Peripartum Cardiomyopathy Due to Myocarditis

Melvin, Kenneth R.; Richardson, Peter J.; Olsen, E. G. J.; Daly, Kieran; Jackson, Graham

doi:10.1056/nejm198209163071207

Cited by 183 publications

(57 citation statements)

References 6 publications

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“…200,201 There are several older reports of lymphocytic infiltrate and myocarditis in patients with PPCM. [202][203][204] In a population of 18 women with PPCM, Bhakta et al 201 and Midei and colleagues 202 found myocarditis in 78% as early as 7 days after presentation and as late as 6.5 months. However, the incidence of lymphocytic myocarditis varies widely in published series and closely parallels the incidence found in biopsy series of other forms of recent-onset cardiomyopathy.…”

Section: Endomyocardial Biopsymentioning

confidence: 99%

Current Diagnostic and Treatment Strategies for Specific Dilated Cardiomyopathies: A Scientific Statement From the American Heart Association

Bozkurt¹,

Colvin²,

Cook³

et al. 2016

Circulation

606

663

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CLINICAL STATEMENTS AND GUIDELINEST he intent of this American Heart Association (AHA) scientific statement is to summarize our current understanding of dilated cardiomyopathies. There is special emphasis on recent developments in diagnostic approaches and therapies for specific cardiomyopathies. Recommendations in this document are based on published studies, published practice guidelines from the American College of Cardiology (ACC)/AHA 1 and other organizations, 2,3 and the multidisciplinary expertise of the writing group. Existing evidence in epidemiology, classification, diagnosis, and management of specific cardiomyopathies is usually derived from nonrandomized observational studies, registries, case reports, or expert opinion based on clinical experience, not large-scale randomized clinical trials or systematic reviews. Therefore, in this document, rather than using the standard ACC/AHA classification schema of recommendations and level of evidence, 4 we have included key management strategies at the end of each section and categorized our recommendations according to the level of consensus. Although the format of our recommendations might resemble the ACC/AHA classification of recommendations used in the ACC/AHA practice guidelines, because of the preponderance of expert opinion or level of evidence C evidence in our document, we elected to use different terminology to provide a distinction from the practice guidelines, in which stronger levels and quality of evidence with randomized clinical trials or meta-analyses are usually present. 4 The levels of evidence follow the AHA and ACC methods of classifying the level of certainty of the treatment effect. 4 DEfINITIoN of DILATED CArDIoMyopAThyThe term dilated cardiomyopathy (DCM) refers to a spectrum of heterogeneous myocardial disorders that are characterized by ventricular dilation and depressed myocardial performance in the absence of hypertension, valvular, congenital, or ischemic heart disease. 5 In clinical practice, the pathogenesis of heart failure (HF) has often been placed into 2 categories: ischemic and nonischemic cardiomyopathy. The term nonischemic cardiomyopathy has been interchangeably used with DCM. Although this approach might be practical, it fails to recognize that nonischemic cardiomyopathy can include cardiomyopathies caused by volume or pressure overload (such as hypertension or valvular heart disease) that are not conventionally accepted under the definition of DCM. 1,5 Again, in general practice and clinical research trials, the term ischemic cardiomyopathy is defined as cardiomyopathy caused by ischemic heart disease. Current use of ischemic cardiomyopathy terminology implies ventricular dilation and depressed myocardial contractility caused by ischemia or infarction. CLASSIfICATIoN of CArDIoMyopAThIESThe first classification on this topic categorized cardiomyopathies as heart muscle diseases with dilated (DCM), hypertrophic, restrictive, arrhythmogenic right ventricular (ARVC), or nonclassifiable cardiomyopathy in 1980. 5 Subse...

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Section: Endomyocardial Biopsymentioning

confidence: 99%

Current Diagnostic and Treatment Strategies for Specific Dilated Cardiomyopathies: A Scientific Statement From the American Heart Association

Bozkurt¹,

Colvin²,

Cook³

et al. 2016

Circulation

606

663

View full text Add to dashboard Cite

show abstract

“…The reason why only some patients recover normal cardiac function is not clear. Immunological or infectious causes have been suspected to be responsible for the decrease of cardiac function [3,[6][7][8] and former histological studies have described the presence of myocardial fibrosis [6,9,10]. Cardiac magnetic resonance imaging (MRI) is now established as a reference technique to assess cardiac Electronic supplementary material The online version of this article (doi:10.1007/ s00330-008-1067-x) contains supplementary material, which is available to authorized users.…”

Section: Introductionmentioning

confidence: 99%

Characterisation of peripartum cardiomyopathy by cardiac magnetic resonance imaging

et al. 2008

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Peripartum cardiomyopathy (PPCM) is a rare cause of heart failure. Only half of the patients recover normal cardiac function. We assessed the usefulness of magnetic resonance imaging (MRI) and late enhancement imaging to detect myocardial fibrosis in order to predict cardiac function recovery in patients with peripartum cardiomyopathy. Among a consecutive series of 1,037 patients referred for heart failure treatment or prognostic evaluation between 1999 and 2006, eight women had confirmed PPCM. They all underwent echocardiography and cardiac MRI for assessment of left ventricular anatomy, systolic function and detection of myocardial fibrosis through late enhancement imaging. Mean (+/- SD) baseline left ventricular ejection fraction (LVEF) was 28 +/- 4%. After a follow-up of 50 +/- 9 months, half the patients recovered normal cardiac function (LVEF = 58 +/- 4%) and four did not (LVEF = 35 +/- 6%). None of the eight patients exhibited abnormal myocardial late enhancement. No difference in MRI characteristics was observed between the two groups. Patients with PPCM do not exhibit a specific cardiac MRI pattern and particularly no myocardial late enhancement. It suggests that myocardial fibrosis does not play a major role in the limitation of cardiac function recovery after PPCM.

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“…It has been postulated that the myocarditis has a viral [30,42] or an autoimmune etiology [17,38,39,43], with pregnancy increasing susceptibility to either [36,39]. The evidence that PP-CMP is associated with high titers of autoantibodies against certain cardiac tissue proteins (adenine nucleotide translocator, branched-chain α-keto acid dehydrogenase) supports abnormal immunological activity as a possible cause [17,43].…”

Section: Pathology and Etiologymentioning

confidence: 96%

“…Nonspecific pathological findings include myocardial cellular hypertrophy and myofiber degeneration with areas of fibrosis, interstitial edema, and, occasionally, lymphocytic infiltration [6,35]. In 1982 Melvin [36] proposed myocarditis as a causal factor, and other reports followed [37,38,39,40,41]. The reported incidence of myocarditis varies from 8.8% [39] to 78% [38].…”

Section: Pathology and Etiologymentioning

confidence: 99%