16-kDa prolactin and bromocriptine in postpartum cardiomyopathy

Curr Heart Fail Rep. 2012 Sep;9(3):174-82. doi: 10.1007/s11897-012-0095-7.


Peripartum cardiomyopathy (PPCM) is a potentially life-threatening heart disease emerging toward the end of pregnancy or in the first postpartal months in previously healthy women. Recent data suggest a central role of unbalanced peri-/postpartum oxidative stress that triggers the proteolytic cleavage of the nursing hormone prolactin (PRL) into a potent antiangiogenic, proapoptotic, and proinflammatory 16-kDa PRL fragment. This notion is supported by the observation that inhibition of PRL secretion by bromocriptine, a dopamine D2-receptor agonist, prevented the onset of disease in an animal model of PPCM and by first clinical experiences where bromocriptine seem to exert positive effects with respect to prevention or treatment of PPCM patients. Here, we highlight the current state of knowledge on diagnosis of PPCM, provide insights into the biology and pathophysiology of 16-kDa PRL and bromocriptine, and outline potential consequences for the clinical management and treatment options for PPCM patients.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Bromocriptine / therapeutic use
  • Cardiomyopathies / diagnosis
  • Cardiomyopathies / drug therapy
  • Cardiomyopathies / metabolism*
  • Female
  • Hormone Antagonists / therapeutic use
  • Humans
  • Oxidative Stress / physiology
  • Peptide Fragments / metabolism*
  • Pregnancy
  • Pregnancy Complications, Cardiovascular / diagnosis
  • Pregnancy Complications, Cardiovascular / drug therapy
  • Pregnancy Complications, Cardiovascular / metabolism*
  • Prolactin / metabolism*
  • Puerperal Disorders / diagnosis
  • Puerperal Disorders / drug therapy
  • Puerperal Disorders / metabolism*


  • Hormone Antagonists
  • Peptide Fragments
  • prolactin 16-kDa fragment, human
  • Bromocriptine
  • Prolactin