Peripartum Cardiomyopathy: an Update

Feriel Azibani, Karen Sliwa, Feriel Azibani, Karen Sliwa

Abstract

Purpose of review: Peripartum cardiomyopathy (PPCM) is an idiopathic disorder defined as heart failure occurring in women during the last month of pregnancy and up to 5 months postpartum. In this review, we outline recent reports about the disease pathogenesis and management and highlight the use of diagnosis and prognosis biomarkers.

Recent findings: Novel data strengthen the implication of endothelial function in PPCM pathogenesis. The first international registry showed that patient presentations were similar globally, with heterogeneity in patient management and outcome. Despite large improvement in patient management and treatment, there is still a sub-group of women who die from PPCM or who will not recover their cardiac function. Remarkable advances in the comprehension of disease incidence, pathogenesis, and prognosis could be determined with multi-center and international registries.

Clinical trials: ClinicalTrials.gov Identifier: NCT02590601.

Keywords: Acute heart failure; Biomarker; Ethnicity; Peripartum cardiomyopathy; Pregnancy; Registry.

Conflict of interest statement

Conflict of Interest

The authors declare that they have no conflict of interest.

Human and Animal Rights and Informed Consent

This article does not contain any studies with human or animal subjects performed by any of the authors.

Figures

Fig. 1
Fig. 1
Pathophysiological mechanisms inducing peripartum cardiomyopathy: role of inflammation, apoptosis, and angiogenic imbalance. Decreased levels of STAT3 and/or PGC-1α increase ROS which will increase cathepsin D and MMP activity. Full-length prolactin (23KDa-PRL), highly expressed before delivery and postpartum, will be cleaved into 16KDa-PRL responsible of (1) increased expression of miR-146a which will inhibit endothelial cell proliferation and survival and induce cardiomyocyte apoptosis and (2) increased expression of CCL2 inducing cardiac inflammation. The angiogenic imbalance induced by 16KDa-PRL is augmented by increased sFlt1 and decreased VEGF and relaxin levels. Abbreviations: 16KDa-PRL, 16-kDa prolactin hormone; CCL2, chemokine ligand 2; CD, cathepsin D; Errb4, tyrosine kinase-type cell surface receptor HER4; IFN-ϒ, interferon-ϒ; MMP, matrix metalloproteinase; MnSOD, manganese-dependent superoxide dismutase; NFκB, nuclear factor-kappa B; PGC-1α, peroxisome proliferator-activated receptor gamma coactivator; PRL, prolactin hormone; ROS, reactive oxygen species; sFlt1, soluble fms-like tyrosine kinase-1; STAT, signal transducer and activator of transcription; VEGF, vascular endothelial growth factor

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