Key result
Peripartum cardiomyopathy stems from inflammation, cardiotoxic prolactin, and hemodynamic stress on a genetic background.
Why the study?
To analyze literature data to examine the pathophysiological mechanisms underlying the development of peripartum cardiomyopathy.
This review highlights that peripartum cardiomyopathy pathogenesis is multifactorial, involving genetic predisposition, inflammation, and the prolactin-cathepsin-prolactin 16 kDa system.
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Does not yet change peripartum cardiomyopathy management; extends multifactorial pathogenesis model and leaves targeted therapies open for prospective trials.
The aim of the study . To analyze literature data in order to study the pathophysiological mechanisms of development of peripartum cardiomyopathy. Research methods and materials . A review of modern Russian and foreign, mainly English-speaking, literature on the pathogenetic mechanisms of IPAH development was carried out. We took into account publications not older than 6 years, published in specialized medical journals and guidelines. Results . According to the data of modern studies devoted to the peculiarities of the development of peripartum cardiomyopathy, much attention is paid to the risk factors of the disease, in particular the age-related obstetric history, pregnancy with twins or more, and arterial hypertension. In addition, the significance of genetic predisposition, inflammatory syndrome has been proven, and the vasculo-hormonal theory is being studied. Difficult issues of the etiopathogenesis of the disease, including myocarditis, the role of the prolactin-cathepsin-prolactin 16 kDa system, and malnutrition are discussed. Conclusion . Pathophysiological mechanism of development of peripartum cardiomyopathy. appears as a complex combination of inflammatory changes in the myocardium with the participation of a cardiotoxic subfragment – prolactin 16 kDa, which causes damage and dysfunction of the endothelium under hemodynamic stress against the background of possible genetic changes, which leads to damage to cardiomyocytes and a decrease in myocardial contractility.
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Kazantseva et al. (2021) conducted a review in Peripartum cardiomyopathy. Peripartum cardiomyopathy develops through a complex combination of inflammatory changes, cardiotoxic prolactin 16 kDa, and hemodynamic stress on a background of genetic predisposition.
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