Peripartum cardiomyopathy: Update 2012

Purpose of review: Peripartum cardiomyopathy ( PPCM ) is a disorder in which initial left ventricular systolic dysfunction and symptoms of heart failure occur between the late stages of pregnancy and the early postpartum period. Incidences vary geographically; it is common in some countries and rare in others. The acute form of PPCM is a clinical syndrome with reduced cardiac output, tissue hypoperfusion, and increase in the pulmonary capillary wedge pressure. Monitoring of the patient with the acute form of PPCM should be initiated as soon as possible. The syndrome carries a high morbidity and mortality and diagnosis is often delayed. This review focuses on new data and aspects in terms of diagnosis, causes of disease, pharmacological therapy, and management of delivery in patients with PPCM. Recent findings: New investigations reveal that PPCM is likely due to multiple factors. It develops based on oxidative stress leading to cleavage of deleterious 16-kDa prolactin, which can be blocked with bromocriptine. New data show furthermore that it is partly a two-hit vascular disease due to imbalances in angiogenic signaling worsening the severity of the disease. Summary: Different mechanisms have been investigated and give rise to promising therapeutic approach, which will be developed based on the new findings

Article Commentary: Acute Heart Failure: Is it Peripartum Cardiomyopathy or Not?

Peripartum cardiomyopathy (PPCM) is a potentially life-threatening disease that occurs in women of childbearing age

Acute heart failure: Is it peripartum cardiomyopathy or not?

Peripartum cardiomyopathy (PPCM) is a potentially life-threatening disease that occurs in women of childbearing age

Parvovirus B19-induced vascular damage in the heart is associated with elevated circulating endothelial microparticles

<div><p>Background</p><p>Diagnosis of viral myocarditis is difficult by clinical criteria but facilitated by detection of inflammation and viral genomes in endomyocardial biopsies. Parvovirus B19 (B19V) targets endothelial cells where viral nucleic acid is exclusively detected in the heart. Microparticles (MPs) are released after cell damage or activation of specific cells. We aimed to investigate whether circulating endothelial MPs (EMPs) in human and experimental models of myocarditis are associated with B19V myocarditis.</p><p>Methods</p><p>MPs were investigated in patients with myocarditis (n = 54), divided into two groups: B19V+ (n = 23) and B19V- (n = 31) and compared with healthy controls (HCTR, n = 25). MPs were also investigated in B19V transgenic mice (B19V-NS1+) and mice infected with coxsackievirus B3 (CVB3). MPs were analyzed with fluorescent activated cell sorting (FACS).</p><p>Results</p><p>In human samples, EMP subpopulation patterns were significantly different in B19V+ compared to B19V- and HCTR (p<0.001), with an increase of apoptotic but not activated EMPs. Other MPs such as platelet- (PMPs) leukocyte-(LMPs) and monocyte-derived MPs (MMPs) showed less specific patterns. Significantly different levels of EMPs were observed in transgenic B19V-NS1+ mice compared with CVB3-infected mice (p<0.001).</p><p>Conclusion</p><p>EMP subpopulations are different in B19V+ myocarditis in humans and transgenic B19V mice reflecting vascular damage. EMP profiles might permit differentiation between endothelial-cell-mediated diseases like myocardial B19V infection and other causes of myocarditis.</p></div

Murine endothelial microparticles (B19V- transgenic mice).

<p>Murine endothelial microparticles (EMPs) in transgenic B19V-NS1-mice with induction by doxycycline (B19V+) after 2, 4 and 6 weeks p.i. compared with controls (C57/Bl6 and transgenic B19V-NS1 mice without doxycyclin). A: EMPs in C57/Bl6 mice compared to transgenic B19V-NS1-mice without doxycyclin showed about the same EMP numbers (p = 0.775). EMPs were significantly increased in transgenic B19V-NS1-mice with doxycyclin after 2, 4 and 6 weeks compared to controls such as C57/Bl6 (p<0.001) and transgenic B19V-NS1-mice without doxycylin (p<0.001, p = 0.003 and p = 0.029). The increase had its maximum after two weeks with a decline after four weeks. B: The increase of EMPs was due to apoptotic EMPs. C: Activated EMPs were not different between the groups.</p

Murine endothelial microparticles (CVB3+ infected mice).

<p>Murine endothelial microparticles (EMPs) in CVB3+ infected mice (CVB3+) after 2, 8 and 28 days p.i. compared with controls (C57/Bl6). A: EMPs were increased in CVB3+ mice two days p.i. (p<0.001 vs. control) with a decline in the following 6 days (p<0.001 vs. control) and 28 days p.i. (p<0.001 vs. control). B: The increase of EMPs was due to apoptotic EMPs. C: Activated EMPs were not different between the groups.</p

Clinical parameters of human samples.

<p>Clinical parameters of human samples.</p