Peripartum Cardiomyopathy: Recent Insights in its Pathophysiology

Peripartum/Postpartum cardiomyopathy (PPCM) is a serious, potentially life-threatening heart disease of uncertain etiology in previously healthy women. Previous clinical and experimental data have identified inflammation, autoimmune processes, apoptosis, and impaired cardiac (systemic) microvasculature as typical features in the pathophysiology of PPCM. However, recent data have shown that unbalanced peri/postpartum oxidative stress is linked to proteolytic cleavage of the nursing hormone prolactin into a potent antiangiogenic, proapoptotic, and pro-inflammatory factor. These observations strongly suggest that prolactin cleavage can operate as a specific pathomechanism for the development of PPCM. Consistent with these findings, inhibition of prolactin secretion by bromocriptine, a dopamine D2 receptor agonist, prevented the development of PPCM in an animal model of PPCM, and first clinical experience are promising in this respect. Thus, inhibition of prolactin release may represent a novel specific therapeutic approach to either prevent or treat patients with acute PPCM. In this review, we are highlighting the current knowledge on risk factors, potential pathomechanisms, and treatment options for PPCM.