Peripartum cardiomyopathy is a distinct entity of dilated cardiomyopathy, and occurs in women between one month antepartum and six months postpartum. Specific risk factors for peripartum cardiomyopathy have not been defined and reports in the literature regarding positive family histories of peripartum cardiomyopathy are rare [
1]. However, the higher incidence of peripartum cardiomyopathy in certain geographic areas, specifically Africa and Haiti, indicates a possible genetic factor [
2].
At present, peripartum cardiomyopathy is treated according to the guidelines for dilated cardiomyopathy with angiotensin converting enzyme (ACE) inhibitors, beta-blockers and diuretics (standard therapy for heart failure) [
2]. Nevertheless, the prognosis is poor, with reported mortality rates up to 15% and full recovery in only 23% of patients, while continuous deterioration is reported in up to 50% of patients despite optimal medical treatment [
2‐
4]. Recently, oxidative stress-mediated generation of anti-angiogenic and pro-apoptotic 16 kDa prolactin and subsequent impaired cardiac microvascularisation have been related to peripartum cardiomyopathy [
5]. A small pilot study suggested that prolactin blockade by bromocriptine in addition to standard therapy prevents repeated episodes of peripartum cardiomyopathy in patients presenting with a subsequent pregnancy [
5]. Following this study, recent case reports have suggested that bromocriptine may also be beneficial in acute peripartum cardiomyopathy [
6‐
8]. A survey of more than 1400 pregnant women who took bromocriptine primarily during the first few weeks of pregnancy found no evidence of increased rates of spontaneous abortion or congenital malformations [
9]. However, safety issues were raised for patients taking bromocriptine in the early postpartum phase: a few case reports describe an increased risk of thrombotic events, such as myocardial infarction and retinal vein occlusion, in these patients [
10‐
12].