. v. Wyeth Corp., et al., MDL ~~Case NO. 03-20220~~

Dear Mike:

~~Enclosed please find for~~ your signature a dismissal without ~~prejudice of Plaintiffs~~ Murray and Thrash in the above-captioned case. If you will sign the order and return it to me, I ~~will circulate the order to~~ the other parties and file it for Judge ~~Bartle's signature~~. Wyeth. of course, takes ho position at this time concerning the propriety of those~~plaintiffs filing a heart valve~~ (IOO or BEOO) claim.

As for plaintiff Meades, our June 6, 2001, orders seem to conflict. ~~I will~~ investigate this and get back to you. In the meantime, I appreciate your agreement to provide us with 2383 records by October 2, 2003 (twenty days from ~~your receipt of our~~ letter requesting records).

Thank you for your cooperation in this matter.

Sincerely,

Geoffrey J. Michael

STIPULATION AND PRETRML ORDER NO.

AND NOW, this __ day of _______, 2003, it is hereby STIPULATED, ORDERED, ADJUDGED, and DECREED, pursuant to Federal Rule of Civil Procedure 41(a)(1)(ii), that the claims of Plaintiffs Katie Murray and Janet Thrash in the above-captioned case are hereby dismissed without prejudice as to all named defendants, with each party to bear its own costs and counsel fees.

EXHIBIT E

ARNOLD PORTER Geoffrey J. Michael Geoffrey Michael@aporter.com 202.342.0352 202.942.5999 Fax 555 Twelfth Street, NW Washington, DC 20004-1208

October 9, 2003

VIA FEDERAL EXPRESS

Michael J. Miller, Esquire Miller Associates 809 Cameron Street Alexandria, VA 22314

Re: Katie R. Murray. et al. v. Wyeth Corp., et al., MDL Case No. 03-20220

Dear Mike:

Last month, you agree to provide Wyeth with PTO 2383 records for plaintiff Meades in this case by October 2, 2003. You also agreed to dismiss plaintiffs Murray and Thrash. However, to date, Wyeth has received neither the 2383 records/certification nor the signed agreed order of dismissal. If we do not receive these items in a timely manner, we will have to seek relief from the Court.

Furthermore, this case has a July 1, 2003 DID. As such, your case specific expert reports were due on October 1, 2003. Wyeth has not received these either, In light of your failure to produce 2383 records as well as to file case specific expert reports, I suggest that we adopt a new discovery schedule in this case whereby the "DID" becomes the date that plaintiff provides 2383 records, and deadlines for case specific expert reports are calculated therefrom per normal MDL tune periods. If this is acceptable to you, let me know and I will circulate an agreed order for your signature and for submission to the Special Master's office upon receipt of the 2383 records.

Sincerely,

Geoffrey J. Michael

EXHIBIT F MILLER ASSOCIATES TRIAL ATTORNEYS

October 20, 2003

Honorable Geoffrey Michael Arnold Porter 555 Twelfth Street, NW Washington, DC 20004-1206

RE: Katie R. Murray, et al. v. Wyeth. Inc., et al. Civil Action No. 2:03cv20220

Dear Honorable Michael:

I have enclosed a Stipulation and Pretrial dismissing the claims of Plaintiffs Katie Murray and Janet Thrash in the above-captioned matter, with prejudice as to all named defendants.

I need to verify that all other possible causes of PPH as to Rebecca Meades have been excluded pursuant to PTO 2383. Either Chris Ide or I will advise you this week if there are any missing medical records.

Thank you for your cooperation. Very truly yours,

MILLER ASSOCIATES

Kenneth W. Smith

IN RE DIET DRUGS (PHENTERMINE/FENFLURAMINE/DEXFENFLURAMINE) PRODUCTS LIABILITY LITIGATION, This Document pertains to: KATIE R. MURRAY, et al. PLAINTIFFS, VS. WYETH. et al. DEFENDANTS MDL Docket No. 1203, CIVIL ACTION NO. 2:03cv20220HB United States District Court, E.D. Pennsylvania

Kenneth W. SMITH, Miller Associates, Alexandria, Virginia, FOR PLAINTIFFS KATIE MURRAY AND JANET THRASH

Nancy Guy Armstrong, Armstrong Guy, LLC, McComb, MS, FOR PLAINTIFFS KATIE MURRAY AND JANET THRASH

Edward A. Williamson, Fenton B. DeWeese, The Edward A. Williamson Law Firm, Philadelphia, MS, FOR PLAINTIFFS KATIE MURRAY AND JANET THRASH

Honorable Amanda Clearman, Bryant, Clark, Dukes, Blakeslee, Ramsey Hammond, Hattiesburg, MS, for Dr. Jerry llgs

Geoffrey J. Michael, Arnold Porter, Washington, DC, for Wyeth

Whitman B. Johnson, III, Juliette V. Wilson, Currie, Johnson, Whitman, Gaines Myers, P.A., Jackson, MS, for Katherine Hensliegh, M.D.

STIPULATION AND PRETRIAL ORDER NO.

HARVEY BARTLE, III, District Judge

AND NOW, this __ day of ________, 2003, it is hereby STIPULATED, ORDERED, ADJUDGED and DECREED, pursuant to Federal Rule of Civil Procedure 41(a)(1)(ii), that the claims of plaintiffs Katie R. Murray and Janet Thrash in the above-captioned case are hereby dismissed with prejudice as to all named defendants, with each party to bear its own costs and counsel fees. This action will proceed as to the claims of the remaining plaintiff, Rebecca Meades, against defendants Wyeth (incorrectly denominated "Wyeth. Inc." in the Complaint) and Professional Weight Loss Center.

Pursuant to Federal Rule of Civil Procedure 41(a)(1)(ii)., all parties in this action who have entered an appearance have executed this dismissal through the undersigned counsel of record.

APPROVED AND SO ORDERED.

EXHIBIT G

ARNOLD PORTER Geoffrey J. Michael Geoffrey_Michael@aporter.com 202.942.6592 202.942.5999 Fax 555 Twelfth Street, NW Washington, DC 20004-1206

November 19, 2003

VIA FIRST CLASS MAIL

Kenneth Smith, Esq. Miller Associates 105 N. Alfred St. Alexandria, VA 22314

Re: In Re Diet Drugs Prod. Liab. Litig. Rebecca Meades v. Wyeth. et. al., MDL No. 03-20220

Dear Ken:

We are currently reviewing medical records you provided pursuant to PTO 2383 concerning Ms. Meades' purported diagnosis of PPH under the Settlement Agreement. In the meantime, please provide us with possible dates for Ms. Meades' deposition.

Sincerely,

Geoffrey J. Michael

EXHIBIT H

ARNOLD PORTER Geoffrey J. Michael Geoffrey_Michael@aporter.com 202.942.6592 202.942.5999 Fax 555 Twelfth Street, NW Washington, DC 20004-1206

November 19, 2003

VIA FIRST CLASS MAIL

Kenneth Smith, Esq. Miller Associates 105 N. Alfred St. Alexandria, VA 22314

Re: In Re Diet Drugs Prod. Liab. Litig. Rebecca Meades v. Wyeth. et. al., MDL No. 03-20220

Dear Ken:

I have not yet received a date from you for Ms. Meades' deposition, requested in my letter to you dated November 19, 2003. Please provide a date as soon as possible. Moreover, I wish to remind you that you had previously promised to provide us with proof of use and product identification information in this case, which we have not yet received.

I look forward to your prompt response.

Sincerely,

Geoffrey J. Michael

EXHIBIT I MILLER ASSOCIATES TRIAL ATTORNEYS

December 21, 2003

Geoffrey J. Michael, Esquire Arnold Porter 555 Twelfth Street, NW Washington, DC 20004-1206

Re: in Re Diet Drugs Prod. Liab. Litig. Rebecca Meades v. Wyeth. et at., MDL No. 03-20220

Dear Geoff:

In response to your letter dated November 19, 2003 which references a prior letter dated November 19, 2003 I send this response, Paul Guy, from Nancy Guy Armstrong's office will be covering Rebecca Meades' deposition. You will receive a call shortly from Paul Guy with potential dates for that deposition. Concerning your request for proof of use and product identification information we provide the following three affidavits.

Very truly yours,

MILLER ASSOCIATES

Micheal J. Miller

EXHIBIT J ARNOLD PORTER Geoffrey J. Michael Geoffrey_Michael@aporter.com 202.942.6592 202.942.5999 Fax 555 Twelfth Street, NW Washington, DC 20004-1206 December 31, 2003 VIA FEDERAL EXPRESS

Michael J. Miller, Esquire Miller Associates 809 Cameron Street Alexandria, VA 22314

Re: Katie R. Murray, et al. v. Wyeth Corp., et al., MDL Case No. 03-20220

Dear Mike:

I am in receipt of your letter dated December 21, 2003. The letter references three attached affidavits; however, I received no affidavits. Please send these as soon as possible.

Also, after reviewing the medical records that you provided pursuant to our PTO 2383 request, we are missing the following records that your are obligated to provide to us under PTO 2383's requirement that you provide us with all medical records relating to Ms. Murray's purported diagnosis with PPH:

• Records/tapes relating to echocardiograms performed on 5/12/03, 9/10/02, 5/27/01 and 4/2/00;

• Records relating to and the actual tracings of heart catheterizations performed on 5/12/03 (RHC), 9/9/02 (LHC) and 9/10/02 (RHC);

• Records relating to a sleep study, if any;

• Records relating to a V-Q scan, if any;

• Records relating to the exclusion of conditions known to cause pulmonary hypertension by a Board Certified Cardiologist or Pulmonologist; and

• Any other medical records' relating to Ms. Murray's purported diagnosis of PPH.

Please provide us with these additional records as well as a "certification that the information being produced is a complete set of medical evidence upon which [Ms. Murray] is relying to establish PPH" as defined in the Settlement Agreement. PTO 2383 at 5.

Finally, I await potential deposition dates for Ms. Murray from Mr. Guy, whom I have copied on this letter.

Sincerely,

Geoffrey J. Michael

MEMORANDUM AND PRETRIAL ORDER NO.

Before the court is the motion of sixty-four claimants[1] represented by attorney Talmadge Braddock to reinstate Blue Forms under the nationwide class action settlement involving Wyeth's diet drugs commonly known as fen-phen.

Under the Settlement Agreement, the AHP Settlement Trust (the "Trust") was established and funded by Wyeth to pay benefits to class members who suffered from ingesting Pondimin and/or Redux. A drug recipient making a claim was required to submit a so-called Blue Form by August 1, 2002 to register to participate in a free screening program and by May 3, 2003 to register for so-called matrix benefits from the Trust or alternatively to be eligible to exercise a back-end opt-out right. Exercising such a right permits the claimant to sue Wyeth in the tort system for compensatory, but not for punitive, damages.

Significantly, the Blue Form contained a detailed "CONDITIONAL RELEASE OF SETTLED CLAIMS AND COVENANT NOT TO SUE." In return for seeking payment from the Trust under the Settlement Agreement, the claimant released Wyeth and others from all settled claims unless the claimant later exercised a back-end opt-out right. The paragraph containing the conditional release concluded with the following sentence in bold letters: "I, THE UNDERSIGNED, HAVE CAREFULLY READ (OR HAVE HAD READ TO ME) THIS RELEASE AND COVENANT NOT TO SUE. I, THE UNDERSIGNED, BELIEVE THAT I UNDERSTAND THE TERMS OF IT, AND AGREE TO BE BOUND BY IT." Following this paragraph is the "Declaration under Penalty of Perjury" which provided in relevant part:

Declaration under Penalty of Perjury. Each person signing below acknowledges and understands that this form is an official Court document sanctioned by the Court that presides over the Diet Drug Settlement, and submitting it to the AHP Settlement Trust is equivalent to filing it with a Court. . . . Each declares under penalty of perjury that the information provided in this form is true and correct to the best of his/her knowledge, information and belief.[2]

Immediately below these words is a signature line, under which is printed "(Signature of Diet Drug Recipient, if Living)" and "(Date)."

On July 25, 2002, the Trust posted the following information about the Blue Form on the Blue Form Filers Page of its website:

It is important to make sure that all Claim Forms are as complete as possible before submitting them to the Trust. With the large number of claims currently being submitted to the Trust (particularly BLUE Forms), the Trust is concerned about patterns of deficient Claims. In response to this concern and to answer questions we have recently received regarding what is required to "register" a Class Member for benefits, please note the following:

To "register" as a Class Member for benefits under the Settlement Agreement, a Class Member must submit a timely . . . BLUE form (the "Form") containing sufficient information to demonstrate that the Form was filled out by a specific individual who is a member of the Class. To make that demonstration, theForm must contain the following:

. . .

3. The Claimant's signature on the Form.

. . .

Moreover, Class Members who delay the completion of their Claim may forfeit their entitlement to particular benefits under the Settlement Agreement . . .

C. Patton Tidmore Aff. ¶ 2 (emphasis added).

Most of the claimants who filed the pending motion not only failed to sign their Blue Forms, thereby submitting incomplete Blue Forms for registration purposes, but also failed to cure the deficiency before the passage of the two submission deadlines imposed by the Settlement Agreement. The forms were signed by Mr. Braddock, their attorney, and postmarked either July 31, 2002 or August 1, 2002.

On April 16, 2003, long after the August 1, 2002 deadline had passed, the Trust notified claimants' counsel that because the Blue Forms lacked claimants' signatures, "after preliminary review, the AHP Settlement Trust . . . deems [claimants] not registered for settlement benefits." It was not until November 3, 2003, some six months after the May 3 deadline, that the pending motion to reinstate the Blue Forms was filed.

According to Wyeth. six claimants Alisa Botto, Gay M. Davenport, Marsha Hodge, Bethany Massey, Debra A. McDade, and Bettye Mims ultimately executed the Blue Forms before May 3, 2003. The remaining claimants have never attempted to cure the deficiency.

We recognize that if a claimant shows excusable neglect, the court will not insist upon strict compliance with a deadline. The excusable neglect standard is a matter of equity and depends on "all relevant circumstances surrounding the party's omission." Pioneer Inv. Serv. Co. v. Brunswick Assoc. Ltd., 507 U.S. 380, 395 (1993). Factors to be considered include: (1) the danger of prejudice to the adverse party; (2) the length of delay and its potential impact on judicial proceedings; (3) the reason for the delay; and (4) whether the movant acted in good faith. See id.; In re Orthopedic Bone Screw Prods. Liab. Litiq., 246 F.3d 315, 322-23 (3d Cir. 2001). We are mindful that an excess of liberality in finding excusable neglect would undermine the finality of judgments in class actions and would discourage settlements. See Pretrial Order No. 2345.

The requirement that the drug recipient, if living, sign the Blue Form under penalty of perjury not only was clearly stated but was of particular significance. By executing the form, a claimant was conditionally releasing important rights and preserving the right to sue Wyeth in the tort system. If a lawyer or some other person signed the form on a claimant's behalf, it is not hard to envision, in a universe of tens of thousands of claimants, never-ending disputes over the authority of those lawyers or other persons to act. The Blue Form was designed to obviate this most unfortunate consequence. This court has emphasized on numerous occasions the importance of a claimant's own signature. See PTO Nos. 997, 1208, 1442, 2316, 3153, and 3154. The lack of a drug recipient's signature is a material omission, not a mere technicality. Without that signature, a claimant is not registered for benefits.

The fifty-eight claimants who have not executed the Blue Forms have offered no reasons, much less reasons constituting excusable neglect, for failing to do so. The requirement that the claimant sign his or her own Blue Form was stated not only on the form but also reiterated on the Trust's website prior to Mr. Braddock's last-minute filing of the Blue Forms at issue. Moreover, allowing these claimants, who have still not signed the Blue Form many months after the last deadline, to proceed at this late date will be unfairly prejudicial to Wyeth. The financial obligations of Wyeth related to this nationwide class action settlement could be adversely affected since it would allow claimants to exercise a back-end opt-out and sue Wyeth in the tort system when they are now precluded from doing so. See In re Orthopedic Bone Screw Prods. Liab. Litiq., 246 F.3d at 323. Accordingly, we will deny the motion to reinstate the Blue Forms as to the fifty-eight claimants who never signed them.

The record before the court is unclear as to the remaining six movants: Alisa Botto, Gay M. Davenport, Marsha Hodge, Bethany Massey, Debra A. McDade, and Bettye Mims. Wyeth states in its brief that they eventually signed Blue Forms before the May 3, 2003 deadline. The affidavit of Denise Kankowski, filed by the Trust, implies to the contrary. It is unclear as to what, if any, deficiencies exist as to their forms. We will hold the current motion in abeyance as to these six movants, pending receipt of additional clarifying affidavits from the Trust, Wyeth. and/or the movants concerning the status and contents of these six Blue Forms. Any such affidavits and brief supplemental legal memoranda shall be filed and served within fifteen days.

PRETRIAL ORDER NO. _____

AND NOW, this ___ day of February, 2004, for the reasons set forth in the accompanying Memorandum, it is hereby ORDERED that:

(1) the motion to reinstate the Blue Forms (Document #204390) is DENIED as to Maranie B. Adams, Patricia G. Bennett, Dina L. Berry, Linda G. Boswell, Vickie Brasher, Latonya Claxton, Elizabeth S. Conner, Jan M. Courtney, Tommie J. Crumbaker, Rena Dear, Rebecca Denton, Carreen Dodd, Michelle Fleenor, Jim Fondren, Sharron Forest, Kelly Freeland, Lisa Gierszewski, Malissa Haase, Dee M. Harvard, Shirley Haywood, Suzanne Heggins, Melissa Henderson, Tamra M. Kite, Amy Hively, Linda Holland, Susie C. Hudson, Marietta Jones, Lisa Kelly, Diana G. Kendrick, Shirley C. Lewis, Jacqueline Lockridge, Mildred Martin, Rebecca K. McCormick, Marcy L. McEntee, Ramona McShan, Phyllis Morgan, Bruce Moss, Mindi D. Mouton, Beverly Nail, Patsy Napier, William

Napier, Angelia Navarre, Misti Nethercut, Tyra L. Nunn, Deborah J. Patterson, Betti C. Perry, Shirley Perry, Donna J. Rivero, Etta Seago, Ace Smither, Rebecca K. Thornton, David C. Thrash, Carolyn J. Tolbert, Ronald E. Tolbert, Kelly 0. Travis, Molly D. Vaughn, Jeanetta P. Watson, Jacqueline D. Wilmore; and

(2) the motion is held in abeyance as to Alisa Botto, Gay M. Davenport, Marsha Hodge, Bethany Massey, Debra A. McDade, and Bettye Mims. The AHP Settlement Trust, Wyeth. and/or movants shall file and serve any affidavits concerning the status and contents of the Blue Forms of these persons, and any brief supplemental legal memoranda, within fifteen days.

The claimants are as follows:

Maranie B. Adams Shirley C. Lewis Patricia G. Bennett Jacqueline Lockridge Dina L. Berry Mildred Martin Linda G. Boswell Bethany Massey Alisa Botto Rebecca K. McCormick Vickie Brasher Debra A. McDade Latonya Claxton Marcy L. McEntee Elizabeth S. Conner Ramona McShan Jan M. Courtney Bettye Mims Tommie J. Crumbaker Phyllis Morgan Gay M. Davenport Bruce Moss Rena Dear Mindi D. Mouton Rebecca Denton Beverly Nail Carreen Dodd Patsy Napier Michelle Fleenor William Napier Jim Fondren Angelia Navarre Sharron Forest Misti Nethercut Kelly Freeland Tyra L. Nunn Lisa Gierszewski Deborah J. Patterson Malissa Haase Betti C. Perry Dee M. Harvard Shirley Perry Shirley Haywood Donna J. Rivero Suzanne Heggins Etta Seago Melissa Henderson Ace Smither Tamra M. Kite Rebecca K. Thornton Amy Hively David C. Thrash Marsha Hodge Carolyn J. Tolbert Linda Holland Ronald E. Tolbert Susie C. Hudson Kelly O. Travis Marietta Jones Molly D. Vaughn Lisa Kelly Jeanetta P. Watson Diana G. Kendrick Jacqueline D. Wilmore

This language became part of the revised Blue Form, which was approved in PTO No. 2355 on January 28, 2002. The original language, which is substantially the same, read as follows:

Declaration under Penalty of Perjury. The persons signing below acknowledge and understand that this form is an official document sanctioned by the Court that presides over the Diet Drug Settlement, and submitting it to the Claims Administrators is equivalent to filing it with a court. Each declares under penalty of perjury that all of the information provided in this form is true and correct to the best of his/her knowledge, information and belief.

SUPPLEMENTAL AFFIDAVIT

DENISE A. RUBIN; being duly sworn, hereby deposes ano says:

1. I am an attorney duly licensed to practice before the Courts of the State of New York, and am associated with the law firm Napoli Kaiser Bern Associates, LLP. counsel for the respondents herein, Dons Weller and Ellen Carey.

2. This Supplemental Affidavit, and the annexed affidavit of Paul N Hopkins, M.D. M.S.P.H, are respectfully offered in further opposition to the Motion already pending against claimants Doris Weller and Ellen Uarey to enforce this Court's anti-suit injunction as set forth in Pretrial Order 1415, paragraph 7.

3. The arguments and exhibits previously submitted on:he motion are adopted by reference here as if fully set forth herein.

4. The affidavit of Pau N. Hopkins, M.D., M.S.P.H. is annexed to this Affidavit.

5. In his affidavit Dr Hopkins, a cardiac epidemologist, explains in cetailed and unassailable fashion how the numbers that were cited to this Court in support of the Settlement Agreement were grossly incorrect, providing for no anticipated claims by patients suffering moderate mitral regurgitation with complications. These numbers, submitted by Class Counsel and produced by their experts, understated the anticipated number of claims by tens of thousands.

6. Clearly then, none of the caimants in this litigation, and particularly Ellen Carey and Doris Weller, wers sufficiently represented, as Class Counsel was basing their representations to this Court about the scope and breadth of the effects of the defendants' diet drug products en estimates that were plainly misstated by their experts.

7. Moreover, these claimants have a constitutional right to challenge a Class action settlement that was not only insufficient to protect their interests, but indeed fiat was based on glaringly faulty epidemiology and estimates from square one This Court, the claimants and their counsel were wholly misled as to the accuracy of the anticipated nunbers and the fairness of the Settlement Agreement as proffered, and justice requires that These claimants be permitted to pursue their claims.

8. As noted in the initial Opposition papers filed cm Ms. Carey's and Ms. Weller's behalf. it is well settled that absent class members may only be bound by a class action judgment they have been afforded the basic requirements of due process: meaningful notice, an opportunity to opt out. and adequate representation by class representatives and counsel. See Phillips Petroleum Co. v. Shutts, 472 U.S. 797, 811-'2.

9. Given the gross misstatement of epidemiology numbers submitted in support of the proposed Settlement Agreement, it cannot be said that Ms. Weller and Ms. Carey were given "meaningful notice" or adequate representation by the class representatives submitting those numbers to the Court.

10. Hence we offer the Hopkins affidavit on the instant motion, and ask this Court to consider its import to the instant motion. as well as to the overall climate 01 this litigation.

Sworn to before me this.

DECLARATION OF PAUL N. HOPKINS. M.D., MSPH

I, Paul N. Hopkins, M.D., MSPH, hereby declare that the following statements are true to the beat of my knowledge, information and belief:

1. I am a physician duly licensed to practice in the State of Utah. I am board certified in Public Health and General Preventive Medicine. My areas of expertise include cardiovascular epidemiology, particularly coronary artery disease risk factors, hypotension, and cardiovascular genetics. My clinical emphasis has been lipid intervention and reduction of coronary risk, I am a Professor of Internal Medicine at the University of Utah School of Medicine, Go-Director of Cardiovascular Genetics (a sub-division of the Cardiology Division), and Director of the Family Lipid Clinic in Preventive Cardiology, Annexed Is a copy of most recent Curriculum Vitae,

2. I have been asked to evaluate and analyze the methodology used by Class Counsel and their experts to predict the total number of potential claims for Fund B benefits (Matrix Benefits) that could be anticipated at the time the settlement with American Home Products Corporation was approved.

3. I have also been asked to evaluate those projections and to comment on whether they had or have today any scientific basis or rationale.

4. Drawing from my past research relating to diet drug exposure, I have also completed a meta-analysis of all of the scientifically reliable epidemiologlcal studies relating to fenfluramine anchor dexfenfluramine and valvular regurgitation. My analysis allowed me to construct a model intended to predict the prevalence of valvular regurgltation in the exposed population and includes a projection of those who would qualify for Fund B benefits based upon the presence of FDA positive mitral regurgitation accompanied by one or more of the complicating factors required by the settlement,

SUMMARY OF MY OPINION

5. Having reviewed all of the material submitted by Class Counsel to support their claims regarding the number of potential class members who could possibly qualify for Fund B benefits, I find major discrepancies between the projections made on behalf of Class Counsel and what may easily be derived from published sources. These discrepancies are of a magnitude that is difficult to believe they were made without a preconceived effort to minimize the extent of the potential damage caused by fenfluramine and dexfenfluramine.

6. I performed a meta-analysis of the prevalence and severity of valvular regurgitation including studies by Wadden.[1] Burger, [2] Dahl, [3] Kancheria, [4] Lepor, [5] Teramae, [6] Khan, [7] Weissman, [8] Shively, [9] Hensrud, [10] Ryan, [11] Gardin, [12] Jollis, [13] and Davidoff.[14] A summary of my findings are given in the table immediately below.

Estimate for settlement Hophins, 2004 Number exposed 6,000,000 6,000,000 Duration of use distribution provided by Wyeth same FDA + AR, number expected Used = 60 days 237,020 217,610 Used 60 days 85,520[***] 256,084 FDA + MR, number expected Used = 60 days 126,000 119,617 Used 60 days 0[*] 79,546 Matrix A, number expected — total 8345 Level I (severe AR+MR) 7511 21,545 Level II (moderate MR+LAE only) 834 24.350-49,161[**] Matrix 8 (use = 60 days). number — total 27,227 Level I (severe AR+MR) 24,504 27,325 Level II (moderate MR+LAE only) 2,723 36,678—74,049[**]

[*] Note that in the settlement, all MR was included only in those exposed 60 days or less and only baseline rate (2.1%) was used, rather than exposed rate.

[**] Percent of patients with MR having left atrial enlargement were derived from two sources. The upper estimate (74.7% of those with moderate MR) was reported in the LIFE study, a analysis of persons with hypertension and left ventricular dysfunction.[15] The tower estimate comes from a Canadian study of healthy, normotensive obese subjects (37%).[16] In the HypgrGEN study, factors which correlate with MR and AR have been published.[17] In further, unpublished analyses of that data set. Dr Hopkins estimated that among the entire population studied, 41% of these with moderate MR and BM) 27+ also had left atrial enlargement (diameter 4.0 cm) — an estimate the is within the range of the published studies.

[***] The reason for (he large discrepancy of FDA+ AR in those using drug 60 days is that no baseline rate was included in the percent estimates for the settlement projections.

7. The estimate that out of an exposed population of 6 million Individuals only 3,345 individuals would qualify for Matrix A benefits while only 27,227 would qualify for Matrix B. under the settlement criteria is at least 3-fold Lora low and as much aa 8-old underestimated.

8. During my review of just how these numbers were calculated I found a series of errors made at each step and assumptions that resulted in gross underestimates of the number affected.

9. These errors kntiudod Ihe use of the background unexpased rate of mitral ragurgitadon, in lieu of the exposed rate, by Dr. Samuel Kursch to calculate the number class members who would have PDA positive mitral regurgitation. Further, this background rate was only applied to those who used the dwgs 60 days or tess. The net result of this failure is an under counting of those who have FDA positive regurgitation, most obviously In those using drugs 61 days or longer —

10. Particularly troubling is the total lack of ary calculations by any of the experts employed by Class Counsel regarding the number of potential claims for Matrix Level II benefits. This oversight results in a laiger discrepancy when one considers that according to the epidemiology relied upon by Glass Counsel there would be expected to be 210,000 class members who would be suffering from FDA positive mitral regurpltatkm (3.5% applied to 6,000,000 users), In my review of the documents and reports which make up the fairness hearing record, I was unable to find any analysis whatsoever as to how many of these class membere would also have any of the other Factors which would allow them to qualify for level benefits, As one of the qualify ing complicaiions 1$left atrial enlargement and considering that left atrfal enlargement is very common in overweight persons, surely some calculation should have been made regarding how many of them would also have left atrial enlargement

11. According to published medical studies available at the time of the settlement, a large percent of overweight persons with moderate mitral regungitation would be expected to have LAE (see footnotes for table above). Thia was apparently overlooked in Class Counsel's projections, either ig norarrHy or knowtngly,

THE CLAIMS PROJECTIONS RELIED UPON BY CLASS COUNSEL AND WYETH

12.In preparation of my analysis I was provided with the following material:

a) Declaration of Dean G. Karalis, M.D., dated February 29, 2000, (Diet Drug Class Exhibit P0095), with attachments;

b) Declaration and Supplemental Declaration on Sanjrv Kaul, M.D., dated March 5, 2000, (Diet Drug Class Exhibit AHP609), with attachments;

c) Declaration of Steven N. Goodman, M.D., M.H.S., Ph.D., dated February 28, 2000 and Supplemental Declaration dated March 20, 2000, (Diet Drug Class Exhibit P0090), with attachments;

d) Expert report, Center For Forensic Economic Studies, dated March 24, 2000, (Diot Drug Class Exhibit P0094), with attachments:

e) Declaration (Feb. 28, 2000) and Supplemental Declaration (May 7, 2000) of Walter F. Stewart, Ph.D., M.P.H., (Diet Drug Class Exhibit AHP611), with attachments;

f) Declaration (Mar. 24, 2000) and Supplemental Declaration (May 8, 2000) of Dr. Mark McCellan, (Diet Drug Class Exhibit AHP614). with attachments;

15. The projections mat formed the basis of the settlement we recalculated based upon the submissions of Goodman, Karalis and Kursh. Each building upon the other.

16. The foundation of the projections is based upon several assumptions. First, it is accepted by Class Counsel that the entire population of exposed class members consists of 6 million users. This number is derived from a marketing study supplied by Wyeth. While this estimate Of ever-users may well be an underestimate, I heve made my projections based on this assumption of 6 million users. Of the six million class members exposed to fenfluramine and/or dexfenfluramine it is asstimed that 4 million took Pondimin and 2 million took Redux. In my estimates I have combined these since associated risk is generally assumed to be identifical.

17. The rate of exposure In turn is determined by Wyeth's marketing data and is presented below.

Pondimin: 4.000.000 total users:

Days of Theraoy Percentage Users

1-30 39.2% 1,568,000

31-60 20.9% 836,000

61-90 11.9% 476.000

91-120 6.3% 332,000

121-150 6.0% 240.000

151-100 4.3% 172,000

161-210 3.3% 132,000

211-240 2.1% 84,000

241-270 1.6% 64,000

271+ 2.4% 96,000

Redux 2,000.000 total users:

Days of Therapy Percentage Users

1-30 55.1% 1.102.000

31-60 19.0% 380,000

61-90 9.8% 196,000

91-120 5.5% 110,000

121-150 3.5% 70.000

151-180 2.3% 46,000

181-210 1.6% 32,000

211-240 1.1% 22,000

241-270 0.6% 16,000

271+ 1.3% 26,000

COMPUTING THE RATE OF FDA POSITIVE REGURGITION

19. In calculating the number of potential class members who would have FDA positive levels of valvular regurgitation Class Counsel relised upon the declaration of Dr. Goodman.

20. Dr. Goodman in his Supplemental Declaration dated March 20, 2000 provides an analysis of the available epidemiological studios and offers hie opinions as to the prevalence of FDA positive levels of regurgitation.

21. With respect to the prevalence of FDA Positive aortic negurgilation Dr. Goodman states that the basaline risk of FDA positive aortic regurgitation is 3.1%. He further states that with exposure to Pondimin and/or Redux the rate increases 1% per month for the first nine months of use. For those who took the drugs for more than 9 months the risk of developing fDA positive aortic ragurg Station is 14.5%.

22. With respect to severity, he conduded that 16.5% of the total exposed population wtio have FOA positive aortic regurgitaiiori will have moderate to severe levels of aortic regurgitatiori

23. In determining the rate of PDA Positive mitral regurgitation Dr Goodman found that the baseline rate of FDA positive mitral ragurgitation was 2.1%. For those exposed to Pondimin and for Redux he conducted that the overall risk of FDA positive milral ragurgitatfion was 3, 5%, with no relationship to duration of exposure.

24. Based upon Or Goodman's conclusions the following projections can be made with respect to the number of potential FDA positive class members.

Pondimm and Redux; 6,000.000 total users:

Days of Therapy Users FDA+AI FDA+MR

1-30 2,670,000 109,470 93,450

31-60 1,216,000 62,016 42,560

61-90 672,000 40,992 23,520

91-120 442,000 31,381 15,470

121-150 310,000 25.110 10,850

151-180 218,000 19.838 7,630

181-210 184,000 16,564 5,740

211-240 106,000 11,766 3,710

241-270 50,000 9,680 2,800

271+ 122.000 17,690 4,270

Total FDA+ AI = 344,508

Total FDA+ MR = 210,000

Total FDA+ 544,506

CLASS COUNSEL'S MATRIX PROJECTION

25. As will shown below, there are few differences with respect to my calculations and analysis gf the total number of FDA+ class members, and the calculations made by Dr. Goodman. However. 1 can find no support for the subsequent calculations made by Dr. Samuel Kursh regarding the projected number of matrix qualifying class members. In fact Dr. Kursh made several errors which contradicted marry of Or. Goodman's conclusions.

26. The most glaring error made by Dr. Kursh was his use of Dr. Goodman's calculation of the background rate of FDA+ mitral regurgitation (2.1%) instead of the exposed rate of 3.5% and applying these number only to persons using drug 60 days or less,

27. The Bafflement sets forttt five tevete of injury which were to be compensated. The criteria for qualifying is set forth in detail in the agreement and was made a part of the material submitted to me for review. For the purposes of this analysis, only Level I and Level II are addressed, since the overwhelming number of class members will qualify at these two levels,

20. Matrix Level is defined as severe aortic or mitral regmyitaticn without complicating factors, measured according to the Sigh criteria, [18]

29. Claims based upon a finding of moderate mitral regurgitation are required to meet the requirements for lever II compensation as set forth in the settlement agreement. The settlement requires that in addition to a finding of moderate mitral regurgitatton. one or more of the following must also be present:

(b) Moderate MR (20% 40%RJA/LAA) or Severe MR ( 40%RJA/LAA) with one or more of the following:

i) Pulmonary hypertension secondary to vaJVuter heart disease witfi peak systofc pulmonary artery pressure 40 mm Hg measured by cardiac cauterizations or with a peak systolic pulmonary artery pressure 45 mm Hg measured by Doppler etectrocarctiography, at rest, utilizing the procedures described in Section F.2.(a)(i),

ii) Abnormal left abial supero-inferior systolic dlmension 5.3 cm (apical four chamber view) or abnormal left atrial anteno-posterior systolic dimension 4-0 cm [parastemal tong axfe vlew)measyred by 2-D directed M-mode or 2-D ecriocardiography with normal sinus rhythm using sites of meafiuremsnt recommended by (he American Society of Echocandjography;

iii) Abnormal left ventricular end-systolic dimension e45 mm 20 by M-mode or 2-D Echocardiogram;

iv) Ejection fraction of 60%;

v) Arrhythmias defined as chronic atrial fibrillation/flutter that cannot be converted to normal sinus rhythm or atrial ¶ requiring ongoing medical therapy, either of which are associated with left ¶ enlargementas defined in Section F.2.(ii).

30. From my analysis of the material submitted to support the settlement there was no effort made to estimate the number of class members who would qualify initially for level II benefits baaed upon the presence of moderate or greater mitral regurgitation and any of the other factors listed above.

31. Instead Dr. Kursh relies upon a series of assumptions provided to him, These assumptions include the declaration of Dean G. Karalis, M.D. that out of the entire population of exposed FDA+ class members only 5-10% could be expected to enter and progross through the severity (payment) matrix.

32. None of the studies cited by Dr. Karalis in paragraph 43 of his declaration provide any data which would allow him to estimate how many people would qualify for level II benefits based upon one or more of the complicating factors died in the settlement.

33. Thus relying solely upon Dr. Karalis' statements, Dr. Kursh concludes that out of me entire population of six million users only 8,345 class members could qualify for Matrix A benefits while 27,727 would qualify for Matrix B benefits. Of these, it was assumed that 90% would fall in level I and 90% in level II.

34. These assumptions result in entirely spurious estimates of those who would qualify for level II benefits,

35. Date existed at the time to permit a more detailed projection as to the number of class members who would initially qualify for benefits at Level I and Level II. The lack of any such effort to estimate the number of potential Matrix Level I is surprising when one considers that Dr. Goodman found that 16.5% of the total exposed population who have FDA positive aortic negurgitation will have moderate to severe levels of aortic regurgttation. Based upon hie findings approximately 57,000 class members would be afflicted with moderate or severe aortic negurgrtatjon, a substantial number of who would qualify for Matrix benefits, even assuming Dr. Karate' assumptions.

IT WAS AND IS POSSIBLE TO ACCURATELY CALCULATE THE NUMBER OF CLASS MEMBERS WHO WOULD QUALIFY FOR MATRIX LEVEL BENEFITS

36. Since 1397 there have been a number of well known published epiderraological studies which have examined the effects of fenfluramine and derfenfturamfne (cited in paragraph 6). All these studies except for Dahl were included in my published analysis of relative risk, In order to determine the prevalence of valvular regurgttation in the exposed population a mata-analysls was performed. Data regarding prevalence of all mild or greater aortic or mitral re-gurgitation reported in each of the cited studies was extracted along with reported levels of severity and exposure duration. Controls in these studies served as a means to estimate baseline (unexposed) levels of aortic and mitraJ mgurgrtation. To estimate overall prevalence of FDA+ valvular disease each study was weighted by number of subjects. An overall estimate of the distribution of severity was made, ¶ regurgitate was significantly related to duration of exposure. Prevalence was modeled as a non-linear logarithmic function of duration as Implemented in SAS Proc NLIM (Statistical Analysts Package. Cary. North CarolinaJ. Similar to Dr. Gooctman's findings, mitral regurgitation was found not to be dearly related to dluration of exposure. Therefore, an overall prevalence was calculated for all users. These estimates of prevalence were used in the attached spreadsheet 1o mode] projected number having regurgitation (exhibit A).

37. To determine of prevalence of left atrial enlargement In the exposed population I based my estimates upon several published studies,

38. The prevalence of ¶ atrial enlargement increases dramatically with BMI, Tliis is especially significant when one considers that the vast majority fen-phen users were overweight.

39. In one study it was found that in normotensiva individuals with BMI 28, 37% of them were found to have left atrial size greater than 4.0 as measured in the posteroartertor dimension This finding is notable because patients were excluded if they had no other potential factors that may have influenced left atrial size.[19]

40. In Gottdiener, et al.[20] BMI was the strongest predictor of LA size. Further, "mean left atrial size differed signfficantly (¶ .0001 by ANOVA) across obesity categories. Based on the Tykey procedure, obese patients had a greater LA size (44.245.7 mm) than overweight (41, 6 ± 5.9 mm) or normal weight (38.9 ± 6.2 mm) patients." The obesity categories were 30, 27-30, and 27 BMt for obese, overweight, and normal weight respectively. The simple correlation between BMI or weight and LA size was between 0.36 and 0.40 (r. correlation coefficients). In this study, systolic and diastolic blood pressures were not determinants of LA size. This would suggest that over 50% of overweight persons would have LA size greater than 40 mn.

41. As Or. Karalis alluded to in his declaration, there is also a relationship between mitral regurgitation and left atrial enlargement (n a study published in 1992. 92 patents had echocardiographic and gngiographfc examinations demonstrating MR-Severe regurgjtatton was found in 45 patients white 47 were found to have mild to moderate regurgitation. For those patients with mild-moderate mitral regurgltation (he mean left atrial size was 48 ± 9, white the mean left atrial size was 51 ± for those with severe mitral regurgitation.[21]

42. Based on the above, I performed estimates of the projected number affected at various levels of severity and compared them with estimates performed previously as part of the settlement. The table in paragraph 6 shows my findings.

CONCLUSION

43. The projections and estimates made by Class Counsel with respect to the number and types of potential claims for Matrix Benefits cannot be considered accurate or reliable. These estimates contain serious errors and severely underestimated, either intentionally orignorantiy. the number of Injured people who could potentiatly quality for benefits.

References Cited

Wadden TA, Berkowitz Rl Silvestry F. Vogt RA, St. John Sulton MG. Stunkard AJ. Foster GD, Aber JL. The fen-phen finale: a study of weight loss and valvular heart disease. Obes Res 1996; 6:278-284.

Burger AJ, Sherman HBT Charlamb MJ, Kim J1 Asinas LA Fllckner SR, Blackburn GL. Low prevalence of valvular heart disease in 226 phenterrnine-ferfluramine protocol subjects prospectively followed for up to 30 months. J Am Coll Cardiol 1999; 34:1153-1166.

Dahl CF. Allen MR, Jeffcoats JA. The prevalence of significant valvular regurgitation and pulmonary hypertension in 753 patients who and phenfennine in a community setting [Abstract], J Am Coll Cardiol 1999; 33:549A

Kancherta MK, Salti HI, Mulderink TA, Parker M, Bonow RO. Mehlman DJ, Echocardiographic prevalence of mitral and/or aortic fegurgltation in patients exposed to either fenfluramine-phenternine combination or to dexfenfluramine. Am J Candiol 1999; 64:1335-1338.

Lepor NE, Gross SB, Daley WL, Samuels BA, Rizzo MJ, Luko SP, Hickey A, Buchbinder MA. Naqvi TZ, Dose and duration of fenfluramine-phentsrmine therapy impacts the risk of significant valvular heart disease. Am J Cardiol 2000; 86:107-110.

Teramae CY, Connolly HM, Grogan MT Milier FA, Jr. Diet drug-ralatad cardiac valve disease: the Mayo Clinic echocardiographic faboratory experience. Mayo Clin Proc 2000; 75:456-461.

Khan MA, Herzog CA, St. Peter JVT Hgrtley GG, Madlon-Kay R, Dick CD, Aslnger RW, Vessey JT. The prevalence of cardiac valvular Insufficiency assessed by transthoracic echocardiography in obese patients treated with appetite-suppressant drugs, N Engl J Med 1998; 339:713-718.

Weissman NJ, Tighe JF, Jr., Gottdiener JS, Gwynne JT. An assessment of heart-valve abnormalities In obese patients taking dexferrfluramine. sustained-ralease dexfenfluramine, or placebo. Sustained-Release Dexfenfhuramine Study Group, N Engl J Med 1998; 339:725-732.

Shively BK, Rotdan CA, Gill EA, Nsjarian T Loar SB, Prevalence and determinants of valvulopathy In patients treated with dexfenfluramine. Circulation 1999: 100:2161-2167.

Hensrud DD. Connolly HM, Grogan M. Miller FA, Bailey KR, Jenson MD. Echocardicgraphic improvement overtime after cossatlon of use of fenfluramine and phentermine. Mayo Clin Proc 1999; 74:1191-1197.

Ryan DHr Bray GA, Helmcke F1 Sander G, Volaufova J. Greenway F, Subramaniam P, Glancy DL. Serial echocardiographic and clinical evaluation of valvular regurgltation before, during, and after treatment with fenfluramine or doxfenfluramine and mazindol or phentermine Obes Res 1999; 7:313-322.

Gardin JM, Schumacher D, Constantine G, Davts KD, Leung C Reid CL Valvular abnormalities and cardiovascular status following exposure to dexfenfluramine or phentermine/fenfluramine.JAMA 2000; 283:1703-1709.

Jotlis JG. Landolfo CK, ¶ J, Constantine 3D, Davis KD, Ryan T. Fenfluramine and phentermine and cardlovasculax findings:effect of treatment duration on prevalence of valve abnormalities Circulation 2000; 101;207t-2077.

Davidoff R.McTieman A, Constantine G, Davls KDF Balady GJ, Mendes LA, Rudolph RE, Bowen DJ, Ectiocandiographk; examination of women previously treated with fenfluramine: long-term follow-up of a randomized, double-blind, placebo-controlled trial. Arch Intern Med 2001; 161:1429-1436.

Gerdts E, Olkarinen L. Palmieri V, Otterstad JE. Wachtell K, Boman K, Dahlof B, Devefeux RB. Correlates of left strial size in hypertensive patients with left ventricular hypertrophy: the Losartan Intervention For Endpoint Reduction In Hypertension (LIFE) Study. Hypertension 2002; 39:739-743.

Sasson Z. Rascoly Y. Gupta R, Rasooly L Left atrial enlargement in heafthy obese: prevatenoe and retention to left ventricular mass and dlastatic function-Can J CardioE 1996; 12:257-263.

Palmied V. Bella JN, Amett DK, Obemian A, Kitzman DW, Hopkjns PN, Rao DC, Roman MJ. Devsreux RB. Associations of aortfc and mitral regurgtlation with body cornpotiitkm and myocardial energy expenditure in adults with hypertension: the Hypertension Genetic EpklemfolOfly Network study. Am Heart J 2003; 145:1071-1077.

Singh JP, Evans JC, Levy D, Ureon MG, Freed LA, Fulter DL. Lehman BT Benjamin EJ. Prevalence and clinical determinants of mitral, tricusptd, and aortic regurgitation (the Framingham Heart Study). Am J Cardlol 1999; 83:897-902.

HNapkins PNT Polukoff Ct. Risk of vatvular heart disease associated with use of fenflunamine. BMC Canttovasc CUsord 2003; 3:5.

Gottdiener JS, Reda DJ, Williams DWT Materson BJ. Left atariaf size in hypertensive men: influence of obesity, race and age. Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents, J Am Coll Cardid 1997; 29:651-658.

Byrwash IG, Blackmore GL, Koilpillai CJ. Useffulneas of teft atrlal and lft ventricular chamber sizes as predictors of the severity of mitral regurgitation. Am J Cardiol 1992; 70:774-779.

Exhibit ACurriculum VitaePaul N, Hopkins, M.D., M.S.P.H.January 2004

Office HomePERSONAL DATAEDUCATIONLOCATION MajorUndergraduateAdvanced DegrsesResidency TraningBoard CertificationSCHOLASTIC HONORS

Cardiovascular Genetics 10418 North Hidden Oak Drive 410 Chipeta Way, Room 157 Highland, UT 84003 Salt Lake City, UT 84108 Phone (501) 756-4S78 Phone (801) 581-3888 ext. 228 Wife: Cynthia (Cindy) FAX (801) 581-6862 Children: Zachary, Ashley, Alexis e-mail: paul@ucvg.med.utalt.edu Birthdate: September 13, 19S2 Social Security #: 545-96-3972 Birthplace: Fort Belvoir, Virginia Medical License #: Utah 173 718-1205 Citizenship: USA DEA #: AH 3263794 Ethnicity: White : 1976 B.S. University of California at Los Angeles Biochemistry : 1978 M.S.P.H. UCLA School of Public Health Nutrition 1984 M.D. University of Utah School of Medicine Medicine : 1984 1985 Mayo Graduate School of Medicine Internal Medicine 1985—1986 University of Utah Preventive Medicine : 1990 American Board of Preventive Medicine 1976 Magna cum laude — Biochemistry, UCLA 1976 Phi Beta Kappa PROFESSIONAL EXPERIENCE 2002—present Professor of Internal Medicine — University of Utah School of Medicine. 1993—2002 Associate Professor of Internal Medicine — University of Utah School of Medicine. Changed front Research to Tenure Tenure February 2000. 1993—2002 Adjunct Associate Professor — Department of Foods and Nutrition, University of Utah. 1986—1993 Assistant Professor of Internal Medicine — University of Utah School of Medicine 1987—1993 Adjunct Assistant Professor — Department of Food and Nutrition, University of Utah. 1985—1966 Staff physician with Humana MedFirst — general and family primary care (30 hours/week), 1978—1986 medical research with Roger R. Williams, M.D. at the University of Utah Department of Cardiovascular Genetics. Full and part time. 1978—1979 Laboratory technician for J. Walter Woodbury, Ph.D. in the Department of Physiology, University of Utah, RESEARCH EXPERIENCE/A WARDS

1. "Genetic and Environmental Determinants of Hypertension", NIH R0-1 grant, 1981 — August 1992. Roger R. Williams, M.D., PI, Participating physician from 1986-1992.

2. "Characterization of Coronary Prone Pedigrees". NIH R0-1 ¶ 1981 — 1991. Roger R, Williams, MD., PI, Participating physician 1986-1991

3. "Genetic Determinants of Response to Diet in Utah Pedigrees with Familial Hypercholestenolemia". CRC protocol #88-07. Pilot completed May 1991. Principal Investigator,

4. "A Double-Blind, Multicenter Study to Evaluate the Safety, Tolerability and Efficacy of Simvastatin and Placebo in Patients with ¶", Sponsored by Merck, Sharpe and Dohme Research Labs, January 1, 1990-March 31, 1991. Principal Investigator for Utah branch,

5. "Effect of ¶ on Controlling Hyperchotesterolemia: A Special Patient Population Study", Bristol-Myers Squibb, December 1991-June 1993. Principal Investigator for Utah branch.

6. "A Randomized, Double-Blind, Placebo-Controlled Multicenter Study of Lovastatin as an Adjunct to Diet in the Treatment of Adolescent Males With Hypertnolesterolemia of Familial Basis", Merck, Sharps and Dohme Research Labs, December 1991 — December 1993. Principal Investigator for Utah branch.

7. "Non-modulation in Essential Hypertension". NIH gram, Collaboration with Gordon Williams, M.D., Richard Lifton, MD., Ph.D., Robert Dluhy, MD., and Norman Hollenberg, M.D. at the Brigham and Women's Hospital, Boston, Mass. Co-investigator responsible for Utah branch of the study. 1986 — 1991,

8. "Genetics of Human Hypertension", NIH grant, July 1991 — May 1996. Continued as component of a SCOR May 1996 — present (renewed February 2001 as "SCOR Molecular Genetics of Hypertension. Project 1 Genetic Determinants of the Reuim-Angiotiensin-Aldosterone System Involved in the Pathaogenesats of Hypertension" NIH 2 P50 HL55000-06), Gordon H. Williams, M.D., PI for SCOR, Principal Ipvestigator for Utah clinical subcontract

9. "Evaluation of Sibting Pairs: a Risk ¶ Trial (ESPRIT)", Zeneca Pharmaceutical Group, April 1992 — December 1956, Co-Principal Investigator of Utah site.

10. "A 54-WEEK Open Label Assessment of the Safety and Efficacy Profile of Atorvastatin as Compared to Fluvastatro, Lovaslattn, Simvastain, and Pravastatin When Used to Optimally Control Primary Hypercholesteroleinia (Type IIa) and Mixed Dyslipidcmia (Type IIb)". Parke-Davis and Pfizer, April 1997 — present. Principal Investigator for Utah site.

11. "A Study to Compare Remnant Like Particle-Cholesterol (RLP-C) immunowparation Reagent Kit with Other Lipoprotein Remnant Methods in Measurement of Remnants in Patients with Type IIb, III, and IV Hyperh'poprottinemii". Otsuka America Pharmaceutical, Inc., June 1997 — November 1998. Principal Investigator for Utah site (of 2 clinical sites).

12. "Genetic Interactions and Atherosclerosis Risk in Familial Hypercholestwolemia". NIH Grant (RO-1). Principal Investigator. Funding August a, 1992-July 31, 1997. Total 5-year budget $1,485,488 direct costs.

13. "A Randomized, Double Blind, Parallel Group Evaluation of Cerivastatin 0.8 mg Compared to Cerivastatin 0.4 mg and Placebo/Pravastatin 40 mg Once Daily in Patients with Hypencholesterolemia". Bayer Corporation (ID 97-008), Feb 1998-May 1999. Principal Investigator for Utah site.

14. "A Multi-Center, Randomized, Double Blind, Placebo Controlled, Parallel 8 Week Ambulatory Blood Pressure Monitoring Study of Three Dose Regiments of Omapatrilat Administered Once-Datly or Twice Daily in the Treatment of Mild to Moderate Hypertension". Bristol-Myers Squibb (CV 137-036), June 1998-August 1999. Principal investigator for Utah site.

15. "A 28-Week, Double Blind and Observer Blind to Lipid Values, Active Controlled, Randomized, Parallel-Group, Multicenter Study to Assess the Safety and EEGcacy of Fluvastatin Slow Release Form (80 mg) Administered Once Daily at Bedtime in Patients with Primary Hypercholesteiolemia Compared to Lescol 40 mg". Novartie Pharamaciticals (XUO F351-00/001), May 1908 — November 1999, Principal Investigator for Uiah site.

16. "A Doublo-Bund, Randomized, P1acebn-Controlled, Crossover Trial of the Effects of Simvastatin on Plasma Lipids in Patients with Abnormal Lipoprotein Rmmant Accuraulalion". Merck Medical School Grant. Approximafely $60.000 direct costs, June 1999 — present Principal Investigator

17. "A Double-Blind, Randomized, Piacebo-Controlled Trial to Evaluate the Efficacy and Safety of Lovastatin in Adolescent Girls (protocol 083-01)". Merck Co., Inc. September 1999-December 2000. Principal Investigator for Utah site.

18. "A 24-Week Randomized Double-Blind Multicenter Multinational Trial to Evaluate the Efficacy and Safety of ZD4522 and Atorvastatin in the Treatment of Subjects with Heterozygous Familial Hypencholesterolemia (ZD4522II/0030)". AstraZeneca Pharmaceuticals, October 1999 — June 2000. Principal Investigator tor Utah site.

19. "A 24-Week Randomized Multicenter Trial to Evaluate the Efficacy and Safety of ZD4522 and NIASPAN, Alone and in Combination, in the Treatment of Subjects with Type IIb and IV Hyperbpidemia (ZD4522II/0029)", AstraZeneca Pharmaceutical, November 1999 — December 2000. Principal Investigator for Utah site.

20. "A 12-Week Multicenter Randumized Double-Blind Placebo-Controlled Trial to Evaluate the Efficacy and Safety of ZD4522 (5, 10, 20, 40, and 80 mg) in the Treatment of Subjects with Hypertriglyceridemia (ZD4522H/0035)". AstraZeneca Pharmaceuticals, November 1999 — January 2001. Principal Investigator for Utah site.

21. "A 12-Week Randomized Open-Label Multicenter Trial to Evaluate the Efficacy and Safety and Toterability of ZD4522 and the Combination of 2D4522 and QUESTRAN Light in the Treatment of Subjects with Severe Hypercholesterolernia (ZD4522IL/0031)"-AstraZeneca Pharmaceuticals, November 1999 — December 2000, Prindnal Investigator for Utah site.

22. "An Open-label, Multinational, Multicenter, Extension Trial to Assess the Long-Term Safety and Efficacy of ZD4522 in Subjects in the ZD4522 Clinical Trial Program (ZD4522IL/0034), AstraZeneca Phamaceuticals, April 2000 — present. Principal Investigator for Utah site.

23. Genetics of Coronary Heart Disease". An ongoing collaboration between Cardiovascular Genetics and Myriad Genetics. Principal Investigator for Cardiovascular Genetics.

24. "A Randomized, Double-Blind, Placebo Controlled Trial of Once Per Day VS. Split Dosing of GT102-279 in Patients with Primary Hypercholesterolernia". Geltex Pharmaceuticals (GTC102-55-202), May 2000 — December 2000, Principal Investigator for Utah site.

25. "A Multicenter, Double-Blind, Randomized, Parallel, 28-Week Study to Evaluate the Efficacy and Safety of Simvestatin 80 mg/day Versus Atorvastatin 80 mg/day in Patients with Hypercholesterolernia, (CHESS: Comparative HDL Efficacy and Safety Study)", Protocol number 188-00/Z0C488. Merck, December 2000-present Principal Investigator for Utah site.

26. "A Multicenter, Randomized, Double-Blind, Parallel Group, Multiple Dose Study of the Safety and Effectiveness of Cerivastatin vs. Placebo in Pediatric or Adolescent Patients with Heterozygous Familial Hypercholesterolernia (BAY-PEDS Trial)". Bayer, January 2001 — present. Principal Investigator for Utah site,

27. "A Dose-Ranging Study of NK-104 in Patients with Primary Hypencholesterolemia: NK-104-209", Sankyo Pharma Development, June 2001 — present

28. "A Six-Week, Dose-Comparison Study to Evaluate the Safety and Efficacy of Rosuvastatin Versus Atorvastatin, Cerivastatin, Pravastatin, and Simvastatin in Subjects with Hypercholesterolernia (4522IL/0065) (STELLAR)". AstraZenica Pharmaceuticals, June 2001-present.

29. "HyperGEN: Genetics of Left Ventricular Hypertrophy". NIH Grant — Donna K, Arnett, Ph.D. is Pl for entire project Principal Investigator for Utah site.

30. "Oxidation Risk Factors and IMT Progression in FH (Familial Hypercholesterolernia)", NIH Giant (R01 HL63349), 5-year award, September 2000-present Principal Investigator for grant.

31. "Genetic Epidemiology Aging in Utah Pedigrees". KTH Aging Institute, 5-ycar award, March 2001 — present Steven C. Hunt, Ph.D., Pl. Co-investigator.

32. "Hostility, Marital Interaction and Health in Aging", NIH Grant, 4-year award, April 2001 — present. Timothy Smith, Ph.D. Pl. Co-Investigator

33. "Treatment of Hypercholesterolemia with Rosuvastatin (protocol 091)", AstraZeneca, Jime 2002-present Pl of Utah center.

34. Participating physician in ongoing collaboration between Cardiovascular Genetics and Jean Marc Lalouel, MD.3 D.Sc. of the Howard Hughes Medical Institute at the University of Utah, Projects include molecular genetic studies of lipoptoteirt metabolism in high-risk. CHD families and, more recently, studies of molecular mechanisms of hypertension.

ADMINISTRATIVE EXPEJBJENCE

1. Chairman, Steering Committee, International and U.S, MEDPED (Mate Early Diagnoses to Prevent Early Deaths in Medkal Pedigrees), an jnteniatiooal humanitarian organisation to find and help persons with familial hypenibolesterolemia. MEDPED was founded by the late Roger EL William M.D. who died in the crash of SwiRsair flight 111 in Geneva, September-2, 1998 cm his way to chair an mternaticDal MEDPED mccdog at the World Health Organization.

2. Director Family Lipid Chmc, Preventive Cardiology, Cardiology Division, University of Utah School of Medicine.

3. Co-Director of Cardiovascular Genetics Research Clinic.

4. Principal investigator for grants listed above (see research experience).

5. Participate in organizational planning and scientific meetings for research projects in Cardiovascular Gcndics.

CLINICAL ACTIV1ESClinical Innoyation and Referral Attraction

1. Developed and direct the Family Lipid Clinic in the Madsen Preventive Cardiology Clink, a model lipid clinic for treatment of familial lipid dieonfere, especially farcilial hypenchoiriesteroienua, familial combined hyperhpidemia, and other severe lipid disorders.

2. Participate in a variety of clinical and research studios with various outreach methods to recruit participants who are then screened and evaluated for cardiovascular risk factors. Some of these pafifents are referred for further medical cere as indicated.

Routine Clinical Activities

1. See patients in Family Upid Clinic (weekly clinic).

2. Occasional consults for lipid abnormalities at University Hospital

3. Advisor for interpretation of ambulatory blood pressure monitor results for Carrtiotogy division.

PROFESSIONAL AND UNIVERSITY COMMUNITY ACTIVITIES

1. Member of (he Diet Evaluation Committee of the Salt Lake County Medical Society (1982-1984).

2. Member of Promotions, Retention and Tenure Committee, University of Utah School of Medicine (1984).

3. Member of the Nutrition Committee, Utah Heart Association (1986 — 1992).

4. Member of the Cholesterol Committee, Utah Medical Association (1989-1993).

5. Member of the Utah Academy of Preventive Medicine (1989-1993)

6. Consultant for AMA Drug Evaluations "Treatment of Disorders of Cholesterol and lipoprotein Metabolism" 1993 Summer supplement.

7. Member Institutional Review Board, University of Utah (1994-1996)

8. Review manuscripts for Annals of Internal Medicine, Arteriosclerosis Thrombosis and Vascular Biology, Circulation, Clinical Chemistry, Diabetes. European Journal of Public Health, Hypertension, Kidney International, JAMA, Journal of Investigative Medicine, Lancet

9. Reviewer for National Heart, Lung, and Blood Institute study section (EDC1), February 1995.

10. Participant in the Special Emphasis Panel on Homocysteinetnia and Cardiovascular Disease, September 1995.

11. Consultant for Roche for studies on ¶, May 1997.

12. Consultant for Pharmacia-UpJohn, July 1997.

13. Consultant for Eli Lily, 1999 — present.

14. Consultant for Merck, 1998 — present

15. Consultant for AstraZeneca 2000 — present.

TEACHING AND PRESENTATIONSPreceptor

1. Clinical diagnosis preceptor for sophomore medical students (1993 — 2000).

2. Internal Medicine residents and Cardiology fellows rotating through Family Lipid Clinic.

3. Diebetics trainees rotating through Family Lipid Clinic.

Graduate Student Committees Theses:

1. Walter Hemelstrand, for Ph.D., Department of Health Education, 1989,

2. Rosana Roberson, R.D., for M.S., College of Health, Division of Poods and Nutrition, 1989-1991.

3. Joseph J. Cimmarusti, for M.S., College of Health, Division of Foods and Nutrition, 1990-1991. Master's thesis defence — August 1992.

4. Mike Manfull, for M.S., College of Health, Division of Foods and Nutrition, 1993-1994

5. Geraldine Wade, M.D. for M.S., Medical Informatics, 1998-1999.

Lectures for Graduste/Medical Students

1. "Prostaglandins and Fish Oil". Yearly lecture to nutrition graduate studects (8-12 students). Started winter quarter 1991.

2. Management of lipids. Yearly lecture to Cardiology Fellows.

3. Hyperlipidemia, Cardiology organ systems lecture for 2nd year medical students.

4. Hypertension. Cardiology organ system; lecture for 2nd year medical students,

5. Introduction to Atherosclerosis. Nutrition graduate students.

Invited Lectures (selected from a longer list)

1. "Cholesterol screening. Vital new developments in cholesterol screening and counseling for the young student." Brigham Young University. March 31, 1987, Approved for I 1/2 hours of category 1 CMD credit

2. "Treatment programs for families with byperlipidcinia." 8th Annual Nutrition in Contetnporary Medicine Symposium. Sponsored by University of Utah Division of Foods and Nutrition and School of Medicine Division of Gastroenterology, February 17, 1989.

3. "Using medical family history data in risk assessment" Southwest Regional meeting of the American College of Sports Medians, Las Vegss, Nevada, Decembers, 1988.

4. "Stearic acid, oleic acid and omega-3's — what do they mean for your patient?" Utah Heart Association Scientific Session, April 7, 1589.

5. "Stratifying patients at risk from ebvaled strum cholesterol," Ogden Clinic. Sponsored by Merck, Sharp Dohme, June 23, 1989.

6. "Diagnosis of Hyperlipidemias." Cottonwood Hospital Sponsored by Merck, Shaip Dohme, August 8, 19S9.

7. "Stratifying patients at risk from elevated scrum cholesterol." Billings Clinic. Sponsored by Merck, Sharp Dohme, October 28, 1989.

8. "High Risk Families for Cardiovascular Disease" Red Lion Hotel, Salt Lake City, At 14th Annual Conference on Cardiovascular Health, "Pamerships in Prevention", Sponsored by the Utah Department of Health and Merck Sharp Dohme, April 6, 1990.

9. "Pathogenesis of Atherosclerosis and Metabolism and Regulation of Lipupruleins Holiday Inn, 31. George, ULah. In a cunlmuing medical educaliun program sponsored by the University of Utah School of Medicine, Department of Internal Medicine and Merck, Sharp Dohme, May 12, 1990.

10. "Hypertension, Hyperhpidcmia, and Ensulin Resistance." Park City, Utah. Sponsored by Rorsr PharmBceuticala; May 16, 19990.

11. "A Practical Approach to High Risk Coronary Families: Risks and Benefits of Exercise and Other InterventionE." A tutorial lecture at the Annual Meeting of the American College of Sports Medicine, Salt Lake City, UT, May 25, 1990.

12. "Women and Coronary Heart Disease," Lakeview Hospital. Sponsored by Parke-Davis, June 14, 1990. Also at Ixjgan Regional Hospital October 17, 1990 and at Salt Lake Clinic May 23, 1991.

13. "Hypeccholestieroleniia — What Lipid Fractions Are Important." Humana Hospital, West Anaheun, CA. 1 hour CME credit, Sponsored by Merck, Sharp Dohme, June 15, 1990.

14. Hypertension: Who to Treat and How to Treat", Part of a Symposium: Management of hypertension and other cardiovascular risk; factors. June 12, 1991, Salt Lake City, UT. Jointly sponsored by Temple University School of Medicine and Pfizer-Roerig.

15. "Cholesterol Lowering Agents", Part of ths 15th annual Castle Country Medical Sympogium June 13, 1991 in Price, UT. Sponsored by Bristol-Myers Squibb.

16. "Nutritional ¶ in Genetic Syndromes Leading to Early Familial Coronary Disease". International Life Sciences Institute, North America 1992 Annual Meeting, January 19-22, 1992, Miami Beach, FL.

17. "Advances in Therapy for Hyperlipidemia", May 1994, Prescott, Arizona. Sponsored by Sandoz.

18. "Secondary Prevention of Coronary Artery Disease". October 4, 1994, Internal Medicine Grand Rounds, Cottonwood Hospital, Salt Lake City, UT. Sponsored by Marion-Merrell-Dow.

19. "Cholesterol Lowering to Prevent a Second MT', March 8, 1995, At FHP, Salt Lake City. Sponsored by Bristol-Myers Squibb.

20. "Secondary Prevention of Coronary Artery Disease", May, 1995, At FHP, Salt Lake City, Sponsored by Sandoz.

21. "Advances in Preventing Coronary Disease". CME credit program, January 26, 1996, McKay-Dee Hospital, Department of Medicine meeting. Sponsored by Bristol-Myers Squibb.

22. "What's New with Coronary Artery Disease", CME credit program, April 23, 1996. St. Mary's Hospital, Grand Junction, CO.

23. Protective Aspects of Diet on Coronary Disease", in Foods as Nutrition symposium May 17, 1996. University of Utah Continuing Education Center, Park City, UT. Sponsored by University of Utah College of Health, Division of Foods and Nutrition.

24. Sponsored ¶ for drug representatives on atherosclerotic disease and intervention-Presented 3 of the 6 lectures including "Management of Coronary Disease; Hopes and Promises", "Proof of the Lipid Hypothesis — Clinical Trials", and "Management of Dyslipidemia". January 21, 1997. Preventive Cardiology, University of Utah, Salt Lake City. Sponsored by Parke-Davis and Pfizer.

25. "New Developments in Treating Hyperlipidemia". CME credit program. March 28, 1997. Dixie Regional Medical Center, St. George, Utah-Sponsored by Parke-Davis.

26. "How Low Should You Go — New Advances in Lipid Intervention to Prevent Coronary Artery Disease". September 16, 1998 (and multiple other dates). Pfizer and Parke-Davis sponsored events.

27. "Triglycerides and Coronary Artery Disease — The Rest of the Lipid Story". September 17, 1998. Internal Medicine Grand Rounds, University of Utah School of Medicine, Salt Lake City.

28. "Pharmacologic Management of Lipid Disorders: The Clinical Rationale far Aggressive Lipid Lowering" a 4D minute presentation in a program entitled "The Cardiovascular Dysmetabolic Profile — Key to Outpatient management of Cardiovascular Disease". September 26, 1998. Hyatt Regency, Sacramento. CME credit program sponsored by The Mercy Heart Institute and The Division of Cardiovascular Medicine, University of California, Davis

29. "Database Issues in Cardiovascular Genetics", November 2, 1999. University of Miami Division of Cardiology and Miami Heart Research Institute, Miami.

30. "Evidence-Based Management of CAD Risk Factors. Lipids and CAD Outcome." November 5, 1999, Winter Sports Park, Parit City, Utah. Sponsored by Merck Co.

31. "Results of the Treatment Support Program in MEDPED". November 6T 1999. Atlanta. Annual MEDPED USA meeting.

32. "Prevention of Atherosclerosis". February 10, 2000. Park City, UT, Advances in Internal Medicine. Sponsored by the University of Utah School of Medicine.

33. "New Approaches in Lipid Intervention to Prevent Coronary Artery Disease: Focus on Cerivastatin. July 20, 2000. St. George Utah. Sponsored by Bayer.

34. "Novel Coronary Risk Factors: Beyond LDL, Triglycerides, and HDL" September 29, 2000. VA Medical Center, Salt Lake City.

35. "Family History: A Major Modifiable Risk Factor for Premature Coronary Artsy Disease". September 30, 2000, Notional Clinical Symposium, American College of Nurse Practitioners, at The Salt Palace, Salt Lake City, Utah.

36. "Aggressive LDL Reduction: Focus cm Primary Prevention". October 3, 2000, Tacoma, Washington. CME program sponsored by the Postgraduate Institute for Medicine and the Veritas Institute for Medical Education, Inc. Supported through an unrestricted education grant from Parke-Davis and Pfizer, facilitated by APEX communications. Also presented in Boise, Westlake, CA, other locations during September — November 2000.

37. "Triglycerides and Coronary Artery Disease, Does Genetic Epidemiology Provide New Insights?" October 7, 2000. Masters Conference on Lipid Management at the LaFonda Hotel, Santa Fe, New Mexico. Sponsored by KU Medical Center, Lipiod, Atherosclerosis Metabolic Clinic, Patrick M. Moriarty, M.D., Director, Supported by a grant from Bayer

38. "The Big Four Drugs of Secondary Prevention (Aspirin, Bela-Blockers, ACE ¶ and Statins). What is Their Role in Primary Prevention?" October 14, 2000 at Homestead Resort in Midway, Utah. Presentation in CME program "Cardiovascular Update. What Works and What's New for Primary Care Providers and Specialists". Sponsored by Intermountain Health Care.

39. "The Genetics of Human Hyperchotesterolemic Syndromes. An Update for the Clinician" University of Utah Internal Medicine retreat. November 2, 2000, University of Utah, Eccles Human Genetics Auditorium,

40. "Genetics of Coronary Artery Disease. Family History as a Major Modifiable Risk Factor for Premature Coronary ¶ Disease". CME lecture for Dixie Symposium, sponsored by Intermoutain Health Care, St. George Holiday Inn, February 23, 2001.

41. "Lipid Lowening: for Whom With What, and Why?" CME lecture for Cardiology Spring Meeting, sponsored by University of Utah Cardiology Division, Stein Eriksen Lodge. Deer Valley, May 10, 2001.

42. "Diet, Antioxidants, and Hormone Replacement: What Should We Now Be Recommending?" CME lecture for Cardiology Spring Meeting, sponsored by University of Utah Cardiology Division, Stein Eriksen Lodge, Deer Valley, May 10, 2001.

43. "Implications of the New Guidelines (NCEP III) for Lifestyle Modification and Lipid-lowering Therapy" CME lecture fur Cardiology Update 2001, sponsored by the University of Utah Cardiology Division, Thanksgiving Point, October 27, 2001.

44. "Managing Multiple Risk Factors in Primary Care: An Interactive Workshop" CME program sponsored by The Impact Group, supported by Pfizer, Staples Center, Los Angeles, December 15, 2001.

45. "Advances in Prevention through Optimizing Lipid Lowering; Utilizing the Most Recent Therapies in Getting Patients to Goal" CME sponsored by The France Foundation, supported by Astra-Zeneca, Log Haven, Salt Lake City, January 15, 2002.

46. "The New NCEP ATP III Guidelines for Lipid Management: How to use them, and do they really make a difference?" CME sponsored by University of Utah School of Medicine, Department of Internal Medicine, Advances in Internal Medicine, The Lodges at Deer Valley Park City, Utah, March 21, 2002.

Abstract Presentations

1. American Heart Association Meetings, November 14, 1989. "Familial Combined Hyperlipidemia (FCHL) and Familial Dyslipidemic Hypertension (FDH): The Most Common Syndromes in Utah Coronary Pedigrees". Abstract #826. Circulation 1989; SO (Suppl II): II-207.

2. American Heart Association Meetings, November 11, 1998, "Type III Hyperlipidemia and Lipoprotein Remnants in Early Onset Familial Coronary Artery Disease". Abstract #4146. Circulation 1998; 98 (suppl P): I-791.

3. American Heart Association Epidemiology Council Meetings, March 1, 2001, San Antonio. "IS the Heat Labile Variant of Methylene Tettahydrofolate Reductase (MTHFR-HL) Associated with Elevated Plasma Total Homocysteine (they) and Premature Coronary Artery Disease (CAD)?" Poster presentation.

4. American Heart Association Epidemiology Council Meetings. March 2, 2001, San Antonio. "Benefits of the MEDPED Treatment Support Program" Poster presentation.

5. American Heart Association Meetings, November 12, 2001. "Gender bias in treatment of lipids among patients with familial hypercholeeterolemia". Abstract #3712, Circulation 2001; 104; II-790.

PUBLICATIONSBooks and Textbook Chapters-[11]

Abstracts and Letter-[27]

Journal Articles. Monograph Chapters

Before 2000[28]-[102]

2000 and later[103]-[153]

Williams RR, Hunt SC, Hopkias PN, Wu LL, Haastedt SJ, Stults BM, Kuida H. Genes, hyperteosion, and early familial coronary heart disease, In: Laragh JH, Brenner BM, eds. Hypertension: pathophysiology, diagposis and management New York: Raven Press; 1990: 127-136.

Hopkins PH Hyperlipidemia: detection and treatment. In: Yanowitz FG, ed. Coronary hejjrt disease prevention A view towards the 21st century. New York: Marcel Dekker, Inc; 1992:189-249.

Hopkins PN, Wit LL, Williams RR. Dyslipideoiias. Jn: Noe DA, Rock RC, eds. Laboratory medicine The selection and interpretation of clinical laboratory studies. Baltimore: Williams Wiltons; 1994:476-511.

Williams RTt, Hopkins PH Hunt SG, Sehumacher MC, Stulta BM, Wu LU Hasstedt S J. Inherited susceptibility to metabolic complications of obesity. In; Bouchaid C, ed. The genetics of obesity. Boca Ratan, Florida CRC Press; 1994:147-159.

Wu LH, WTI JTf Hopkins PN Apalipopnotein E: laboratory determinations and clinical significance. In: Rifai N, Wamicfc GR, Dominiczak MH, eds. Handbook of [ipopiotein testing, Washington, D.C.: AACC Press; 1997:329-356.

Williams RR, Hopkins FN, Wu LL, Scoumacher MC, Hunt SC Bvalualing fkuily history to prevent early CHD. In: Pearaon TA, Diqui MH, Luepker RV, Oberman A, Winston M, eds. Primer in preventive cardiology. Dallas: American Hieait Association; 1994:93-106.

Hunt SC, Hopkins PN, WiHiarns RR-Hypertensiott: genetics and mechanisms. In: Fuster V, RDSJJ R, Topol FJ3 eds. Atherosclerosis and coronary artery disease, Philadelphia: Uppincott-Raven Publishera; 1996:209-235.

Williams RK, Hunt SC, Hopkins PN, Wu L, Stephenson S. Practical baiefita from understanding the genetics of chronic diseases. In: Day I, Humptuiea S, eds. Genetics of coranum diseases: future therapeutic and diagnogtic possibilities. Oxford: BIOS Scientific Pubhshos Limited; J9?7:185-202.

Hopkins PN, Hunt SC, Wu LL, Williams RR, Family history and genetic factors. IF: Wong ND, ed. Preventive cardiology. New Yoik; McGraw-HiU; 2000:93-132.

Wilfcams RJR, Hopkins PN, Wu LL, Hunt SC. Applying genetic strategies to prevent atherosclerosis. In: Khoury MJ, Burke W, Thomsou EJ, eds. Genetics and public health in the 21^st century. New York: Oxford University Press; 2000:463-435.

Smith TW, Hopkitts PN, Psychosocial wnsBidcrations in essential hypertension, coronary heart dU$a$a, and end-stage renal disease. In: Scbein LA, Bernard HS, Spitz HI, Muskin PRj eds. Psyctosgcial treatment for medical conditiona: principles and techniques. New York; ttttnmer-Routledge; 2003:133-179.

Hopkrdfi PN. Phenylpcopanolamine; an ineffective and potentially dangerous over-die-counter appetite suppressant. Utah State Medical Association Bulletin 1964; 32:2-3.

Hopkins PN, Willi ams RR, Hunt SC. Coronary heart disease and sm oking (letter). West J Med 1935; 143; 631-682.

Hunt SC, Wu LLt Hopkins PN, Stults BM, Kuida H, Laloucl J-M. Williams RR. Characteristics of familial dyslipidemio hypertension and its nelattonehip to familial combined hvperlipidemia [abstract], Cincutation 1938; 78 (suppl n):II-481.

Hunt SC, Wu LL, Hopkins PN, Will jama RR, Elevated Na-Li coxmtertransport and lasting insulin in patients with familial combined hyperlipidemia and hypertension [abstract], Hypertension 1989; 14:345.

Hegele RA, Rni M, Wu L, Hopkins PN, Lalouel JM, Williams KR. Anapolipoprotein B gone mutation normalizes the lipid profile in a paiient with a gene for familial hypeicholcstepoleinia fabstract], Clm Res 1939; 37:129A.

Williams RR, Hopkins PN, Hunt SC, Wu LL, Hasstedt SJ, Laiouel JM, Ash KO, Stults BM, Kuida H. Fumilial combined hypedipidetnia (FCHL) and familial dyslipidemic hypertension (FDH): The moat common syndromes in Utah conjnary pedigrees [abstract]. Circulation 1939; 80 (Suppl n):II-207.

Hunt SC, Stephenson SH, Hopkins PN, Hasstedt SJ, Williams RR. A 7-year prospective study of sodium-lithium countertransport (SLC) and hypertension [abstract]. Am J Hypertens.

Hopkins PN, Wu LL, Williams RR, Leary ET, Waug T, Nakajjma K. Type III hypertipidemia and lipoproteiti remnants in early onset familial coronary artery disease. Circulation 1998; 98 (suppl 1);I-791.

Amett DK, Devereux RB, Hong Y, Rao DC, Oberman A, Kitzman D W, Hopkins PN. Strong heritability of left ventricular mass in hypertensive African Americans and relative wall thickness in hypertensive whites: The HyperGEN Echocardiography Study, Circulation 1998; 98 (suppl I):I-658.

Amen DK, Bella IN, Paranicas M, Rao DC, Obennan A, Kitzman DW, Hopkins PN. Differences between African American and whites in left ventricular mass and geometry: The HyperGEN Echocardiography Study, Circulation 1998; 98 (suppl I); 1-204.

Palmieri V, de Simone G, Amett DK, Bella JN, Liu JE, Kitsaaan DW, Obennan A, Hbpkuis PN, Fishman D, Devereun RB. Impact of lean body mass on left ventricular mass and hemodynamics in obese and non-obese hypertensive: The HyperGEN Study, Circulation 1999; 100:J-741.

Amett DK, Deveneus RB. Rao DC, Kitzman D W, Obetmai: A, Hopkins PN. A genome search in hypertensive African American and white siblings detects a locus mapping to chromosome 7 that infteunces variation in left ventricular mass; The HyperGEN Study. Circulation 1999; 100:1-193.

Djousse L, Pankow IS, Eckfeldt JH, Folsom AR., Hopkins PN, Province MA, Hong Y, Ellison RC, Relation between dietary lujolenic fatty acid and coronary heart disease in the NHLBI Family Heart Study [abstiact]. Circulation 2001; 103:1346.

Hopkins PN, Rozen R, Hunt SC, Is the heal labile variant of metfiylene tetrahydrofolate reductese (MTHFR-HL) associated wilh elevated plasma total homocystcinc (tHey) cmd premature coronary artery disease (CAD)? [abstract]. Circulation 2001; 103:1354.

Hopkins PN, Stephenaon SH, Laninaga-Shum S. Benefits of MEDPED Treatment Support Program (TSP) for patients with familial hypercholesterolemia [abstract]. Circulation 2001; 103:1368.

Hopkins PN, Stephenson SH, Lairinaga'Shum S. Gender bias in treatment of lipids among patients with familial hypercholesterotemia. Circulation 2001; 104 (Suppl II):II-790.

"Williams RR, Hopkins PN. Salt, hypertension, aud geraetic-cnvirunmental interactiDns. Id; Siog CF, Skolnict M, eds. The genetic analysis of common diseases. New York: Alan R-Liss, Int., 1979:183-194.

Hopkins PN, Williams RR. A simplified approach to lipoprotein kinetics and factors affecting serum cholesterol and triglyccridc concentrations. Am J Clin Nutr 1981; 34:2560-2590.

Hopkins PN. Williams RR. A survey of 246 suggested coronary risk factors-Atherosclerosis 1981; 40:1-52.

Williams RR, Dadone M, Hunt SC, Jorde LB, Hopkins PN, Smith JB, Ash KD, Kuida H, The genetic epidemiology of hypertension: review of past studies and current results for 948 persons in 48 Utah pedigrees, In: Rao DC, Blston RC, Kuller LH, Feinleib M, Carter C, Havlik R, eds. Genetic epidemiology of coronary heart disease: pasl, present, and future. New York: Alan R Liss, Inc, 1984:419-444.

Hopkins PN, Williams RR, Hunt SC. Magnified risks from cigarette smoking for coronary prone families in Utah. West J Med 1984: 141: 196-202.

Hopkins PN, Williams RR Identification and relative weight of cardiovascular risk factora. Cardiology Clinics 1986; 4:3-31.

Hunt SC, Blickenstaff K, Hopkins PN, Williams RR. Coronary disease and risk factors in close relatives of Utah women with early coronary death. West I Med 1986; 145:329-334.

Hopkins PN, Williams RR, Kuida H, Stalls BM, Hunt SC, Barlow GK, Ash KO. Family history as an independent risk factor for incident coronary artery disease in a high-risk cohort in Utah. Am I Cardiol 1988; 62:703-707.

Williams RR, Hunt SC, Wu LL, Hasstedt SJ, Hopkins PN, Ash KO. Genetic and epidemiological studies on electrolyte transport systems in hypertension, Clin Physiol Biochem 1988; 6:136-149.

Dluhy R G, Hopkins PN, Hollenberg NK, Williams GH, Williams RR. Heritable ¶ of the ¶ system in essential hypertension. J Cardiovasc Pharmacol 198g; 12 (suppl 3):S149-S154.

Williams RR, Hunt SC, Hopkins PN, Stults BM, Wu LL, Hassledt SJ, Barlow GK, Stephenson SH, Lalouel J-M, Kuida H. Familial dyslipidemic hypertension. Evidence from 5S Utah families for a syndrome present in approximately 12% of patients with essential hypertension, JAMA 1988; 259:3579-3586.

Lifted RP, Hopkins PN, Williams RR, Hollenberg NK, Williams GH, Dluhy RG. Evidence for heritability of non-modulating essential hypertension, Hypertension 1989, 13:884.

Hunt SC, Hasstedt SJ, Kuida H, Stulla BM, Hopkins PN, Williams RR, Genelic heritability and common environmental components of resting and stressed blood pressures, lipids, and body mass index in Utah pedigrees and twins. Am J Epidermiol 1939; 129:625-638.

Williams RR, Hunt SC, Hopkins PN, Stults BM, Wu LL, Hasstedt SJ, Barlow GK, Stephenson SH, Lalouel J-M, Kuida H, Un nouveau syndrome; Thypertension dyslipidemique femiliale JAMA 1989; 14:109-111.

Williams RR, Hunt SC, Hasstedt SJ, Hopkins PN, Wu LL, Stults BM, Berry TD, Barlow GK, Kuida H, inherited bimodal traits and susceptibility to hypertension in Utah pedigrees. In: Rettig R, Ganten D, Luft eds, eds. Salt and hypertension. Heidelberg, Germany: Springer-Verlag; 1989:139-155.

Williams RR, Hunt SC, Hasstedt SJ, Hopkins PN, Wu LL, Berry TD, Stults B, Barlow GK, Schumacher MC, Kuida H. Current knowledge regarding the genetics of human hypertension. J Hypertens 1989; 7 (suppl 6):58-S13.

Williams RR, Schumacher MC, Hunt SC, Wu LL, Hopkins PN, Kuida H The genetics of hypertension, coronary atherosclerosis, and non insulin dependent diabetes mellitus (NIDDM): heterogeneity and covariation; In: Nerup J, Mandrup-Poulson T, Hokfelt B, ods, Genes and gene products in the development of diabetes mellitus, New York: Eisevier Science. Publishers; 1989:387-397.

Hopkins PN, Williams RR. Human genetics and coronary heart disease: a public health perspective. Armu Rev Nutr 19S9; 9:303-345.

Hopkins PN, Williams RR., Kuida H, Slults BM, Hunt SC, Barlow GK, Ash KO. Predictive value of a short dietary questionnaire for changes in serum lipids In high-risk Utah families. Am J Gin Nutr 1969; 50:292-300.

Hegele RA, Ermi M, Wu LL, Hopkins PN, Williams RR, Lalouel JM. Clinical application of deoxy ¶ acid markers in a Utah family with ¶. Am J Cardiol 1989; 63:109-112.

Hunt SC, Wu LL, Hopkins PN, Stults BM, Kuida H, Ramirez ME, Lalouel JM, Williams RR. ¶, low density lipoprotein subfraction, and insulin associations with familial combined hyperlipidermia: Study of Utah patients with familial dyslipidemic hypertension, Arteriosclerosis 1989; 9:335-344.

Williams RR, Malinow MR, Hunt SC, Upson B, Wu LL, Hopkins PN, Stults BN, Kuida EL Hyperhomocyst(e)injemia in Utah siblings with early coronary disease. Cor Art Dis 1990; 1:681-685.

Williams RR, Hunt SC, Hasstedt SJ, Hoptins PN, Wu LL, Berry TD, Stults BM, Barlow GK, Kuida H, Hypertension: genetics and nutrition. World Rev Nutr Diet 1990; 63:116-130.

Williams RR, Hopkins PN, Hunt SC, Wu LL, Hasstedt SJ, Lalouel JM, Ash KO, Stulta BM, Kuida H. Population-based frequency of dyslipidernia syndromes in coronary prone families in Utah, Arch Intern Med 1990; 150:582-588.

Williams RR, Hunt SC, Hasstedt SJ, Hopkins PN, Wu LL, Berry TD, Stults BM, Barlow GK, Kuida H. Genetics of hypertension: what we know and don't know, Clin Exp Hypertens [A] 1990; 12:865-876.

Williams RR, Hunt SC, Wu LL, Hopkins PN, Hasstedt SJ, Schumacher MC, Stults BM, Kuida H. Concordant dyslipidemia, hypertension and early coronary disease in Utah families, Klin Wochenschr 1990; 68:52-58.

Williams RR, Hum SC, Haastedt SJ, Hopkins PN, Wu LL, Berry TD, Stilts BM, Barlow GK, Schumacher MC, Lifton RP, Lalouel JM, Multigenic human hypertension: evidence for subtypes and hope for haplotypes, J Hyperten 1990; 8 (suppl 7):S39-S4C.

Jorde LB, Williams RR, Hopkim PN. Family history as an independent risk factor for coronary artery disease. Cardiology Boani Review 1990; 7:31-48.

Williams RR, Hunt SC, Hasstedt SJ, Hopkins PN, Wu LL, Beary TD, Stults BM, Bartow GK, Schumacher MC, Lf Aon KP, Lalouel JM. Are there imteractions and relations between genetic and environmental factors predisposing to high blood pressure? Hypertension 1991; 18 (suppl 1):I-29-I-37.

Hegde RA, Sutherland S, Robertson M, Wu LL, Emi M, Hopkins PN, Williams RR, Lalouel JM. The effect of genetic determinauts of low density lipoprotein levels on lipoprotein(a). Clin Invest Med 1991; 14:146-152.

Williams RR, Hunt SC, Hasstedt SJ, Hopkins PN, Wu LL, Schumacher MC, Berry TD, Stults BM, Barlow GK, Lifton RP, Lolouel J-M. A population perspective for genetics research and applications to control cardiovascular disease in Utah. In: Berg K, Bulyzhenkov V, Christen Y, Corvol P, eds, Genetic approaches to coronary heart disease and hypertension. Berlin: Springer-Verlag 1991:8-19.

Williams RR, Hunt SC, Wu LL, Hopkins PN, Schumaduw MC, Elbein S, Haasbedt S, Lalouel JM, Stults BM, Kuida N. Dyslipidernia hypertension in families with hypertension, non-insulin-dependent diabetes mellitus, and coronary heart disease. Athemselar Rev 1991; 22:107-111.

Williams RR, Hasstedt SJ, Hunt SC, Wu LL, Hopkins PN, Berry TD, Stults BM, Bartow GK, Kuida H. Genetic traits related to hypertension and electrolyte metabolism. Hypertension liJiJl; 17 (suppl 1):I-69-1-73.

Williams RR, Hunt SC, Schunaacher MC, Hopking PN, Wu LL, Barlow GK, Stults BM, Wilson DE, Lalouel I-M, Genes, hypertension and coronary heart disease: evidene for shared metabolic pathophystology. Nn: Smith U, Bruun NE, Hedner T, H"kfelt B, eds. Hypertension as an insulin-resistant disorder Genetic factors and cellular mechanisms, Amsterdam: Elsevier Science Publishers B. V.; 1991:89-101.

Hunt SC, Stephenson SH, Hopkins PN, Williams RR. Predictors of an increased risk of future hypertension in Utah. A screening analysis. Hypertension 1991; 17:969-976.

Hunt SC, Stephenson SH, Hopkins PN, Hasstedt SJ, Williams RR, A prospective study of sodium-lithium countertransport and hypertension in Utah. Hypertension 1991; 17:1-7.

Emi M, Hegele RM, Hopkins PN, Wu LL, Plaetke R, Williams RR, Lalouel JM Effects of three genetic loci in a pedigree with multiple lipopratein phenotypes, Arteriosclerosis 1991; 11:1349-1355.

Hopkins PN, Wu LL, Scbumacher MC, Emi M, Hegele RM, Hunl SC, Lalouel JM, William* KB. Type III dysfipoproteinemia in patients heterozygous for familias hypercholesterolemia and apolipoprotein E2. Evidence for a genc-gene interaction. Arterioscler Throrab 1991; 11:1137-1146.

McMurry MP, Hopkins PN, Gould R, Engclbcrt FK, Schumacher C, WuLL, Williams RR. Family-oriented nutrition intervention for a lipid clinic population. J Am Dietet Assoc 1991; 91:57-65.

Williams RR, Hunt SC, Barlow GK, Wu LL, Hopkins PN, Schumacher MC, Hasatedt SJ, Ware I, Chamberlain, RM, Weinberg AD. Prevention of famitial cardiovascular disease by screening for family history and lipids in youths. Clin Chem 1992; 38:1555-1560.

Williams GH, Dluny RG, Lifton RP, Moore TI, Gleason R, Williams R, Hnnt SC, Hopkins PN, Holleuberg NK. Non-modulation as an intermediate phaiotype in essential hypertension. Hypertension 1992; 20:788-796.

Williams RR, Hunt SC, Hopkins PN, Hasstedt SI, Wu LL, Stults BM, Schumacher MC, Kntda H, Lalouel JM, Hypertension and dyslipidemia in high risk families, In Gotto AM, Lenfant C, Paoletti R, Soma M, eds. Multiple risk foctors in cardiovascular disease. Dordrecht: Kluwer Academic Publishers; 1992-11M15.

Jeunennaitre X, Soubrier F, Kotelevtsev YV, Lifton RP, Williams CS, Charru A, Hunt SC, Hopkins PN, Williams RR, Lalouel J-M, Corvol P. Molecular basis of human hypatertsion; role of angiotensinogen. Cell 1992; 71:169-180.

Williams RR, Hunl SC, Hopkins PN, Wu LL, Schumacher MC, Stalts BM, Ball L, Ware J, Hasstedt SJ, LaJouel J-M. Evidence for genc-environmental interactions in Utah families with hypertension, dysbpidacmia and early coronary heart disease. Clin Esp Pharmacol Physiol 1992: 19(soppl 20):1-6.

Williams RR, Hopking PN, Hunt SC, Schumscher MC, Elbein SC, Wilson DE, Stults BM, Wu LL, Hasstedt SJ, Lalouel J-M. familial dyshpidaemic hypertension and other multiple metabolic syndromes. Ann Med 1992; 24:469-475.

Hopkins PN, Effects of dietary cholesterol on scrum cholesterol: a meta-analysis and review. Am J Clin Nutr 1992; 55:1060-1069.

Williams RR, Hunt SC, Hopkins PN, Wu LL, Hasstedt SJ, Beny TD, Barlow GK, Stults BM, Schumacher MC, Ludwig EH, Elbdn SC, Wilson DE, Lifton RP, Lalouel JM. Genetic basis of familial dyslipideinia and ¶ 15 — yrar results from Utah. Am J Hyperlens 1993; 6:319S-327S.

Williams RR, Hunt SC, Scbumacher MC, Hegele RA, Leppeit MF, Ludwig EH, Hopkins PN. Diagnosing heterozygous familial hypercholcstcrolemia using new practical criteria validated by molecular genetics. Am J Cardiol 1993; 72:171-176.

Williams RR, Hunt SC Hopkins PN, Wu LL, Lalouel JM. Evidence for single gene contributions to hypertension and lipid disturbances: definition, genetics, and clinical significance, Clin Genet 1994; 46:80-87.

Wu LL, Wu J, Hunt SC, James BC, Vincent GM, Williams RR, Hopkins PN, Plasina homocyst(e)ine as a risk factor for early familial coronary artery disease. Clin Chem 1994; 40:552-561.

Williams RR, Hunt SC, Barlow GK, Hopkins PN, Ware JL, J3outyjenkov V. MED PED: preventve medicine for high risk pedigrees. In Yamamoto A. ed Multiple risk (actors in cardiovascular disease. Tokyo: Churchill Livingstone Japan; 1994:173-179.

Williams R.R. Schumacher MC, Hopkins PN, Hunt SC, Wu LL, Hasstedt SJ, Stults BM, Ware JL, James BC, Vincent GM, Pratt M, Latham BD, Bulyzhenkov V, Practical approaches for finding and helping coronary prone pedigrees. In: ¶ U, de Faire U, Berg K, eds. ¶ factors in coronary heart disease. Dordrecht, Boston, London: Kluwer Academic Publishes; 1994:425-445.

Wiliams RR, Hunt SC, Hopkins PN, ¶ SJ, Wu LL, Lalouel J-M, Tsbulations and expectations regarding the genetics of human hypertension. Kidney Int 1994; 45 (suppl 44): S-57-S-64.

Hopkins PN, Wu LL, Wu J, Hunt SC, James BC, Vincent GM, Williams RR. Higher ptaema homocy 51(e)ine and increased susceptibility to adverse effects of low folate in early familial coronary artery disease. Arterioscler Tbromb Vase Biol 1995; 15:1314-1329.

Williams RR. Hunt SC, Hopkins PN, Hasstedt SJ, Wu LL, Lalouel JM. Finding the genes for human hypertension. In: Woodford FP, Davignon J, ¶ A, eds. Atherosclerosis X. New York: Elsevier Science B. V.; 1995:856-861.

Williams RR, Hopkins PN, Wu LL, Hunt SC. Guidelines for managing severe familial lipid disonders. Primary Cardiology 1995; 21:47-53.

Gaboury CL, Hollenberg NK, Hopkins PN, Williams R, Williams GH, Metabolic derangements in nonmodulating hyperteflsion. Am J Hypertens 1995; 8;870-875.

Hopkins PN, Litton RP, Hotlenberg NK, Jeunemaitre X, Hallouin MC, Skuppin J, Williams CS, DIuhy RG, Latouel JM, Williams RR, Witiams GH. Blunted renal vascular response to angiotensin II is associated with a common variant of the angiotsisirogen gene and obesity. J Hypertens 1996; 14: 199-207.

Hopkins PN, Wu LL Hunt SC, Jaraea BC, Vincent GM, Williams RR. Higher serum bilinibin is associated with decreased risk for eaily familial coronary artedry disease. Aiterioscler Thromb Vase Biol 1996; 16:250-255.

Hopkins PN, Hunt SC, Wu LL, Williams GH, Williams RR Hypertension, dyslipidemia, and insulin resistance; links in a chain or spokes on a wheel? Curr Opin Lipidol 1996; 7:241-253.

Hunt SC, Wu LL, Hopkins PN, Williams RR-Evidence for a major gene elevating serum bilirubin concentration in Utah pedigrees. Arterioscler Thrarnb Vase Biol 1996; 16:912-917.

Hopkins PN, Wu LL, Hunt SC, James BC, Vincent GM, Williams RR lipopnrtein(a) iMeracdoas with lipid and non-lipid risk factors in early familial coronary artery disease, Arterioscler Thromb Vase Biol 1997; 175783-2792.

Lndwig EH, Hopkins PN, Alien A, Wu LL, Williams RR, Andoson JL, Ward RH, Lslouel I-M, fonerarity TL, Association of garetic vaiiaiioiis in opolipoprotcta B with hypercholesterolemia, coronary artery disease, and receptor binding of low density tipoproteins, J Lipid Res 1997; 38: 1361-1373.

Hopkins PN, Hunt SC, Schrciner PJ, Eokfeldt JH, Borecki B, Ellison CR, Willison RR, Stegmund KD. Lipopnoten(a) interactions with lipid and non-lipid risk faclons in patieota wilh early onset coronary artery disease. Results from the NHLBI Family Heart Study. Atherosclerosis 1998; 141:333-345.

Hopkins PN. An approach to dyBlipidcmia. J Am Acad Phys Assist 1998; September.

Day 1NM, Hopkins PN. Clinical criteria for the diagnosis of FH. In: Familtal Hypercflolestenolemia Report of a WHO Consultation. Paris: World Health Organkation; 1998.

Yaraaki E, Hirayama T, Wu LL, Hopkions PN, Williams RR, Emi M. VTolccular genetic diagnosis of a family with hypercholesterolemia by a mismatched PCR-KFLF method for genotypiug single base substitution of the LDL receptor gene, Jpn Heart J 1998; 39:681-686. PGPage 17

Bmi M5 Yamaki E, Hirayama T, Kateumata H, Poxharov Vf Wu LL, I lopfcine PN, Williams RR-Familial hypercholesteioleinm kindred in Utah with novel C54S mutations of (he LDL receptor gene, Jpn Heart J 199$; 39:785-789.

Stein EA, Htmgworth DR. Kwilerovieh PG, Jr., Liacouras CA, Slimes MA, Jacobson MS, Breweter TG, HopkUw P, Davideon M, Graham EC, ArensnMn F, Knopp RH, DuJovne C, Williams CL, Isaacsohn JL, Jacobsen CA, Laskarzcwski PM, Ames S, Gormley GJ, Efficacy and safety of Icvastatin in adolescent males with heterozygous familial hyperchdegterotcroia: a randomized controlled trial. JAMA 1999; 261:137-144.

Haddad L, Day INM, Hunt S, Williams RB, Humphries SE, Hopkins PN. Evidence for A (binl genetic locus causing familial hypercholesterolafimia: a uon-LDLR, non-apoB kindred J Lipid Res 1999; 40:1113-1122.

Wang T, Nakaj iraa K, Lcary ET, Wamick GR, Cohn JS, Hopkins PN, Wu LL, Cilia DD, Zhong J, Havel RJ. Ratio of remnant-like particle-cholesterol to serum total trielycerides is an effective alternative to uJtracentrifiigpl and elettrophoretic methods in (he diagpsosis of famtfial type IH Jiypertipoproteinemia, din Cbern 1999; 45:1981-1987.

Kateumato H, Enii M, N-ob" Yd Naksqima T, Hirayama T, Wu LL, Stephenson SH, Hopkins PN, Williams RR. Familial hyperchofesteFolemia in Utah kindred with novel R1Q3W mutations in exon 4 of tbe IDL recqitor gene. Jpn Heart J 1999; 40:443-449.

Nobe Yt Emi M, Katsumala H, Naltajima Tt Hirayania T, Wu LL, Stephens(tm) SH, Hopkins PN, Williams RR. Familial hypercholesterolemia in Utah kindred with novel 2412-5 Ins G mutations in eion 17 of the LDL receptor gene. Jpn Heart J 1999; 40:435-441.

Hopkins PN, Wu LL, Stephenson SH, Xia Y, Katsumata H, Nobe Y, Nataj iraa T, Hjiayama T, Emi M, Williams RR. A novel LDLR mutation, H190Y, in ft Utah fcifldred with famital hypercoolestKolemia, J Hum Genet 1999; 44:364-367.

Williams RR, Hopkins PN, Stephenson S, Wu L, Hunt SC. Primordial prevention of cardiovascular disease through applied genetics, Prev Med 1999; 29; S41-S49.

Giaocfoe M, Vuagnat A, Hunt SC, Hopkins PN, Fisher ND, Azizi M, Corvol P, Williams GH, Jcuncmiitre X. AldwteioDe stimuUition by angiotengin II: influence of gendW, plasma renin, and familial resemblance, Hypertensioo 2000; 35:710-716.

Koit EN, BalHngcr LX5f Ding W, Hunt SC, Bowen BR, Abkevich V, Bulka K, Campbell B, Capener C, Gutin A, Harshman K, McDcnnott M, Tbome Tf Wang H, Waidetl B, Wong J, Hopkins PN, SkoEnick M, Samuels M. Evidence of linkage of familiai hypercholesterolemia to a novel locus on chromosome 1 Iq23. Am J Hum Genet 2000; 66:1845-1856.

Hunt SC, Hopkins PN, Balka K, McDennott MT, Thorae TL, WatdeU BB, Bowen BR, Ballmger DG, Skolnick MH, Samuels ME, Geneuc localisation to ctromosome ip32 ot the thini locus for familial hypercholesterolemia in a Utah kindred. Artcrioscler Thuomb Vase Btol 2000; 20:1089-1093.

Williams GH, Fisher ND, Hunt SC, Jeunemaitre X, Hopkins PN, Holleriberg NXL Effects of gender and genotype on the phemotypic expression of nonmodulatiug essential hypertension. Kidney Int 2000; 57:1404-1407.

Wu LU Hopkins PN, Xin Y, Stephenson SII, WiUiams RR, Nobe Y, Kajita M, Nakajuna T, Emi M, Co-segregation of elevated LDL with a novel mutation (D92JC) of the LDL receptor in a kindred with multiple lipoprotejn abnormalities, J Hum Genet 2000; 45:154-158.

Manxnuc C, Hopkins PN, Wang T, Leaiy ET, Nakajima K, Davignon J, Cohti J S. Remnaot-)Jkc particle cholesterol and trigtyceride levels pf hypertrigiyceridemcc patients in the fed and fasted state. J Upid Res 2000; 41:1428-1436.

Williams KRT Hunt SC, Heiss G, Province MA, Bensen JT, Higgins M, Chamberlain RM, Ware J, Hopkins PN, Usefulness of cardiovascular famHy history data fiwpopuMon-based preventive medicine and medical research (The Health Family Tree Study and the NHLBI Family Heart Study), Am I Cardkil 2001; 87:129-135.

Palmieri V, Bella JK, Amett DK, Liu JE, Obennan A, Schuck MY, Kitansn DW, Hopkins PN, Morgan D, Ran DC, Devaeux RB. Effect of type 2 diabetes mellitus on left ventricular geometry and systolic function in hypertoasive subjects r hypertension genetic epidemiology network (HyperGEN) study, Circulation (Online) 2001; 103:102-107.

Raji A, Williams GH, Jcunenuitre X, Hopldns PN, HuntSC, Hollenterg NK, Seely EW. Insylm reaigtance in hypertensives: effect of salt sensitivity, renia status and sodium intake. J Hyperteos 2001; 19:99-105.

Huiwitz S, Potter B, Weiss RJ, Jeunemadtre X, Hopkins PN, Hunt SC, Litchfield WR, Williams GH. Influence of sodium intake on the reliability of active renin as a measure cf the reran-angiotmsin system in essential hypertensiotL Am J Clin Psthol 2001; 115:304-312.

Hopkins PN, Stephereon S, WuLL, Riley WA, Xin Y, Hunt SC. Evaluation of coronary risk factors in patients with heterozygous familial hypercholesbemlBmia. Am J Cardiol 2001; 87:547-553.

Pankow JS. Foteom AR. Cushman M. Borecki IB, Hopkins PN, Eckfeldt JH, Tracy KP. Familid and genetic determinants of systemic markers of inflammation: the NHLB1 Faintly Heart Study, Atherosclerosis 2001; 154:681-689.

Hunt SC, Kronenberg F, Eekfoldt JH, Hopkins PN, Myers RH, Heiss G, Association of plasma bilirubin with coronary heart disease and segregation of bilirubin oe a major gene trait: the NHLBI family heart study. Atherosclerosis 2001; 154:747-754.

Hong Y, Rautaharju PM, Hopkins PN, Amett DK, Djousse L, Pankow JS, Shulinsky P, Rao DC, Province MA Familial aggregation of QT-iolerval variability in a getrenal population: results from the NHLBI Family Heart Study. Cltn Geiiet 2001; 59:171-177.

Samuels M, Forbey K, Reid J, Abkevich V, Bulka K, Wardell B, Bowen B, Hopkins P, Hunt S, Ballinger D, Stolnick M, Wagner S, Identification of a common variant in. the lipoprotein lipase gene in a large Utah kindred ascotained for coronary heart disease; the-93G/D9N variant prediqxjses to low HDL-C/high (riglycaides, Clin Genet 2001; 59:88-98.

Hollenberg NK, Anzalone DA, Falkner B, Fisher ND, Hopkins PN, Hsueh W, Hutchinaon H, Krauss FM, Price DA, Raskm P, Reaven GM, Familial factors in the antihyperteasive response to lisiitoprit. Am JHypertens 2001; 14:218-223.

Palmieri V, Bella JN, Amett DK, Roman MJ, Oherman A, Kitaman DW, Hopkins PN, Paranricas M, Rau DC, Devereux RB. Aortic root dilatation at sinuses of valsalva and aortic regurgjtBlion in hypertensive and normotensive snibjeck: the hypertension genetic epidemiology network study. Hypeitaialoii 2001, 37. 1229-1235.

Deirtsreux RB, Bella JN, Pahnieri V, Oberman A, Kitsman DW, Hopkins PN, Rao DC, Morgan D, Peranicas M, Fiahman D, Arnctt DK, Left ventricular systobc dysfunction in a biracial sample of hypertensive adults: The Hyper GEN Study. Hypertension 2001; 38:417-423.

Bella JN, Palmieri V, Uu Liu, Kitztnan DW, Oberman A, Hunt SC, Hupkins PN, Rao DC, Amett DK, Devereux RB. Relationship between left ventricular diastolic relaxation and syfitolk fimction in hypertension: the hypertension genetic epidemiology network (HyperGBN) study. Hypertension 2001; 38:424-428.

Amett DK, Devereux RB, Kitzman D, Oberman A, Hopkins P, Atwood L, Dewan A, Rao DC. Linkage of left ventricular contractility to chromosome 11 in humajis: The HyperGEH Study. Hypertension 2001; 38:767-772.

Djousse L, Pankow as, Eckfeldt JH, folsom AR, Hopkins PN, Province MA, Hong Y, Ellison RC. Relation between dietary linolecic acid and coronary artery disease in the National Heart, Lung, and Blood Institute Family Heart Study. Am J Clin Nutr 2001; 74:612-619.

Palmieri V, de Simone G, Amctt DK, Bella JN, Kilanan DW, Oberman A. Hopkins PN, Province MA, Devereux RB. Relation of various degrees of body mass index in patients with systemic hypertension to left ventricular mass, cardiac output, and peripheral resistance (The Hypertension Genetic Epidemiology Network Study). Am J Candiol 2001; 88:1163-1168.

Coon H, Leppert MF, Eckfeldt JH, Oberman A, Myers RH, Peacock JM, Province MA, Hopkins PN, Heiss G. Genome-wide linkage analysis of Jipids in the Hypertension Genetic Epidemiology Network (Hyper GEN) Blood Pressure Study. ArtfirinsclerThioinb VASC Biol 2001; 21:1969-1976.

Amett DK. Hong Y, Bella JN, Oberman A, Kitzman DW, Hopkins PN, Rao DC, DCVCTCUX RB. Sibling correlation of left ventricular mass and geometry in hypertensive African Americans and whites the HypesrGEN study, Hypertension Genetic Epidemiology Network. Am J Hypertens 2001; 14:1226-1230.

Vuagnat A, Giacche M, Hopkins PN, Azizi M, Hunt SC, Vedie B, Corvol f, Williams GH, leunenwtre X. Blood pressure response to angiotensin II, low-density lipoprotein cholesterol and polymorphisms of the angiaiensin II type 1 receptor gene in hypertensive sibling pairs. J Mol Med 2001; 79:175-183.

Hopkins PN. Familial Hypercholesterolemia. Current Treatment Options in Cardiovascular Medicine 2002; 4:121-128.

Grant FD, Romero JR, Jeunemaitre X, Hunt SC, Hopkins PN, Holleoberg NH, Williams GH, Low-renin hypertension, altered sodium homeostasis, and an alpha-adducin polymorphism Hypertension 2002; 39:191-196.

de Simone G, Palmieri V, Bella JN, Celentano A, Hong Y, Oberman A, Kilzman DW, Hoptdna PN, Amett DK, Devereux RB. Association of left ventricular hypertrophy with metabolic risk factors: the HyperGEN study-J Hypertenfi 2002; 20:323-331.

al'Absi M'Devereux RB, Lewis CE, Kitzman DW, Rao DC, Hopkins H. Markovoz J, Amett DK. Blood pressure responses to acute stress and left ventricular mass (The Hypertension Genetic Epidemiology Network Study). Am I Cardiat 2002-89:536-540.

Fisher ND, Hurwitz S, Jeunemaitre X, Hopkins PN, Hollenberg NK., Williams GH. Familial aggregstion of low-renin hypertension. Hypertension 2002; 39;914-918.

Hopkias PN, Hunt SC, Jeunemaitre X, Smith B, Solorio D, Fisher ND, Holleabctg NK, Williams GH Angiotensinogen genotype affects renal and adrenal responses to angiotensin II in essential hypertension. Circulation 2002; 105:1921-1927.

¶ F, Coon H, Ellison Etc, Borecki I, Arnett DK, Province MA, Eckfeldt JH, Hopkins PN, Hunt SC. Segregation analysis of HDL cholesterol in the NHLBI Family Heart Study and in Utah pedigrees. Eur J Ham Genet 2002; 10:367-374.

Palmieri V, Arnett DK, Roman MT, Liu IB, Bella JN, Oberroan A, Kitzman DW. Hopkins PN, Morgan D, de Siroone G, Devereux RB, Appetite suppressants and valvular heart disease in a population-based sample: the HyperGEN study. Am J Med 2002; 112:710-715.

Tang W, Devereux KB, Rac DC, Oberman A, Hopkins PN, Kitzman DW, Amett DK. Associations between ¶ gene variants and left ventricular mass and function in the HyperGEN study. Am Heart J 2002; 143:854-860.

Wilk JB, Myera RH, Zhang Y(Lewis CE, Atwood L, Hopkins PN, Ellison RC, Evidence for a gene influencing heart rate on chromosome 4 among hypertensives. Hum Genet 2002; III:207-213.

Bella JN, Palmieri V, Kitzman DW, Liu JE, Oberman A, Hunt SC, Hopkins PN, Rao DC, Amett DK, Devereux RB, Gender differemce in diastolic function in hypertersion (the HyperGEN study). Am J Cardiol 2002; 89:1052-1056. PGPage 20

Srikumar N, Brown NJ, Hopkins PN, seunemaitre X, Hunt SC, Vaughan DE, Williams GH. PAT-1 in human hypertension: relation to hypertensive groups. Am J Hypertens 2002; 15:683-690.

Kronenberg F, Coon H, Gutin A, Abkevich V, Samuels MR, Ballinger DG, Hopkins PN, Hunt SC, A genome scan for loci influencing anti-atherogenic serum bilirabin levels. Eur J Hum Genet 2002; 10:539-546.

Tang W, Amett DK, Devereux RB, Province MA, Atwood LD, Oberrnan A, Hopkins PN, Kitzman DW. Sibling resemblance for left ventricular structure; contractility, and diastotic filling. Hypertension 2002; 40:233-238.

Hunt SC, Hasstedt SJ, Coon H, Camp NJ, Cawthon RM, Wu LL, Hopkins PN, Linkage of creatinine clearance to chromosome 10 in Utah pedigrees replicates a locus for end-stage rend disease in humans and renal failure in the fawn-booded rat. Kidney Int 2002; 62:1143-114$.

Takada D, Emi M, Ezura Y, Nobe Y, Kawamura K, lino Y, Katayama Y, Xin Y, Wu LL, Larringa-Shiun S, Stephenson SH, Hunt SC, Hopkins PN. Interaction between the LDL-receptor gene bearing a novel imitation and a variant in the apolipoprotein A-II promoter; molecular study in a 1135-member familial hypercholeaterolemia kindred, J Hum Genct 2002; 47:656-664.

Hurwitz S, fisher MD, Feni C, Hopkins PN, Williams GH, Holtenberg NK, Controlled analysis of blood pressure sensitivity to sodium intake: interections with hypertension type. J Hypertens 2003: 21:951-959.

Takada D, Elura Y, Ono S, lino Y, Katayama Y, Xin Y, Wu LL, Larringa-Shum S, Stephenson SH, Hunt SC, Hopkins PN, Emi M, Apolipoprotein H variant modifies plasma triglyceride phenotype in familial hyperebolcholester A molecular study in an eight-generation hyperlipidemic family, J Atherosdcr Thromb 2003; 10:79-84.

Hopkins PN. Familial hypeaxholesterolemia — Improving treatment and meeting guidelines, Int J Cardiol 2003; 89:13-23.

Hopkins PN, Polukofif GL Risk of valvular heart disease associated with use of fenfluramine. BMC Cardiovase Disord 2003; 3:5.

Hopkins PN, Heiss G, Ellison RC, Province MA, Pankow JS, Eckfeldt JH, Hunt SC, Coronary artery disease risk in familial combined hyperlipidemia and familial ¶ a case control comparison from the National Heart, Lung, and Blood Institute Family Heart Study. Circulation 2003; 108:519-523.

Takada D, Ezura Y, Onu S, lino Y, Kateyama Y, Xin Y, Wu LL, Larringa-shum S, Stephenson SH, Hunt SC, Hopkins PM, Rmi M. Growth hormone receptor variant (L526T) modifies plasma HDL cholesterol phenotype in familial hypercholesterolemia: intra-familial association study in an eight-generation hyperitpidemic kindred. Am J Med Genet 2003; 121 A: 136-140.

Camp NJ, Hopkins PN, Hasstedt S J, Coon H, Malhotra A, Cawthon RM, Hunt SC, Genome-wide multipoint parametric linkage analysis of pulse pressure in large, extended Utah pedigrees. Hypertension 2003; 42:322-328.

de Simone G, Devereux RB, Palmieri V, Bella JN, Oberman A, Kjtzman DW, Hopking PN, Rao DC, Aniett DK. Influence of fat-free mass on detection of appropriateness of left ventricular mass: the HyperGEN Study. J Hypertens 2003; 21:1747-1752.

Tang W, Miller MB, Rich SS, North KE, Pankow IS, Borecki IB, Myers RH, Hopkins PN, Leppert M, Amelt DK. Linkage analysis of a composite Factor for the multiple metabolic syndrome: The National Heart, Lungs and Blood Institute Family Heart Study. Diabetes 2003 52:2840-2847.

Tang W, Devereux KB, Kitzman DW, Province MA, Leppert M, Obemian A, Hopkins PN, Arnelt DK The Arg16Gly polyroorphiani of the beta2-adrenergic receptor and left ventricular systolic function. Ana J Hypertens 2003; 16:945-951.

In re Diet Drugs Products Liability Litigation

Opinion

DECLARATION OF TERI R. RICHARDSON

FACTUAL BACKGROUND

II. WYETH'S REPEATED REQUESTS FOR MEDICAL EVIDENCE FROM MS. MEADES

III. WYETH'S REPEATED REQUEST FOR MS. MEADES' DEPOSITION

ARGUMENT

CONCLUSION

PRETRIAL ORDER NO. _____

EXHIBIT A

STIPULATION AND PRETRIAL ORDER NO.

AGREED ORDER OF DISMISSAL WITH PREPUPICE

STIPULATION AND PRETRIAL ORDER NO.

STIPULATION AND PRETRIAL ORDER NO.

REPORT MID RECOMMENDATION NO. 6 OF SPECIAL MASTER(AS TO MOTION TO ENFORCE PARAGRAPH 7 OF PRETRIAL ORDERNO. 1415 ABAIHST CAROL ANNETTE BRADY)

EXHIBIT CMILLER ASSOCIATESTRIAL ATTORNEYS

ORDER

EXHIBIT D

September 16, 2003

STIPULATION AND PRETRML ORDER NO.

EXHIBIT E

October 9, 2003

EXHIBIT F MILLER ASSOCIATES TRIAL ATTORNEYS

October 20, 2003

STIPULATION AND PRETRIAL ORDER NO.

EXHIBIT G

November 19, 2003

EXHIBIT H

November 19, 2003

EXHIBIT I MILLER ASSOCIATES TRIAL ATTORNEYS

December 21, 2003

MEMORANDUM AND PRETRIAL ORDER NO.

PRETRIAL ORDER NO. _____

SUPPLEMENTAL AFFIDAVIT

DECLARATION OF PAUL N. HOPKINS. M.D., MSPH

SUMMARY OF MY OPINION

THE CLAIMS PROJECTIONS RELIED UPON BY CLASS COUNSEL AND WYETH

COMPUTING THE RATE OF FDA POSITIVE REGURGITION

CLASS COUNSEL'S MATRIX PROJECTION

IT WAS AND IS POSSIBLE TO ACCURATELY CALCULATE THE NUMBER OF CLASS MEMBERS WHO WOULD QUALIFY FOR MATRIX LEVEL BENEFITS

CONCLUSION

Exhibit ACurriculum VitaePaul N, Hopkins, M.D., M.S.P.H.January 2004

In re Diet Drugs Products Liability Litigation

In re Diet Drugs Products Liability Litigation

Case Details

CitationsCopy Citation

**EXHIBIT CMILLER ASSOCIATES*TRIAL ATTORNEYS***

Citations