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Peripartum Cardiomyopathy

Key Findings

Pubmed MONDO:0018920

Key Findings

  1. Angiogenic imbalance is the primary vascular mechanism: elevated sFlt1 from the placenta antagonizes VEGF/PlGF signaling, causing endothelial dysfunction and impaired cardiac angiogenesis (PMID:22596155)

  2. 16-kDa prolactin is a central mediator: STAT3 deficiency leads to enhanced cathepsin D activity, cleaving prolactin into a cardiotoxic 16-kDa fragment that is anti-angiogenic and pro-apoptotic (PMID:17289576)

  3. Bromocriptine shows therapeutic promise: blocks prolactin secretion, preventing 16-kDa fragment generation; proof-of-concept RCT showed LVEF recovery from 27% to 58% vs 36% with standard therapy alone (PMID:20308616)

  4. TTN truncating variants are the most common genetic risk factor, found in ~10% of PPCM patients, similar to the prevalence in dilated cardiomyopathy (PMID:26735901)

  5. Preeclampsia is present in 22% of PPCM cases (4x background rate), sharing anti-angiogenic pathobiology (PMID:24013055)

  6. Autoimmune mechanisms including anti-M2 muscarinic receptor autoantibodies independently predict worse cardiac recovery (PMID:34963460)

  7. Prognosis: ~10% mortality; >50% recover LV function within 1 year; high relapse risk in subsequent pregnancies (PMID:37414337)