Breastfeeding, Cellular Immune Activation, and Myocardial Recovery in Peripartum Cardiomyopathy

Visual Abstract
Highlights • The impact of breastfeeding on prolactin, cellular immune activation, and myocardial recovery was analyzed in 100 women with peripartum cardiomyopathy • Cardiac function was assessed by echocardiography at presentation and at serial intervals over the first year postpartum • The levels of circulating prolactin were assessed by ELISA, and cellular immunophenotyping by flow cytometry, and compared between breastfeeding and nonbreastfeeding women • Prolactin levels were higher in breastfeeding women and correlated with significant increases in CD8+ T cells • Despite significantly higher prolactin levels and increased CD8+ cells, myocardial recovery was similar in breastfeeding and nonbreastfeeding women
Summary The etiology of peripartum cardiomyopathy remains unknown. One hypothesis is that an increase in the 16-kDa form of prolactin is pathogenic and suggests that breastfeeding may worsen peripartum cardiomyopathy by increasing prolactin, while bromocriptine, which blocks prolactin release, may be therapeutic. An autoimmune etiology has also been proposed. The authors investigated the impact of breastfeeding on cellular immunity and myocardial recovery for women with peripartum cardiomyopathy in the IPAC (Investigations in Pregnancy Associated Cardiomyopathy) study. Women who breastfed had elevated prolactin, and prolactin levels correlated with elevations in CD8+ T cells. However, despite elevated prolactin and cytotoxic T cell subsets, myocardial recovery was not impaired in breastfeeding women.