Peripartum Cardiomyopathy_JAMA

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CLINICAL CARDIOLOGY

Peripartum CardiomyopathyNational Heart, Lung, and Blood Institute andOffice of Rare Diseases (National Institutes of Health)Workshop Recommendations and ReviewGail D. Pearson, MD, ScD

Jean-Claude Veille, MD

Shahbudin Rahimtoola, MD

Judith Hsia, MDCelia M. Oakley, MD

Jeffrey D. Hosenpud, MD

Aftab Ansari, MD

Kenneth L. Baughman, MD

HEART FAILURE IN THE PUERPE-rium has been recognizedsince the 18th century, butcardiomyopathy was not

identified as its cause until an article byGouley et al was published in 1937.1

Peripartum cardiomyopathy (PPCM) isnow considered to be a cardiomyop-athy of unknown cause that occurs inthe peripartum period in women with-out preexisting heartdisease.2,3 Peripar-tum cardiomyopathy is relatively rare,but can be devastating, with reportedmortality rates between 18%and56%.3-5

Survivors may not recover completelyand may require heart transplantation.Even if left ventricular function does re-turn to normal, exercise tolerance mayremain abnormal and the long-term se-

quelae, including risks of future preg-nancies, are not known.In April 1997, the National Heart,

Lung, andBlood Institute (NHLBI)andtheOfficeof RareDiseasesof theNationalInstitutes of Health (NIH) convened aWorkshopon PeripartumCardiomyop-athyto foster a multidisciplinaryreview.Experts in cardiovascular medicine,ob-

Author Affiliations: Division ofHeartand VascularDis-eases, National Heart, Lung, and Blood Institute, Na-tional Institutes of Health, Bethesda, Md (Dr Pearson);

Department of Obstetrics and Gynecology, BowmanGraySchool of Medicine, Winston-Salem, NC (DrVeille);Divisionof Cardiology, University of Southern Califor-nia, Los Angeles (Dr Rahimtoola); Division of Cardiol-ogy, George Washington University School of Medi-cine and Health Sciences, Washington, DC (Dr Hsia);Emeritus Professor of Cardiology,Imperial CollegeMedi-cal School, London, England (Dr Oakley); Division ofCardiovascular Medicine, Medical College of Wiscon-sin, Milwaukee (DrHosenpud); Departmentof Pathol-ogy and LaboratoryMedicine, EmoryUniversitySchool

of Medicine, Atlanta, Ga (Dr Ansari); and Division ofCardiology, Johns Hopkins UniversitySchoolof Medi-cine, Baltimore, Md (Dr Baughman).

Corresponding Author and Reprints: Gail D. Pear-son, MD, ScD, National Heart, Lung, and Blood In-stitute, 6701 Rockledge Dr, Room 9146, MSC 7940,Bethesda, MD 20892-7940 (e-mail: [email protected]).Clinical Cardiology Section Editors: Bruce Brun-dage,MD, University of California, Los Angeles, Schoolof Medicine; Margaret A. Winker, MD, Deputy Edi-tor, JAMA.This article is one of a series sponsored by the Ameri-can Heart Association.

Objective Peripartum cardiomyopathy (PPCM) is a rare life-threatening cardiomy-opathy of unknown cause that occurs in the peripartum period in previously healthywomen. In April 1997, the National Heart, Lung, and Blood Institute (NHLBI) and theOffice of Rare Diseases of the National Institutes of Health (NIH) convened a Work-

shop on Peripartum Cardiomyopathy to foster a systematic review of information andto develop recommendations for research and education.

Participants Fourteen workshop participants were selected by NHLBI staff and rep-resented cardiovascular medicine, obstetrics, immunology, and pathology. A repre-sentative subgroup of 8 participants and NHLBI staff formed the writing group for thisarticle and updated the literature on which the conclusions were based. The work-shop was an open meeting, consistent with NIH policy.

Evidence Data presented at the workshop were augmented by a MEDLINE searchfor English-language articles published from 1966 to July 1999, using the terms peri-partum cardiomyopathy, cardiomyopathy, and pregnancy. Articles on the epidemi-ology, pathogenesis, pathophysiology, diagnosis, treatment, and prognosis of PPCMwere included.

Recommendation Process After discussion of data presented, workshop partici-pants agreed on a standardized definition of PPCM, a general clinical approach, andthe need for a registry to provide an infrastructure for future research.

Conclusions Peripartum cardiomyopathy is a rare lethal disease about which littleis known. Diagnosis is confined to a narrow period and requires echocardiographicevidence of left ventricular systolic dysfunction. Symptomatic patients should receivestandard therapy for heart failure, managed by a multidisciplinary team. If subse-quent pregnancies occur, they should be managed in collaboration with a high-riskperinatal center. Systematic data collection is required to answer important questionsabout incidence, treatment, and prognosis.

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stetrics,immunology,and pathologymetto discuss the availableinformation andmakerecommendations(alistofpartici-pants appears at theend of this article).The objectives for the Workshop onPPCM, modeled on a previous NHLBI

Workshopon IdiopathicDilated Cardi-omyopathy,6 were to (1)summarizeex-istinginformationon PPCM,specificallyitsdefinition,epidemiology,cause,clini-cal characteristics, treatment, andprog-nosis;(2) reviewdiagnostic criteriaanddiscuss means of differentiating earlysymptomsof heartfailure fromnormalphysiological changes associated withpregnancy,suchastachypneaandfatigueduringthe thirdtrimester of pregnancy;(3)developrecommendationsfor futureresearchonPPCM; and(4) discuss edu-cationalmeasuresto increaseawareness

of PPCM andthus facilitate prompt di-agnosis.A representative subgroup of 8participantsandNHLBIstaffformedthewritinggroupforthisarticleandupdatedthe literature on which the conclusionswerebased.Theworkshopwasanopenmeeting consistent with NIH policy.

PPCM: LITERATURE REVIEW

Data presented at the workshop wereaugmented with a MEDLINE litera-ture search (English language) for theyears 1966 to July 1999 that included

the terms peripartum cardiomyopathy,cardiomyopathy,and pregnancy. The lit-erature search was updated followingthe workshop to provide the mosttimely references.The bibliographies ofarticles identified in this fashion weresearched for additional references, andthe search was further supplemented

with articles recommended by work-shop participants. This review, whichworkshop participants felt to be im-portant because of the reported rarityof the condition, the consensus that thecondition may be more prevalent than

reported, and because of new data con-cerning cause, includes the majority ofarticles identified through these pro-cesses covering epidemiology, patho-genesis, pathophysiology, diagnosis,treatment, and prognosis of PPCM.

Definition

Peripartum cardiomyopathy is de-fined on the basis of 4 criteria, adaptedfrom work by Demakis et al3,7 and sum-marized in TABLE 1. The importance ofadhering to the interval from 1 monthbefore delivery to 5 months postpar-

tum was emphasized to exclude pre-existing causes of cardiomyopathy thatmaybe exacerbatedby pregnancy ratherthan arising as a result of pregnancy.For example, heart failure occurringearlier in pregnancy may be caused bypreviously unsuspected dilated cardi-omyopathy unmasked by the hemody-namic or hormonal stress of preg-nancy. Peripartum cardiomyopathy isdefined as occuring only in those pa-tients with no prior history of recog-nizable heart disease and can be diag-

nosed only in the absence of anotherexplanation for the cardiomyopathy.

Incidence and Risk Factors

The incidence of PPCM is not knownbecause population-basedestimates arenot available, and the diagnosis of thisrare disease is not always straightfor-ward. Incidence rates reported in indi-vidual studies are based on the expe-rience at a particular institution andmay reflect referral bias as well as in-dividual practicepatterns.Althoughthe

reported incidence rates range from 1per 14858 to 1 per 15 000,9 the cur-rently accepted estimate of incidence isapproximately 1 per 3000 to 1 per 4000live births, which wouldtranslate to be-tween 1000 and 1300 women affectedeach year in the United States.10

Risk factors for PPCM classicallyidentified in the literature include mul-

tiparity, advanced maternal age, mul-tifetal pregnancy, preeclampsia and ges-tational hypertension, and AfricanAmerican race.3 It is unclear whetherracerepresents an independent riskfac-tor or whether it is the interaction of

race with hypertension that increasesthe risk of PPCM. Until risk factors canbe delineated confidently, it is diffi-cult to develop recommendations forscreening high-risk populations.

Etiology

Workshopparticipants concurredthatPPCM is a distinct entity, rather than aclinically silent underlying cardiomy-opathy unmasked by the hemody-namicstresses ofpregnancy,because thereported incidence is higher than theincidence of idiopathic cardiomyop-

athy,6 and because the high frequencyof myocarditis would not be expectedin a population presenting with decom-pensation of preexisting heart diseasedue to hemodynamic stress. However,reliable data comparing the incidenceof cardiomyopathyin pregnantwomencompared with age-matched nonpreg-nant women are not available. A num-ber of possible causes have been pro-posed forPPCM, including myocarditis,abnormal immune response to preg-nancy, maladaptive response to the

hemodynamic stresses of pregnancy,stress-activated cytokines, and pro-longed tocolysis. In addition, therehavebeen a fewreports of familial PPCM,11-13

raising the possibility that some casesof PPCM are actually familial dilatedcardiomyopathy unmasked by preg-nancy. The key hypotheses are pre-sented below.

Myocarditis. There is more evi-dence for myocarditis as a cause ofPPCM than for other purported etiolo-gies. Melvin and colleagues14 first re-

ported myocarditis by endomyocardialbiopsy in 3 consecutive patients withPPCM. The incidence of myocarditis insubsequent authors series has varied.The variability is likely due to the in-clusion of patients outside the ac-cepted time frame of PPCM, the inher-ent difficulties in establishing thediagnosis of myocarditis by endomyo-

Table 1. Definition of PeripartumCardiomyopathy

ClassicDevelopment of cardiac failure in thelast month

of pregnancy or within 5 monthsof deliveryAbsence of an identifiable cause for the

cardiac failureAbsence of recognizable heart diseaseprior to

the last month of pregnancyAdditional

Left ventricular systolic dysfunctiondemonstrated by classicechocardiographic criteria,such as depressed shorteningfraction or ejection fraction

PERIPARTUM CARDIOMYOPATHY

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cardial biopsy,15,16 the variability in theinclusion of patients with borderlinemyocarditis with those with histologicmyocarditis as defined by theDallas his-tologic criteria, the potential geo-graphic variability of patient popula-

tions affected, and the variable intervalbetween presentation and the perfor-mance of the endomyocardial biopsy.The highest incidence of myocarditis inPPCM (76%) was reported by Midei andcolleagues.17 This group performed en-domyocardial biopsies on patients withsymptoms of congestive heart failure atthetime ofpresentation andincluded pa-tients with histologic borderline myo-carditis as well as those with active myo-carditis.

The absent or muted immune re-sponseduring pregnancy may allow for

unchecked viral replication and thusa greater likelihood of myocarditisin the setting of a viral infection. Stud-ies in pregnant mice demonstrate en-hanced susceptibility to viral myo-carditis due to coxsackieviruses andechoviruses.18,19 In thenear future, elec-tron micrography combined with mo-lecular biological techniques shouldpermit not only identification of viralparticles in myocardium, but also theputative viruses implicated. The pre-sumption is that if viral genetic prod-

ucts are evident, the postviral im-mune response of the patient may havebeen inappropriately directed againstotherwise cryptic cardiac tissue pro-teins, leading to ventricular dysfunc-tion.

Abnormal Immune Response toPregnancy. Several reports have docu-mented the occurrence of chimerism ofthe hematopoietic lineage cells fromthe fetus to the mother during preg-nancy.20-23 It is postulated that fetal cellsmay escape into the maternal circula-

tion and remainthere without being re-jected, due to weak immunogenicity ofthe paternal haplotype of the chimericcells, or to the naturally occurring im-munosuppressive state of the mother,or both. If chimeric hematopoietic cellstake up residence in cardiac tissue dur-ing the immunosuppressed pregnantstate and, following postpartum recov-

ery of immune competence, are recog-nized as nonself by the maternal im-mune system, a pathologicautoimmuneresponse may be triggered. Prior expo-sure to paternal major histocompatibil-ity complexantigens expressed by sper-

matozoa or previous immunizationfrom prior pregnancies may play a rolein inducing local tissue inflammatoryresponse. Cytokines and similar sig-nalingmoleculesare thenreleased,lead-ing to nonspecific bystander myocyto-toxicity and myocarditis. The evidence(TABLE 2) that PPCM is associated withhigh titers of autoantibodies against se-lect cardiac tissue proteins (eg, ad-enine nucleotide translocator, branchedchain-keto acid dehydrogenase) sup-ports abnormal immunologic activityas a possible cause of PPCM.24

Response to Hemodynamic Stressesof Pregnancy. During pregnancy, bloodvolume(preload)andcardiacoutput in-crease and afterload decreases. An echo-cardiographic assessment of cardiachemodynamics in normal pregnan-cies performed by Geva et al25 demon-strated a 10% increase in left ventricu-lar end-diastolic volume, a 45%increasein cardiac output, and a 26% to 28% de-crease in end-systolic wall stress, a sen-sitive measure of myocardial after-load. In addition, the left ventricle

remodels in response to the hemody-namics of pregnancy, resulting in tran-sient hypertrophy. The research byGeva et al25 and other studies26 have

shown a reversible decrease in left ven-tricular systolic function in the sec-ond and third trimesters that per-sisted into the early postpartum period,but returned to baseline shortly there-after. It is possible that PPCM may be

due, in part, to an exaggeration of thisdecrease in systolic function, al-thoughthere areno data in women sup-porting this hypothesis.27

Other Etiologic Factors. Othercauses for PPCM that merit furtherstudy have been suggested and in-clude the following: (1) prolonged to-colysis4,28; (2) stress-activated proin-flammatory cytokines such as tumornecrosis factor or interleukin 1 thathavebeen implicatedin the pathophysi-ology of idiopathic dilated cardiomy-opathy29; (3) abnormalities of relaxin,

primarily an ovarian hormone pro-duced during pregnancy, recently foundin cardiac atria, shown to have posi-tive inotropic and chronotropic prop-erties30 and potentially involved inexcessive relaxation of the cardiac skel-eton; and (4) deficiency of selenium,31

which may make the heart more sus-ceptible to injury from viral infection,hypertension, or hypocalcemia.

DIAGNOSIS ANDMANAGEMENT OF PPCM

The diagnosis of PPCM rests on theechocardiographic identificationof newleft ventricular systolic dysfunction dur-ing a limited period surrounding par-

Table 2. Serum Levels of Antibodies to Cardiac Muscle Proteins in Patients With PeripartumCardiomyopathy (CM) and Idiopathic Dilated Cardiomyopathy*

Patient Group

Antibody Titer Levels

1:20 1:20-1:160 1:160

ANT

Idiopathic CM 16/56 (28) 29/56 (52) 11/56 (20)

Peripartum CM 1/10 (10) 1/10 (10) 8/10 (80)

BCKD

Idiopathic CM 30/56 (53) 21/56 (38) 5/56 (9)

Peripartum CM 0/10 (0) 2/10 (20) 8/10 (80)

Myosin

Idiopathic CM 18/56 (32) 27/56 (48) 11/56 (20)

Peripartum CM 1/10 (10) 1/10 (10) 8/10 (80)

*A. Ansari, MD, unpublished data, 1997.Reciprocal of the highest dilation of serum samples showing reactivity arbitrarily divided into those with low ( 1:20),

medium (1:20-1:160), andhigh (1:160) titers. ANTindicates adeninenucleotidetranslocator; BCKD, branchedchain-keto acid dehydrogenase. Data presented as No./Total (%) of patients in each group.





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turition. This presents a challenge be-cause many women in the last monthof a normal pregnancy experience dys-pnea, fatigue, and pedal edema, symp-toms identical to early congestive heartfailure. Peripartum cardiomyopathy

may, therefore, go unrecognized, lead-ing to underestimation of incidence.Symptoms andsigns thatmight raise thesuspicion of heart failure include par-oxysmal nocturnal dyspnea, chest pain,cough, neck vein distention, new mur-murs consistent with atrioventricularvalve regurgitation, and pulmonarycrackles. There are no specific criteriafor differentiating subtle symptoms ofheart failure from normal late preg-nancy, so it is important that a high in-dex of suspicionbe maintained to iden-tify the rare case of PPCM.

The diagnosis of PPCM requires ex-cludingother causes ofcardiomyopathyandisconfirmedbystandardechocardio-graphicassessmentofleftventricularsys-tolic dysfunction, including depressedfractional shortening and ejection frac-tion.Strongconsiderationshouldbegivento screening family members of PPCMpatientsbecausePPCMmaybetheformefruste of a genetic predisposition to car-diomyopathy.

In the absence of systematic studiescomparing therapeutic approaches in

PPCM,standardheartfailuretherapy(di-uretics, vasodilators, and digoxin32 asneeded)should be initiated. Careful at-tention must be paid to fetal safety andto excretionofdrug or drug metabolitesduring breastfeedingafter delivery. Col-laborationamongmedicalspecialists,in-cluding obstetricians,cardiologists,peri-natologists,andneonatologists,is essen-tial. Thediscussion thatfollows shouldbeconsideredageneralguide,ratherthana specific algorithm.

Angiotensin-converting enzyme in-

hibitors are contraindicated duringpregnancy because of teratogenicity, butshould be considered a mainstay oftreatment for PPCM after delivery. Safealternatives during pregnancy includehydralazineand nitrates. Calciumchan-nel blockers can be used during preg-nancy to control blood pressure (anddecrease uterine contractility),but most

have negative inotropic properties thatmay make them unacceptable for usein this situation. Amlodipine, a dihy-dropyridine calcium channel blocker,has been shown to improve survival innonischemic cardiomyopathy pa-

tients

33

and may have a role in man-agement of PPCM. Plasma levels ofinterleukin 6, a proinflammatory cy-tokine, were reduced among amlo-dipine recipients in the ProspectiveRandomized Amlodipine SurvivalEvaluation (PRAISE) trial,34 provid-ing an additional potential rationale forits use in PPCM.

Second-generation -adrenorecep-tor antagonists have beneficial effectsin selected patients with dilated cardi-omyopathy. Studies of-adrenorecep-tor antagonists in patients with con-

gestive heart failure have demonstratedsafety and modest clinical benefit, butconflicting results regarding sur-vival.35 Vasodilating-blockers such ascarvedilol alsoreduce afterload through1 adrenergic blockade. Data from theUS Carvedilol Heart Failure Programsuggest a potential clinical benefit, in-cluding mortality reduction, in di-latedcardiomyopathy.36 These drugs arenot contraindicated in pregnancy, butas with other agents, there are no dataevaluating their use in PPCM. A rea-

sonable approach wouldbe to use-ad-renoreceptor antagonists in the post-partum period in patientswho continueto have symptoms and echocardio-graphicevidence of left ventricular com-promise despite more than 2 weeks ofstandard heart failure management.

With mild left ventricular dysfunc-tion, therapy can be initiated in the out-patient setting. Patients with severeheart failure may require hospitaliza-tion and more aggressive support, in-cluding intravenous inotropic agents,

oxygen, and invasive monitoring. Pa-tients with significantly depressed leftventricular function (ejection fraction35%) may benefit from anticoagula-tion therapy (heparin before delivery,warfarin afterward) to prevent throm-bosis and emboli. Arrhythmias shouldbe treated according to standard pro-tocols. Immunosuppressive therapy

may be considered in patients withmyocarditis documented by endomyo-cardial biopsy who fail to improvespon-taneously within 2 weeks of initiationof standard heart failure therapy. TheMyocarditis Treatment Trial failed to

demonstrate an overall advantage forimmunosuppressive therapy, but didnot evaluate its merits in women withPPCM.37 A more recent retrospectivestudy suggested that women withPPCM treated with intravenous im-mune globulin had a greater improve-ment in ejection fraction during earlyfollow-up than patients treated con-ventionally.38 Women who fail maxi-mal medical management may be can-didates for cardiac transplantation. Onestudy of 10 PPCM patients who under-went heart transplantation reported

survival comparable to age-matchedwomen undergoing heart transplanta-tion for other indications, but noted amarginally higher rate (P = .05) of bi-opsy-proven early rejection, necessi-tating increased cytolytic therapy.39

Salt and water restriction are impor-tant in patient management, particu-larly in women with symptoms andsigns of heart failure. Once heart fail-ure symptoms have been controlled,modest exercise may improve symp-toms as well as peripheral muscular and

arterial tone. The need for early deliv-ery and the mode of delivery should beassessed through collaboration withcar-diologists and anesthesiologists. Thereis little systematic evidence that in-fantsborn to women with PPCM aread-versely affected,althoughonestudy didreport a prematuredelivery rate of 21%in 14 women.40

PROGNOSIS FOR WOMENWITH PPCM

The prognosis for women with PPCM

appears to depend on the normaliza-tion of left ventricular size and func-tion within 6 months after delivery. Inone study, approximately half of 27women studied had persistent left ven-tricular dysfunction. In this group, thecardiac mortality rate was 85% over 5years, compared with the group inwhom cardiac size returned to nor-





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mal, who experienced no reported car-diac mortality in the same time inter-val.3 A more recent study corroboratesthese results: 50% (7/14) of patientshaddramatic improvement soon after de-livery, but 6 of the 7 remaining pa-

tients died.

41

Survivors were found tohave a higher mean ejection fraction(23% vs 11%) and smaller mean leftventricular cavity size (5.8 vs 6.9 cm)at diagnosis.

Currently, there is no consensus re-garding recommendations for futurepregnancy after PPCM. Patients whoseleft ventricular size or function does notreturn to normal should be counseledstrongly to avoid subsequent preg-nancy3 and treated accordingly, includ-ing adopting a heart-healthy diet andlifestyle. Patients whose cardiomyop-

athy apparentlyresolves completely area more difficult group to counsel. In thelong-term follow-up study reported byDemakis et al,3 8 of 14 patients whoseheart size returned to normal after thefirst episode of PPCM had subsequentpregnancies. Of the 8 patients, 2 de-veloped PPCM with subsequent preg-nancies. Sutton and colleagues41 re-ported normal subsequent pregnanciesand normal leftventricular function(byechocardiography) in 4 women whoseheart size returned to normal after

PPCM in a prior pregnancy. BecausePPCM has been associated with mul-tiparity in some studies, the risk of ir-reversible cardiac damage may in-crease with eachsubsequentpregnancy.In addition, even though the left ven-tricular size and function return to nor-mal, there is evidence that contractilereserve is impaired,42 and recurrence ofPPCM despite rapid return of heart sizeand function to normal in the prior af-fected pregnancy has been reported.43

Therefore, subsequent pregnancies, if

they cannotbe avoided,shouldbe man-aged in collaboration with a high-riskperinatal center.

SUMMARY ANDRECOMMENDATIONS

Peripartum cardiomyopathy is a raredisease of unknown cause that strikeswomen in the childbearing years, may

recur, andis associatedwitha high mor-tality rate. Hypotheses about the causecenter on interactions of peripartumphysiology with infectious, inflamma-tory, genetic, hormonal, or metabolicfactors. Diagnosis of PPCM is challeng-

ing and requires vigilance. Once PPCMis identified based on the workshopcri-teria, the primary goal of therapy is toalleviate symptoms of congestive heartfailure. If left ventricular size returns tonormal after pregnancy, the short-term prognosis is likely to be favor-able, although long-term sequelae, par-ticularlywithrepeat pregnancy, stillarenot known. Failure of heart size to re-turn to normal is associated with ex-cess morbidity and mortality.

Based on the information presentedat the workshop and on the identified

gaps in knowledge, participants madethe following clinical and research rec-ommendations:

Adherence to the criteria in Table1, especially the timing and the neces-sity for echocardiographic demonstra-tion of left ventricular systolic dysfunc-tion, is important in making thediagnosis of PPCM.

Once the diagnosis is made, closecollaboration between specialists in ob-stetrics, perinatology, and cardiology isessential. If the diagnosis is made be-

fore birth, the team should include an-esthesiology and neonatology as well,and transfer to a high-risk perinatal cen-ter should be considered.

For affected patients, family his-tory may be revealing and should beelicited.

Therapy should be initiated us-ing standardheart failure protocols. An-giotensin-converting enzyme inhibi-tors should be avoided prenatally, butare a mainstay of therapy otherwise.

Immunosuppressive therapy can

be considered if an endomyocardial bi-opsy indicates myocarditis, and if thereis no improvement after 2 weeks ofstandard heart failure therapy.

Subsequent pregnancies remaincontroversial, but at the very leastshould be managed in a high-riskperinatal center if they cannot beavoided.

Workshopparticipants alsomaderec-ommendations about the need for addi-tional research and dissemination of in-formation:

An internationalregistryshouldbeestablished to capture prospectively all

women with PPCM to facilitate thefollowing: (1) development of better in-cidence and prevalence estimates, (2)determinationofriskfactorsandprognos-ticvariables,(3) ascertainment ofcardio-vascularrisksfor subsequentpregnancies,(4)establishment ofa centralized serumand tissue bank to help facilitate identi-fication of the cause of PPCM, and (5)evaluation of therapeutic interventions.

A review of current knowledgeabout PPCM should be prepared forpublication. This article fulfillsthat rec-ommendation.

Because PPCM is an under-rec-ognized obstetrical problem, an edu-cational brochure should be preparedfor broad dissemination to individualsinvolved in the care of women of child-bearing age.

Participants, Peripartum Cardiomyopathy Work-shop, April 14,1997: Judith Hsia,MD, Chair, GeorgeWashington University Schoolof Medicineand HealthSciences,Washington, DC; Aftab Ansari,MD, EmoryUniversity School of Medicine, Atlanta, Ga; SusanneL. Bathgate, MD, George Washington UniversitySchool of Medicine and Health Sciences; Kenneth L.Baughman, MD, Johns Hopkins University School ofMedicine, Baltimore, Md; Gautam Chaudhuri, MD,

PhD, University of California, Los Angeles School ofMedicine; Heidi M. Connolly, MD, Mayo GraduateSchoolof Medicine, Rochester,Minn; Maria RosaCos-tanzo, MD, Rush-Presbyterian-St LukesMedical Cen-ter,Chicago, Ill;JudithHibbard, MD,Universityof Chi-cago, Chicago, Ill; David Homans, MD, University ofMinnesota Medical School, Minneapolis; Jeffrey D. Ho-senpud, MD, Medical College of Wisconsin, Milwau-kee; Celia M. Oakley, MD, Imperial College MedicalSchool, London, England; ShahbudinRahimtoola, MD,University of Southern California, Los Angeles; Jean-Claude Veille, MD, Bowman Gray School of Medi-cine, Winston-Salem, NC; and Renu Virmani, MD,Armed ForcesInstituteof Pathology,Washington, DC.National Heart, Lung, and Blood Institute Staff:GailD. Pearson, MD, ScD,ConstanceWeinstein, PhD.

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