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Case 3:99-cv-00305-G Document 60 Filed 01/02/07 Page 1 of 46 PageID 788

IN THE UNITED STATES DISTRICT COURT
FOR THE NORTHERN DISTRICT OF TEXAS

DALLAS DIVISION

CINDY BURTON,
Plaintiff,

V.

WYETH-AYERST LABORATORIES
DIVISION OF AMERICAN HOME
PRODUCTS CORPORATION, ET AL.,
Defendants.

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CIVIL ACTION NO.

3:99-CV:0305-G



ECF

________________________________________________________________

WYETH’S BRIEF IN SUPPORT OF

MOTION FOR PARTIAL SUMMARY JUDGMENT



________________________________________________________________








Case 3:99-cv-00305-G Document 60 Filed 01/02/07 Page 2 of 46 PageID 789

TABLE OF CONTENTS

Page No.

Table of Contents .............................................................................................................. i

Index of Authorities........................................................................................................... iii

I. Summary Judgment Standard ...................................................................................... 1

II. Wyeth is Entitled to Summary Judgment on Plaintiff’s Claim of Exercise

Induced Pulmonary Arterial Hypertension................................................................... 2

A.

Summary...................................................................................................... 2

1.

Introduction ....................................................................................... 2

B.

Factual Basis for Motion .............................................................................. 2

1.

2.

3.

4.

Pulmonary Arterial Hypertension ....................................................... 2

Course of Diseases............................................................................. 4

Diet Drugs and PAH Causation .......................................................... 4

Plaintiff Does Not Have the Progressive, Potentially Fatal
Condition Studied in IPPHS............................................................... 6

a. Plaintiff Does Not Have Elevated Resting Pulmonary

Artery Pressures .......................................................................... 6

b. Plaintiff’s Experts Agree That the Course for Exercise

Induced PAH is Different from Resting PAH............................... 12

C.

Argument and Authorities ............................................................................ 14

1.

Plaintiff Must Present Legally Sufficient Evidence of
Causation........................................................................................... 14

a. Texas Law Requires Epidemiological Evidence ........................... 15

(1). Study Must Show Doubling of the Risk ....................... 16

(2). Finding Must be Statistically Significant...................... 17

(3). Study Must Show Results for Specific Injury or

Condition At Issue ....................................................... 17



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(4). At Least Two Studies are Required .............................. 18

(5). Case Reports are Not Reliable Evidence ...................... 18

(6). Unpublished Data is Suspect ........................................ 21

(7). The Plaintiff Must Show Similarity to Those

Studies ......................................................................... 21

2.

3.

4.

Havner is Substantive Texas Law....................................................... 21

Plaintiff Cannot Meet Havner’s Requirements.................................... 25

a. No Epidemiological Study Links Exercise Induced PAH to

Diet Drugs................................................................................... 25

Causation Evidence Relating to Resting PAH or PPH is
Inapplicable ....................................................................................... 29

CONCLUSION........................................................................................................... 31

III. Plaintiff has No Private Cause of Action for Negligence Per Se. ................................ 32

A.

B.

Summary...................................................................................................... 32

Argument and Authorities ............................................................................ 32

IV. Plaintiff Has No Evidence to Support a Conspiracy Claim .......................................... 35

A.

B.

Summary...................................................................................................... 35

Argument and Authorities ............................................................................ 35

CERTIFICATE OF SERVICE .......................................................................................... 38



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INDEX OF AUTHORITIES

Cases









Page No.

1999 WL 811334 (152nd Dist. Ct., Harris County, Tex. June 7, 1999)................33,34

(Tex.App. – Texarkana 2000, no pet.) ..................................................................... 16

(5th Cir. 1999), subsequent appeal, 180 F.3d 175 (5th Cir. 1999) .........................24,25

Anderson v. Liberty Lobby, Inc., 477 U.S. 242 (1986) ..................................................... 1

Austin v. Kerr-McGee Refining Corp., 25 S.W.3d 280


Ayres v. Sears Roebuck & Co., 789 F.2d 1173 (5th Cir. 1986) ........................................ 22

Baker v. Smith & Nephew Richards, Inc., No. 95-58737,


Bartley v. Euclid, Inc., 158 F.3d 261 (5th Cir. 1998), vacated, 169 F.3d 215


Black v. Food Lion, Inc., 171 F.3d 308 (5th Cir. 1999) ..............................................19,24

Cano v. Everest Minerals Corp., 362 F. Supp. 2d 814 (W.D. Tex 2005)...............23,24,25

Caraker v. Sandoz Pharmas. Corp., 172 F. Supp. 2d 1046 (S.D. Ill. 2001).................... 19

Casey v. Ohio Med. Prods., 877 F. Supp. 1380 (N.D. Cal. 1995)................................... 20

Castellow v. Chevron USA, 97 F. Supp. 2d 780 (S.D. Tex. 2000) .................................. 19

Castillo v. First City Bancorporation of Texas, 43 F.3d 953 (5th Cir. 1994) .................. 36

Celotex Corp. v. Catrett, 477 U.S. 317 (1986) ................................................................. 1

Cimino v. Raymark Indus., Inc., 151 F.3d 297 (5th Cir. 1998) ....................................... 21

Coastal Tankships, Inc. v. Anderson, 87 S.W.3d 591


Copley v. Smith & Nephew, Inc., No. H-97-2910, 2000 WL 223404


Current v. Atochem N. Am., Inc., No. W-00-CV-332, 2001 WL 1875950


Daniels v. Lyondell-Citgo Refining Co., 99 S.W.3d 722 (Tex. App. – Houston



(W.D. Tex. Dec. 17, 2001) (unpublished)................................................................ 24

[14th Dist.] 2003, no pet.) ...................................................................................... 16

(Tex. App. — Houston [1st Dist.] 2002, pet. denied)............................................. 18

(S.D. Tex. Feb. 1, 2000) (unpublished).................................................................... 24



iii

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[14th Dist.] 2003, no pet.) ....................................................................................... 18

(Tex. App.-Houston [14th Dist.] Dec. 7, 2006, no pet. h.) ....................................... 20

Daubert v. Merrell Dow Pharm, Inc., 509 U.S. 579 (1993)......................................... 4,23

E. I. DuPont de Nemours v. Robinson, 923 S.W.2d 549 (Tex. 1995) .........................14,23

Erie R. Co. v. Tompkins, 304 U.S. 64 (1938) ................................................................ 21

Exxon Mobil Corp. v. Altimore, No. 14-04-01133-CV, 2006 WL 3511723


Firestone Steel Prods. Co. v. Barajas, 927 S.W.2d 608 (Tex. 1996). ............................. 35

Freudiger v. Keller, 104 S.W.3d 294 (Tex. App.—Texarkana 2003, pet. denied) .......... 32

Frias v. Atlantic Richfield Co., 104 S.W.3d 925 (Tex. App. — Houston


General Elec. Co. v. Ingram, 513 U.S. 1190 (1995)....................................................... 22

Glastetter v. Novartis Pharma. Corp., 252 F.3d 986 (8th Cir. 2001).............................. 18

Hackett v. G.D. Searle & Co., 246 F. Supp. 2d 591 (W.D. Tex. 2002).......................33,34

Hall v. Baxter Healthcare Corp., 947 F. Supp. 1387 (D. Or. 1996)................................ 19

Hamburger v. State Farm Mut. Auto. Ins. Co., 361 F.3d 875 (5th Cir. 2004) ................. 22

Ideal Mut. Ins. Co. v. Last Days Evangelical Ass’n, Inc.,


In re Breast Implant Litig., 11 F. Supp. 2d 1217 (D. Colo. 1998)................................... 19

In re Paoli R.R. Yard PCB Litig., 35 F.3d 717 (3rd Cir. 1994),


Jones v. United States, 933 F. Supp. 894 (N.D. Cal. 1996) aff'd,


Jones v. Wal-Mart Stores, Inc., 870 F.2d 982 (5th Cir. 1989) ........................................ 22

Little v. Liquid Air Corp., 37 F.3d 1069 (5th Cir. 1994) (en banc) ................................... 1

McMahon v. Smith & Nephew Richards, Inc., No. 14-99-00616,




2000 WL 991697 (Tex. App.—Houston [14th Dist.]
July 20, 2000) (not designated for publication)........................................................ 33

783 F.2d 1234 (5th Cir. 1986) ................................................................................. 22

cert. denied sub. nom, General Electric. Co. v. Ingram, 512 U.S. 1190 (1995)........ 22

127 F.3d 1154 (9th Cir. 1997) ................................................................................. 19



iv

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978 S.W.2d 183 (Tex.App. — Texarkana 1998, pet. denied)...............................16,17

(Tex. App. – San Antonio 2002, no pet.) .............................................................16,18

(E.D. Ark. 1996) aff'd, 133 F.3d 1132 (8th Cir. 1998) ............................................. 19

(Tex. 1997) .......................................................................................................passim

Merrell Dow Pharmaceuticals Inc. v. Havner, 953 S.W.2d 706


Minnesota Mining & Manufacturing Co. v. Atterbury,


Mo. Pac. R.R. Co. v. Navarro, 90 S.W.3d 747


Moore v. Ashland Chem. Inc., 151 F.3d 269 (5th Cir. 1998). ....................................... 31

Muzzey v. Kerr-McGee Chem. Corp., 921 F. Supp. 511 (N.D. Ill. 1996)........................ 19

Nat'l Bank of Commerce v. Dow Chemical Co., 965 F. Supp. 1490


Nebraska v. Wyoming, 507 U.S. 584 (1993). ................................................................... 1

Newton v. Roche Laboratories, Inc., 243 F. Supp. 2d 672 (W.D. Tex. 2002) ................. 19

Page v. Gulf Oil Co., 812 F.2d 249 (5th Cir. 1987)........................................................ 34

Peavy v. WFAA-TV, Inc., 221 F.3d 158 (5th Cir. 2000).................................................. 36

Perry v. S.N., 973 S.W.2d 301 (Tex. 1998)................................................................33,34

Reeder v. Daniel, 61 S.W.3d 359 (Tex. 2001)............................................................32,33

Revels v. Novartis Pharmaceuticals Corp., No. 03-98-231-CV,



Reynolds v. Murphy, 188 S.W.3d 252 (Tex. App.—Fort Worth 2006, pet. denied) ........ 32

Rhynes v. Branick Mfg. Corp., 629 F.2d 409 (5th Cir. 1980).......................................... 35

Rider v. Sandoz Pharms. Corp., 295 F.3d 1194 (11th Cir. 2002) ...............................18,19

Siharath v. Sandoz Pharms. Corp., 131 F. Supp. 2d 1347 (N.D. Ga. 2001).................... 19

Smith v. Louisville Ladder Co., 237 F.3d 515 (5th Cir. 2001) ........................................ 24

Smith v. Merritt, 940 S.W.2d 602 (Tex. 1997) ............................................................... 33


1999 WL 644732 (Tex. App.-Austin Aug. 26, 1999, pet. denied)
(not designated for publication)............................................................................... 20



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2004 WL 2058796 (N.D. Tex. 2004) (unpublished). ............................................... 25

(Tex. App. — Houston [14th Dist.] 1995, writ denied)............................................ 36

aff'd, 46 F.3d 1120 (3d Cir. 1994) ........................................................................... 20

2004 WL 3170789 (N.D. Tex. Nov. 15, 2004) (unpublished) .................................. 36

Solomon v. Walgreen Co., 975 F.2d 1086 (5th Cir. 1992) .............................................. 34

Taylor v. Bristol Myers Squibb Co., No. 5:01-CV-166-C,


Tigue Inv. Co., Ltd. v. Chase Bank of Texas, N.A., No. 3:03-Cv-2490-N,


Torres v. Oakland Scavergh Co., 487 U.S. 312 (1988) .................................................. 22

Tutor v. Ranger Ins. Co., 804 F.2d 1395 (5th Cir. 1987)................................................ 22

Tri v. J.T.T., 162 S.W.3d 552 (Tex. 2005)...................................................................... 35

Vosko v. Chase Manhattan Bank N.A., 909 S.W.2d 95


Wade-Greaux v. Whitehall Labs., Inc., 874 F. Supp. 1441(D.V.I. 1994),


Wallace v. Texas Tech Univ., 80 F.3d 1042 (5th Cir. 1996) ............................................. 1

Zavala v. Trujillo, 883 S.W.2d 242 (Tex. App.—El Paso 1994, writ denied) ................. 32

Statutes and Rules

28 U.S.C. § 1652 ........................................................................................................... 21

FED. R. CIV. P. 56(c)........................................................................................................ 1

Miscellaneous

Appetite-Suppressant Drugs and the Risk of Primary Pulmonary Hypertension,


REFERENCE MANUAL ON SCIENTIFIC EVIDENCE


Sean P. Gaine, et al., Unmasking of Anorexigen-Induced Primary Pulmonary
Hypertension by Exercise, (1999) .................................................................................. 26

International Primary Pulmonary Hypertension Study (IPPHS) ...................................... 5


(Fed. Judicial Ctr., 2d ed. 2000) .............................................................................. 18

335 N. ENGL. J. MED. 610 (1996)........................................................................... 5,6



vi

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167 AM. J. RESPIR. CRIT. CARE MED. 167, A692 (2003) ......................................... 28

Snow, et al., Noninvasive Evaluation of Exercise-Associated Pulmonary
Hypertension in Patients with Exposure to Anorectic Agents,


David F. Bernstein, The Admissibility of Scientific Evidence After Daubert v.
Merrell Dow Pharmaceuticals, Inc., 15 CARDOZO L. REV. 2139 (1994)................... 28

David Rosenberg, The Causal Connection in Moss Exposure Cases: A “Public


Law” Vision of the Tort System, 97 HARV. L. REV. 851 (1984). .............................. 29



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I.


Summary Judgment Standard

Summary judgment is proper when it appears from the record “that there is no




genuine issue as to any material fact and that the moving party is entitled to a judgment

as a matter of law.” FED. R. CIV. P. 56(c). The movant must identify those portions of

the pleadings, depositions, or other evidence that demonstrates the absence of a genuine

issue of material fact. See Celotex Corp. v. Catrett, 477 U.S. 317, 323 (1986); Anderson

v. Liberty Lobby, Inc., 477 U.S. 242, 247-48 (1986).



After adequate time for discovery, a defendant may assert the absence of evidence

as a grounds for summary judgment. Little v. Liquid Air Corp., 37 F.3d 1069, 1075 (5th

Cir. 1994) (en banc). A defendant need not negate each element of the plaintiff’s case.

See Wallace v. Texas Tech Univ., 80 F.3d 1042, 1047 (5th Cir. 1996) (citing Little, 37

F.3d at 1075). Once a proper motion has been made, the nonmoving party must present

affirmative evidence, setting forth specific facts, to show the existence of a genuine issue

for trial. See Celotex Corp., 477 U.S. at 322-23; Anderson, 477 U.S. at 247-48.

“Summary judgment is mandated if the nonmovant fails to make a showing sufficient to

establish the existence of an element essential to her case on which she bears the burden

of proof at trial.” Nebraska v. Wyoming, 507 U.S. 584, 590 (1993).



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II.


Wyeth is Entitled to Summary Judgment on Plaintiff’s

Claim of Exercise Induced Pulmonary Arterial Hypertension.



Summary

1.

Introduction

A.





This is a products liability personal injury case. Plaintiff took Pondimin and

Redux, two diet drugs formerly marketed by Wyeth, in 1996-97. She now claims that

they injured her, causing two distinct diseases: 1) heart valve regurgitation and

2) Exercise Induced Pulmonary Arterial Hypertension. Because, Plaintiff lacks legally

sufficient evidence under Texas law to demonstrate that diet drugs caused her Exercise

Induced Pulmonary Arterial Hypertension, Wyeth is entitled to summary judgment on

this claim.

B.

Factual Basis for Motion





1.

Pulmonary Arterial Hypertension

Pulmonary Hypertension (PH) is a physical finding of elevated blood pressure in

the lungs. Many different diseases and conditions, including congenital abnormalities of

the lungs, valvular heart disease, and pulmonary venous hypertension, can cause elevated

pulmonary pressures. See generally, Amended Expert Report of Stephen Koenig, M.D.,

(“Koenig Report”) Appendix 1 to Wyeth’s Brief in Support of Motion for Partial

Summary Judgment (hereafter “App.”) at p. 1.1

As required by the Local Rules, each page of the Appendix is sequentially numbered. Each


1
separate document is identified by its own number as well. Where a witness has been deposed more than
once, the deposition date is included in the references.



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PH is best diagnosed by a right heart catheterization, considered the “gold

standard” diagnostic tool, which directly measures the pressures in the pulmonary artery.

A physician trained in administering right heart catheterizations typically will measure

pressures while a patient is at rest. A resting pressure greater than or equal to 25 mmHg

is considered elevated, and the patient may be diagnosed with resting pulmonary

hypertension or “PH.” If the PH is due to changes in the pulmonary arteries in the lungs

(as opposed to, for example, problems in the left side of the heart, breathing disorders,

sleep apnea, or a number of other common causes of pulmonary hypertension) then the

condition is referred to as Pulmonary Arterial Hypertension or “PAH.”2



Even if a patient has no elevated pulmonary artery pressures at rest, then in some

cases, the physician also might conduct a right heart catheterization while the patient

exercises with the catheter in the heart in order to obtain a measurement of the pulmonary

artery pressure during exercise. If the pulmonary artery pressure is greater than or equal

to 30 mmHg during the exercise catheterization, and other possible causes have been

ruled out, this elevated pressure on exercise might be referred to as Exercise Induced

Pulmonary Arterial Hypertension.



Pulmonary artery pressures also may be estimated by an echocardiogram (a

sonogram of the heart), which gives only an estimated pressure reading rather than a

direct measurement. An echocardiogram is a noninvasive procedure.


2
PAH for which physicians can find no cause is referred to as “Idiopathic PAH,” or under older
nomenclature, “Primary Pulmonary Hypertension” (PPH). This is a diagnosis of exclusion that requires
ruling out of all potential secondary causes, of which there are many. “Idiopathic PAH” and “PPH” may
be used interchangeably.



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Plaintiff has had six right heart catheterizations since 1996; in each, she was found

to have normal resting pulmonary artery pressures, with elevated pressures in some of

these catheterizations only upon exercise. Thus, Plaintiff’s medical experts have

diagnosed her with Exercise Induced Pulmonary Arterial Hypertension.3





2.

Course of Diseases

While it is generally acknowledged that the course of resting PAH or PPH (that is,

PAH diagnosed by a resting right heart catheterization), when left untreated, can progress

to a debilitating or even fatal outcome, Plaintiff’s medical expert witnesses uniformly

have testified that the course or “natural history” for Exercise Induced PAH is unknown.

They therefore admit that they cannot state to a reasonable degree of medical probability

that Plaintiff’s prognosis is the same as that for resting PAH or PPH, or even that her

condition will progress or worsen.4



3.

Diet Drugs and PAH Causation

There is only one case-controlled epidemiological study addressing the relationship

between diet drugs and resting PAH (referred to as Primary Pulmonary Hypertension

“PPH” throughout the study). Significantly, pursuant to the study’s Protocol, this study did

not include patients diagnosed with Exercise Induced PAH; the subjects of this study all

had elevated resting pressures.


3
For purposes of this motion only, Wyeth will refer to Plaintiff’s condition as Exercise Induced
Pulmonary Arterial Hypertension (“Exercise Induced PAH”) but reserves the right to argue at trial that
her elevated pulmonary artery pressure on exercise is due to a secondary cause (i.e., pulmonary venous
hypertension).

4
Daubert v. Merrell Dow Pharm, Inc., 509 U.S. 579 (1993) to exclude testimony of poor prognosis for
PAH or PPH. See Motion to Exclude Plaintiff’s Expert Testimony Regarding Pulmonary Hypertension
Medical Prognosis.


The inability of Plaintiff to present evidence of a poor prognosis is the subject of a motion under

4

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The final results of this European epidemiological study known as the International

Primary Pulmonary Hypertension Study (IPPHS) were published in August, 1996. (See

generally, Koenig Report; App. 1 at p. 1). The IPPHS studied a group of patients

diagnosed with PPH based on a finding of elevated resting pressures, and then examined

risk factors potentially associated with that disease, including diet drugs or “anorexigens.”

The IPPHS is the only case-controlled epidemiological study and the most complete,

reliable study to date on the potential risk factors of PPH. (See Appetite-Suppressant

Drugs and the Risk of Primary Pulmonary Hypertension, 335 N. ENGL. J. MED. 610

(1996) and excerpted Protocol, § 5.2; App 2 at pp. 13, 26). Previously, there had been

anecdotal evidence, such as case reports, of a possible association between diet drugs and

PPH, but the IPPHS is the only case-controlled epidemiological study to analyze any

association scientifically. The IPPHS found that a patient’s use of anorexigens for more

than three months was associated with a statistically significant increase in the risk of

developing PPH based on a finding of elevated resting pressures if the initial symptom of

PPH was reported within one year after the patient last used the drugs. The IPPHS also

confirmed that the risk of developing PPH, even in association with diet drugs, is

extremely rare. Indeed, even among those who have used diet drugs, the risk of

contracting PPH is far less than 1 in 10,000 (less than .01%). The causes of PPH largely

remain unknown, however, as the great majority of PPH patients never used a diet drug.



5

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Most importantly for this motion, none of the study subjects in IPPHS had Exercise

Induced PAH, the condition at issue here; the IPPHS Protocol reflects that the study

included only those who had “the presence of a mean pulmonary artery pressure of greater

than 25 mmHg at rest.” (IPPHS Protocol, § 5.2.1, App. 2 at p. 26) (emphasis added).

Thus, the only epidemiological study to examine the association between diet drugs and

PAH is inapplicable to Plaintiff’s condition.

4.



Plaintiff Does Not Have the Progressive, Potentially Fatal Condition
Studied in IPPHS

Plaintiff Does Not Have Elevated Resting Pulmonary Artery
Pressures

a.



Those patients determined to have elevated pulmonary artery pressures at rest, for

whom no treatable secondary cause is identified, are at risk for progression to a serious,

debilitating, sometimes fatal condition. But Plaintiff does not have this condition; her

experts and treating physicians all have testified that she does not have elevated resting

pulmonary artery pressures. Plaintiff has four medical experts to testify about her claimed

PAH: Dr. Harold Palevsky, Dr. Richard Channick, Dr. Waenard Miller, and Dr. Michael

Poon. (Plaintiff’s Witness and Exhibit List, December 7, 2006; App. 3 at pp. 43-46).



Each confirmed in his deposition that Plaintiff does not have elevated resting

pressures, and that her pulmonary artery pressures are elevated only on exercise, resulting

in a diagnosis only of Exercise Induced PAH.







Dr. Palevsky testified:

Q With respect to Cindy Burton, I understand from your report that you have
diagnosed her with, I think you phrased it, "exercise-associated pulmonary
arterial hypertension"?

Yes.

A


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Q Would you agree that Ms. Burton has normal resting pulmonary artery

. . .

pressures?

Yes.


A


(Deposition of Dr. Harold Palevsky, December 15, 2006, p. 18:13-18, 23-25; App. 4, at

p. 48).



Dr. Channick also agreed that Plaintiff’s resting pulmonary artery pressures were

normal. Discussing Plaintiff’s five heart catheterizations done from 1996 to 2004,

Dr. Channick confirmed that she never had resting pulmonary hypertension:

[From 1996 to 2004] [s]he was not worse, correct?

Correct. . . . [It] certainly wasn’t worse than it had been previously, and she
did not have resting pulmonary hypertension.

She’s never had resting pulmonary hypertension that we know of, correct?

Correct. . . .

Q

A


Q

A


(Deposition of Dr. Richard Channick, April 5, 2005, pp. 46:19 – 47:4; App. 5 at pp. 72-

73). Recently, Dr. Channick performed an additional heart catheterization on Plaintiff in

May, 2006. Again, he testified that her pulmonary artery pressures at rest are normal:

Did this cath indicate to you, that is this cath of May ’06 indicate to you,
that Ms. Burton continues to have normal pressures at rest?

She does have normal pressures at rest, correct.

Q


A


(Deposition of Dr. Channick, November 1, 2006, p. 174:21-24; App. 6 at p. 86). Instead

he found her only to have Exercise Induced PAH. Id. He later confirmed that his

diagnosis of PAH was based solely upon the exercise pressures:

A Well, the diagnosis of pulmonary hypertension was based on my evaluation



of the patient in August of 2004.

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Q

A

And that right heart cath . . . She was normal at rest, right?

Her pulmonary artery pressures were normal at rest, correct.

(Deposition of Dr. Richard Channick, November 1, 2006, pp. 197:10-15; 174:25 - 175:5,

App. 6 at pp. 86-88). Dr. Waenard Miller likewise confirmed that Plaintiff has normal

resting pressures, and that his diagnosis of PAH is dependent on the elevated pressures on

exercise catheterization:

Q Would it be fair to say that the catheterization [done by Dr. Poon]

demonstrates at rest that her main pulmonary artery pressure was normal?


A

Q


A

Q


A

Q


A


That is my understanding, yes. . . .

And I think Dr. Poon concluded that there was exercise-induced pulmonary
hypertension, correct?

Exactly.

Is it fair to say that each of the caths and echoes in this case demonstrate
normal resting pulmonary artery pressures?

That is my recollection, yes.

So with regard to the issue of primary pulmonary hypertension, the issue
becomes whether or not she in fact has exercise-induced pulmonary
hypertension?

Correct.

(Deposition of Dr. Waenard Miller, August 30, 2002, pp. 28:16 – 29:10; App. 7 at pp. 96-

97).



In a second deposition, Dr. Miller confirmed his diagnosis of Exercise Induced

Pulmonary Hypertension based also upon echocardiograms that provided an estimate (as

opposed to the direct measurement of the catheterization):



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Q

Based on the [echocardiograms] that your office performed on Ms. Burton,

would you agree that she does not have resting pulmonary hypertension?

A

I would agree with that.

(Deposition of Dr. Waenard Miller, May 6, 2005, p. 44:16-19; App. 8 at p. 102).



While one February 2006 echocardiogram performed at a Fort Worth hospital

estimated her pulmonary artery pressure was elevated at rest (Deposition of Dr. Waenard

Miller, October 27, 2006, p. 24:13-22; App. 9 at p. 107), Dr. Miller testified that given

the results of the many heart catheterizations (direct measurements) of Plaintiff’s

pressures, he would not diagnose her with resting pulmonary hypertension based on the

estimated reading:

Q


A

Given the results of the various heart catheterizations that have been
performed on Ms. Burton, you wouldn’t diagnose her with resting
pulmonary hypertension based on that 2006 echo alone, would you?

No. I would want confirmation.

(Id. at p. 26:10-14; App. 9 at p. 108). Another treating physician one time estimated what

he considered to be an elevated pressure in a 1998 echocardiogram, but at deposition, he

testified repeatedly that this was just an "estimate," and that the direct measurement of

pressures by catheterization are both "more reliable" and the "most accurate" way to

measure pressures:

Q

A

Q

A

Can you estimate pulmonary artery pressures based on an echo?

Yes.

And it would be an estimate opposed to the reading that you would get —

Right.

Q — on a cath?



9

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A

Correct.

Q Which is more reliable in determining pulmonary artery pressures, an

echocardiogram or a cardiac catheterization?

A Well, a direct measurement is — is always the most accurate. So cardio

catheterization would be the most accurate.

(Deposition of Dr. John Willard, September 10, 2002, pp. 17:18 – 18:6; App. 10 at pp.

112-113). And the two heart catheterizations (direct measurements) Dr. Willard

performed both before and after this echocardiogram reading showed that Plaintiff had no

elevated pressures. (Id. pp. 40:3-13, 71:15-22; App. 10 at pp. 115-116). In explaining

his reading that he estimated slightly elevated, he testified:

A

. . . keep in mind, that these are estimates. These are not direct
measurements. So there is some range of expected error.

(Deposition of Dr. John Willard, September 10, 2002, p. 39:18-20, App. 10 at p. 114).5

Q

And the two catheterizations that you performed in November 1996 and
November 1998 did not show any pulmonary hypertension, correct?

A

That’s correct.

(Deposition of Dr. John Willard, September 10, 2002, p. 71:19-22; App. 10 at p. 116).

Dr. Miller confirmed that this earlier echo was not sufficient on which to base a finding

of pulmonary hypertension (Deposition of Dr. Waenard Miller, August 30, 2002, p. 55:6-

20; App. 7 at p. 98). Dr. Palevsky recently confirmed that the “most reliable” and

“accurate” measurements were the catheterizations and that he did not rely on

echocardiogram estimates:

In any event, Plaintiff’s counsel discounted this echocardiogram reading when he made a running


5
objection that Dr. Willard was not qualified to read echocardiograms. (Deposition of Dr. John Willard,
September 10, 2002, p.18:14-22; App. 10 at p.113).



10

Case 3:99-cv-00305-G Document 60 Filed 01/02/07 Page 19 of 46 PageID 806

. . .[D]o you intend to render any opinions regarding her pulmonary artery
pressures based on any echoes that have been done on her,
echocardiograms?

No. The most reliable information we have are from the exercise
hemodynamics.

Q


A




Q Will you give an opinion in this case that any of her echocardiograms

demonstrate pulmonary hypertension?

. . .


[Objection omitted]

A

No. The diagnosis of exercise pulmonary hypertension has been made by
right heart catheterizations repeatedly.


Q Would you rely on her catheterizations to reflect most accurately her resting

and exercise pressures?


A


Yes.

(Deposition of Dr. Harold Palevsky, December 15, 2006, pp. 94:1-6; 95:6-18; App. 4 at
pp. 50-51)


Dr. Michael Poon also examined Plaintiff in June 2002 and June 2003 and



performed a right heart catheterization. (Deposition of Dr. Michael Poon, March 29,

2005, pp. 105:20 – 106:22; 112:10-13; App. 11 at pp.120-122). He testified that while

she had elevated pressures upon exercise, she did not have elevated pulmonary artery

pressures at rest:

. . . [W]hat were the results of the left and right heart catheterization
that you performed on Ms. Burton in June 2003?

She was found to have mild exercise-induced pulmonary
hypertension . . .

Q


A




Q What was the mean pulmonary artery pressure at rest, Doctor?




11

. . .

Case 3:99-cv-00305-G Document 60 Filed 01/02/07 Page 20 of 46 PageID 807

18.

A

Q Would you consider that would be pulmonary hypertension or no?

A


No.

(Id. at pp. 112:22 – 113:3; 113:20-25; App. 11 at pp. 122-123) (emphasis added).

Plaintiff’s experts are thus unanimous that she does not have elevated pulmonary

artery pressures at rest, and that on direct measurement of her pressures by catheterization,

her pressures are elevated only upon exercise. Thus, Plaintiff has been diagnosed solely

with Exercise Induced PAH, which distinguishes her from those patients with resting PAH.

Plaintiff’s Experts Agree That the Course for Exercise Induced
PAH is Different from Resting PAH.

b.



Plaintiff’s experts and doctors unanimously agree that Exercise Induced PAH does

not have the same course or prognosis as resting PAH or PPH. Instead, they all concede

that they cannot testify to a reasonable degree of medical certainty as to the prognosis for

Plaintiff’s condition. No expert or treating physician can testify that her condition will

progress to the debilitating and sometimes fatal resting PAH or PPH outcome. Dr.

Palevsky testified that he cannot predict, and there is no medical literature to help him

predict, Plaintiff’s prognosis. (Deposition of Dr. Harold Palevsky, December 15, 2006, pp.

131:3 – 132:1; App. 4 at pp. 66-67). He admitted that there was “no way” to predict her

course with exercise PAH (Id. at pp. 131:23 – 132:1; 133:3-12 App. 4 at pp. 66-68):

Q

A

Q

If we look at a prognosis for the future . . . is there any published data which
is going to help you predict for Ms. Burton what is likely to happen?

So, no. . . . [T]here’s no way to predict likelihood of remaining stable versus
likelihood of progressing over the next five years.

. . .

Is there any way to state to a reasonable degree of medical certainty that she
will need [certain medications for progressive PAH] or interventions such as



12

Case 3:99-cv-00305-G Document 60 Filed 01/02/07 Page 21 of 46 PageID 808

that?

A

No. Those are possibilities, what we would use if there was progression, but
there’s — if there’s no way to predict stability, there’s no way to predict
progression.

(Deposition of Dr. Harold Palevsky, December 15, 2006, pp. 131:3 – 132:1; 133:3-12;

App. 4 at pp. 66-68). He cannot say to a reasonable degree of medical probability that she

will progress to a state of resting pulmonary arterial hypertension, as it is “incompletely

understood:”

Q

A

Q

A

In your report, you say that, “The prognosis of exercise-associated
pulmonary arterial hypertension is incompletely understood at this point in
time.” Is that correct?

You read that well.

All right. Can you say to a reasonable degree of medical certainty that she
will progress to a state of resting pulmonary arterial hypertension?

No . . . we would hope she will not be progressing to fixed pulmonary
hypertension.

(Id. at pp.104:20 – 105:10; App. 4 at pp. 52-53). Dr. Channick confirmed that he could not

say with certainty that Plaintiff has a fatal disease, that in his own unpublished case study

(rejected for publication), 70% of those with exercise induced PAH do not progress or

deteriorate, and that he was unaware of medical literature that supports the proposition that

she would progress to develop elevated pressures at rest. (Deposition of Dr. Richard

Channick, April 5, 2005, pp. 61:24 - 62:6, 143:6-9, 146:10-20; 148:20-23, App. 5 at pp.

74-75 and 80-82; Deposition of Dr. Richard Channick, November 1, 2006, p. 234:18-24;

App. 6 at p. 92).

Dr. Poon acknowledged that Plaintiff’s prognosis for the condition of Exercise

Induced PAH is “significantly better” than that for the PAH disease of resting elevated

pressures. (Deposition of Dr. Michael Poon, March 29, 2005, p. 120:9-18; App. 11 at p.



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Case 3:99-cv-00305-G Document 60 Filed 01/02/07 Page 22 of 46 PageID 809

124).6 Indeed, Plaintiff’s expert concedes that a drug used to treat patients with elevated

resting pressures has not been studied in patients with Plaintiff’s condition, and that use of

the drug for her is an “off label” or unapproved use of the drug. (Deposition of Dr. Harold

Palevsky, December 15, 2006, pp. 92:2-9; 105:11 – 106:8; 107:22-25; App. 4 at pp. 49 and

53-55). Thus, Plaintiff’s medical experts concede that the condition at issue here, Exercise

Induced PAH, is distinct from the resting PAH or PPH condition that may lead to a

debilitating, sometimes fatal outcome. This distinction is important, as Plaintiff must

establish that her condition was caused by diet drugs.

C.

Argument and Authorities

1.

Plaintiff Must Present Legally Sufficient Evidence of Causation

As set forth in Section (C)(2), Texas substantive law applies in this case. In Merrell

Dow Pharmaceuticals Inc. v. Havner, 953 S.W.2d 706(Tex. 1997), the Texas Supreme

Court adopted strict standards for legally sufficient evidence of causation in cases like this

one, where there is no direct biological evidence that the defendant’s product caused the

plaintiff’s illness or injury and, therefore, she must use epidemiological studies to establish

causation. A plaintiff can raise a fact issue on causation only by proving she is similar to

the test subjects in at least two epidemiological studies whose results indicate that it is

“statistically more likely than not that [each test subject’s] disease was caused by the drug.”

Id. at 717; see also id. at 714-24.7 In addition, Havner requires a plaintiff’s expert to rule

out alternative plausible causes of her illness or injury to a reasonable degree of medical

certainty. Id. at 711-12; E.I. du Pont de Nemours & Co. v. Robinson, 923 S.W.2d 549,

Dr. Waenard Miller testified that he will not offer testimony of the prognosis for Exercise


6
Induced PAH (Deposition of Dr. Waenard Miller, May 6, 2005, p. 45:21-24; App. 8 at p. 103).

7
single study does not reliably indicate “that it is ‘more probable than not’ that an association [between the
substance and the disease] exists.” 953 S.W.2d at 727.


A plaintiff must have at least two epidemiological studies meeting certain criteria because a

14

Case 3:99-cv-00305-G Document 60 Filed 01/02/07 Page 23 of 46 PageID 810

556-57 (Tex. 1995). These requisites are not mere technicalities: as the Havner court

explained, epidemiological studies standing alone just show correlation and cannot

establish the probable, actual cause of any plaintiff’s injury, unless certain additional

requirements are met. 953 S.W.2d at 715.

The Havner court reviewed the necessary elements of “general” and “specific”

causation in pharmaceutical cases:

General causation is whether a substance is capable of causing a particular
injury or condition in the general population, while specific causation is
whether a substance caused a particular individual’s injury.


Id. at 714. Havner then set out what a party must show to establish that a drug is

capable of causing an injury that also occurs in people who did not take the drug. In

brief, Havner requires a plaintiff lacking direct experimental proof to produce,

among other things:

 At least two properly designed and executed epidemiological studies;

 That show a relative risk or odds ratio of 2.0 or greater;

 For the specific injury or condition complained of;

 And that she is similar to the subjects of the study. 8



a.

Texas Law Requires Epidemiological Evidence



In the absence of direct experimental proof of causation, Texas law requires the

plaintiff to supply epidemiological studies meeting specific criteria in order to prove

general causation — i.e., that the drug is capable of causing the injury complained of.

Havner, 953 S.W.2d at 714. Numerous Texas courts following Havner have required

The studies must meet additional standards not relevant here, since Plaintiff has no


8
epidemiological studies at all to support her claim of association.



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Case 3:99-cv-00305-G Document 60 Filed 01/02/07 Page 24 of 46 PageID 811

such proof.9 Havner requires such epidemiological evidence unless the plaintiff has

direct proof of causation through controlled experiments, which is unavailable in most

toxic tort and drug injury cases:

Particularly where, as here, direct experimentation has not been conducted,
it is important that any conclusions about causation be reached only after an
association is observed in studies among different groups and that the
association continues to hold when the effects of other variables are taken
into account.



Id. at 727 (emphasis added). The court found that requiring scientifically reliable studies

that show more than a doubling of the risk of injury “strikes a balance between the needs

of our legal system and the limits of science.” Id. p. 718.



The Texas Supreme Court set specific rules for use of epidemiological studies in

Texas courts:

(1). Study Must Show Doubling of the Risk



First, to constitute some evidence of general causation, such a study must show a

relative risk or odds ratio of at least 2.0.10 In other words, the study must show that the

risk of the injury among those who took the drug is at least twice that of those who did

See, e.g., Daniels v. Lyondell-Citgo Refining Co., 99 S.W.3d 722 (Tex. App. – Houston [14th


9
Dist.] 2003, no pet.) (workplace exposure to benzene allegedly caused decedent’s lung cancer); Mo. Pac.,
R.R. Co. v. Navarro, 90 S.W.3d 747, 749 (Tex. App. — San Antonio 2002, no pet. h.) (allegation that
exposure to diesel exhaust caused decedent’s multiple myeloma); Austin v. Kerr-McGee Refining Corp.,
25 S.W.3d 280 (Tex.App. — Texarkana 2000, no pet.) (decedent exposed to Benzene subsequently
contracted chronic myelogenous leukemia); Minnesota Mining & Manufacturing Co. v. Atterbury, 978
S.W.2d 183 (Tex.App. — Texarkana 1998, pet. denied) (silicone gel breast implants allegedly linked with
various diseases and symptoms such as multiple sclerosis).

10
substance and the injury it allegedly causes. An “odds ratio” is used in a retrospective case control study.
Havner, 953 S.W.2d at 721.



“Relative risk” and the “odds ratio” are measures of the strength of the association between the

16

Case 3:99-cv-00305-G Document 60 Filed 01/02/07 Page 25 of 46 PageID 812

not. Id. at 718-22. A finding of 1.0 would indicate no association, and findings between

1.0 and 2.0 are simply too weak to be legally sufficient evidence in Texas. Id. at 718.11

(2). Finding Must be Statistically Significant



The 2.0 or greater finding also must be statistically significant —i.e., not

attributable to chance. This can be determined through the concepts of “confidence

intervals” and the “confidence level.” The confidence interval “shows a ‘range of values’

within which the results of a study sample would be likely to fall if the study were

repeated numerous times.” Id. at 723. If this range of values includes 1.0 or a lower

number, then it includes the possibility that there is no association and the relative risk

finding is not statistically significant. Id. The confidence level shows what percentage of

the time the study results would be the same.

(3). Study Must Show Results for Specific Injury or Condition

At Issue





The study results must support an association between the drug and the specific

condition at issue. Havner dismissed an expert who “testified about published studies on

Bendectin that did show statistically significant results, but they dealt with birth defects

other than limb reduction defects [the injury at issue]. These studies cannot of course

support a finding that Bendectin causes limb reduction defects.” Havner, 953 S.W.2d at

725 (emphasis by the court).

The court did not decide whether a study with a relative risk of less than 2.0 could ever be


11
considered scientifically reliable if “coupled with other credible and reliable evidence.” Id. at 719. The
court did state, however, what other kinds of evidence are not “credible and reliable” in this context. See
also Atterbury, 978 S.W.2d at 198 (study showing less than a statistically significant doubling of the risk
must be supported by other credible, reliable evidence which cannot include animal studies, clinical
experience and case reports).





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Case 3:99-cv-00305-G Document 60 Filed 01/02/07 Page 26 of 46 PageID 813

(4). At Least Two Studies are Required




A single epidemiological study, even if it is well-designed and executed, and even

if it meets all of the criteria specified in Havner, is not sufficient to raise a fact issue

regarding causation. As the court noted, “We do not hold … that a single epidemiological

test is legally sufficient evidence of causation.” Havner, 953 S.W.2d at 718. Instead,

where “direct experimentation has not been conducted, it is important that any

conclusions about causation be reached only after an association is observed in studies

among different groups and the association continues to hold when the effects of other

variables are taken into account.” Id.12

(5). Case Reports are Not Reliable Evidence



Case reports, case series studies, random experience, and anecdotal evidence of

association are not good enough because they provide “no more than a false appearance

of direct and actual knowledge of a causal relationship.” Havner, 953 S.W.2d at 720.13

Expert testimony of this kind, the court concludes, “cannot be used to shore up

epidemiological studies that fail to indicate more than a doubling of the risk.” Id.

The court expressly rejected the argument that it is unfair to early claimants to wait until an


12
association found in one study is confirmed by others. Id. at 728. “Our legal system requires that
claimants prove their cases by a preponderance of the evidence. In keeping with this sound proposition at
the heart of our jurisprudence, the law should not be hasty to impose liability when scientifically reliable
evidence is unavailable.” Id. Other courts likewise have required more than one epidemiological study
to show causation. Mo. Pac. R.R. Co. v. Navarro, 90 S.W.3d 747 (Tex. App. — San Antonio 2002, no
pet.); Frias v. Atlantic Richfield Co., 104 S.W.3d 925 (Tex. App. — Houston [14th Dist.] 2003, no pet.);
Coastal Tankships, Inc. v. Anderson, 87 S.W.3d 591, 616-17 (Tex. App. — Houston [1st Dist.] 2002, pet.
denied) (Brister, J., concurring).

13
Case studies are “reports in medical journals describing clinical events involving one individual
or a few individuals. They report unusual or new disease presentations, treatments, or manifestations, or
suspected associations, between two diseases, effects of medication . . . Case reports lack controls and
thus do not provide as much information as controlled epidemiological studies do.” Reference Manual on
Scientific Evidence at 474-75 (Fed. Judicial Ctr., 2d ed. 2000). See Rider v. Sandoz Pharma. Corp., 295
F.3d 1194, 1199 (11th Cir. 2002) (“case reports are merely accounts of medical events”); Glastetter v.
Novartis Pharma. Corp., 252 F.3d 986, 990 (8th Cir. 2001) (“case report is simply a doctor’s account”).


18

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Similarly, the court indicated that courts should reject opinion testimony by “a physician,

even a treating physician, or other expert who has seen a skewed data sample” because

such experts are “not in a position to infer causation,” and "the scientific community

would not accept as methodologically sound a ‘study’ by such an expert.” Id. at 719-20.

See Black v. Food Lion, Inc., 171 F.3d 308, 313 n.2 (5th Cir. 1999) (approving

conclusion that case reports do not provide causation evidence); Newton v. Roche

Laboratories, Inc., 243 F. Supp. 2d 672 (W.D. Tex. 2002) (concluding “isolated,

anecdotal case reports” were not an "acceptable scientific foundation[]” for causation

opinion); Caraker v. Sandoz Pharmas. Corp., 172 F. Supp. 2d 1046, 1050 (S.D. Ill. 2001)

(rejecting experts’ opinions relying on case reports); Siharath v. Sandoz Pharms. Corp.,

131 F. Supp. 2d 1347, 1361 (N.D. Ga. 2001) (case reports “cannot establish general

causation"), aff’d sub nom., Rider v. Sandoz Pharms. Corp., 295 F.3d 1194 (11th Cir.

2002); Castellow v. Chevron USA, 97 F. Supp. 2d 780, 787 (S.D. Tex. 2000) (agreeing

“attempts to form opinions regarding medical causation based on documents such as

[anecdotal case reports or collections of case reports] are unscientific and speculative”)

(amendments in original, citation omitted); In re Breast Implant Litig., 11 F. Supp. 2d

1217, 1231 (D. Colo. 1998) (noting case reports “no not isolate and exclude potentially

alternative causes . . . and do not investigate or explain the mechanism of causation”)

(citation omitted); Nat'l Bank of Commerce v. Dow Chemical Co., 965 F. Supp. 1490,

1520 (E.D. Ark. 1996) (concluding case studies did not establish causation), aff'd, 133

F.3d 1132 (8th Cir. 1998); Hall v. Baxter Healthcare Corp., 947 F. Supp. 1387, 1411 (D.

Or. 1996) (“case reports and case studies are universally regarded as an insufficient

scientific basis for a conclusion regarding causation because case reports lack controls”);


19

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Jones v. United States, 933 F. Supp. 894, 899 (N.D. Cal. 1996) (recognizing anecdotal

case reports, reviews of research done by other people, or studies lacking a control group

are “not derived through the scientific method”), aff'd, 127 F.3d 1154 (9th Cir. 1997);

Muzzey v. Kerr-McGee Chem. Corp., 921 F. Supp. 511, 519 (N.D. Ill. 1996) (“Anecdotal

reports. . . are not reliable bases to form a scientific opinion about a causal link”); Casey

v. Ohio Med. Prods., 877 F. Supp. 1380, 1385 (N.D. Cal. 1995) (explaining “case reports

are not reliable scientific evidence of causation, because they simply described reported

phenomena without comparison to the rate at which the phenomena occur in the general

population or in a defined control group; do not isolate and exclude potentially alternative

causes; and do not investigate or explain the mechanism of causation. . . . [T]he study . . .

does not have the degree of clarity required for a validation