Article Text

other Versions

PDF
Predicting the future in peripartum cardiomyopathy
  1. Petronella G Pieper
  1. Correspondence to Dr Petronella G Pieper, Department of Cardiology, University Medical Center Groningen, University of Groningen, PO Box 30.001, Groningen 9700 RB, the Netherlands; p.g.pieper{at}umcg.nl

Statistics from Altmetric.com

Heart failure caused by primary muscle disease and occurring as a complication of pregnancy was already described in 1849.1 In 1937 and 1938 two series of women with pregnancy-associated heart failure were reported in the literature, and the condition was then named ‘postpartal heart failure’.2 Since 1971 when Demakis defined diagnostic criteria of peripartum cardiomyopathy (PPCM), the definition has been modified several times. For many years the definition included the development of clinical heart failure associated with systolic left ventricular dysfunction according to stringent echocardiographic criteria and occurring in the last month of pregnancy or within 5 months postpartum.2 A recent position paper from the European Society of Cardiology Working Group on PPCM stated that such strict definitions may result in underdiagnosis of PPCM. They proposed that PPCM should be defined as ‘an idiopathic cardiomyopathy presenting with heart failure secondary to left ventricular systolic dysfunction towards the end of pregnancy or in the months following delivery, where no other cause of heart failure is found. It is a diagnosis of exclusion. The left ventricle (LV) may not be dilated but the ejection fraction is nearly always reduced below 45%’.3

The incidence varies according to race and region from 1 : 300 in Haiti to 1 : 9800 in Hispanic USA inhabitants.3 The cause of PPCM remains unknown, and multiple factors may be involved in the inflammation process leading to manifest cardiomyopathy. These factors include cytokine imbalance, viral infection, genetic susceptibility and altered immune response due to pregnancy which may be aggravated by hormones and nutrient deficiency.3 ,4 Recent data suggest involvement of oxidative stress activating cathepsin D, which subsequently cleaves prolactin leading to increased serum levels of the 16 kDa prolactin fragment that …

View Full Text

Request permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Linked Articles