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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.

OBJECTIVE: The aim of this work was to evaluate the hypothesis that the distribution of circulating immune cell subsets, or their activation state, is significantly different between peripartum cardiomyopathy (PPCM) and healthy postpartum (HP) women. BACKGROUND: PPCM is a major cause of maternal morbidity and mortality, and an immune-mediated etiology has been hypothesized. Cellular immunity, altered in pregnancy and the peripartum period, has been proposed to play a role in PPCM pathogenesis. METHODS: The Investigation of Pregnancy-Associated Cardiomyopathy (IPAC) study enrolled 100 women presenting with a left ventricular ejection fraction of

Introduction: Poor health literacy is associated with worse outcomes in patients with heart failure; however, the role of health literacy in predicting outcomes in patients implanted with left ventricular assist devices (LVADs) has not yet been studied. We hypothesized that health literacy would independently influence clinical outcomes in patients implanted with continuous-flow LVADs (CF-LVADs). Hypothesis: Poor health literacy is associated with worse outcomes in patients with end-stage heart failure implanted with CF-LVADs. Methods: We performed a prospective, single center, cohort study of adult patients with implanted CFLVADs. We identified 118 patients implanted with a Heart Mate II (n5101) or an HVAD (n517) implanted between 8/2005 and 9/2013. Health literacy was assessed using the Rapid Estimate of Adult Literacy in Medicine (REALM), with adequate health literacy defined as a score $ 61 (REALM IV) and poor literacy defined as a score ! 61 (REALM I-III). The primary outcome was combined all-cause death, stroke, gastrointestinal bleeding (GIB), LVAD-related infection, or hemolysis/pump thrombosis; components of the combined primary outcome were analyzed separately as secondary outcomes. Results: The majority of patients were implanted with Heart Mate II LVADs and had an INTERMACS profile of 2. The poor health literacy group (n538) had significantly more patients with a history of smoking (76% vs. 49%, p 5 0.005), a destination therapy strategy (53% vs. 30%, p 5 0.05), and a history of GIB (58% vs. 26%, p 5 0.003). There were no significant differences between cohorts with respect to age, date of implant, BMI, race, sex, etiology of cardiomyopathy, or history of diabetes. During a follow-up period of 88.8 patient-years there were 89 events: 32 in the poor health literacy group and 57 in the adequate health literacy group (84% vs. 71%, HR 1.56, CI 1.01-2.42, p 5 0.0466), see figure. This was driven primarily by GIB events of which there were 22 in both groups (58% vs. 28%, HR 2.57, CI 1.56-5.81). There were no significant differences in individual secondary outcomes of all-cause death