Cardiomyopathy around the time of delivery is rare and prolactin release associated with breastfeeding is hypothesized to worsen the condition. A new prospective study, published in JACC: Basic to Translational Research, calls into question that connection.
For the Investigations in Pregnancy Associated Cardiomyopathy study, 100 women with postpartum cardiomyopathy (PPCM) were enrolled at 30 centers during the first 13 weeks after giving birth. None had a history of cardiovascular disease or structural heart disease and all had left ventricular ejection fractions ≥ 45% at time of enrollment and had developed nonischemic cardiomyopathy in late pregnancy or soon after delivery.
At presentation and at serial intervals during the first year postpartum, the women’s cardiac function was assessed with echocardiography. Levels of circulating prolactin were assessed using ELISA, and cellular immunophenotyping by flow cytometry, and compared between the women who breastfed and those who did not.
The women who breastfed had higher levels of prolactin than the women who did not and those levels correlated with significant increases in CD8-positive T cells. Despite these elevations, myocardial recovery was not impaired in the women who breastfed.
The authors noted that their study “is the first to demonstrate the impact of BF [breastfeeding] on maternal cellular immunity in a cohort of women with PPCM and that this change in cellular immunity (increased cytotoxic T cell) was correlated with prolactin.” The results, they said, argue against the hypothesis that breastfeeding worsens cardiomyopathy.
“Women with PPCM who are more gravely ill at the time of diagnosis may potentially benefit from prohibition of BF via bromocriptine therapy,” the researchers concluded, “but a recommendation regarding the use of bromocriptine in these patients with PPCM should be based on a rigorous large randomized controlled study comparing the use of bromocriptine versus placebo in patients with PPCM who are at higher risk for poor outcomes, all of whom should also be concomitantly treated with guideline-directed heart failure therapies.”