Background: Black women have greater than a three-fold risk of pregnancy-associated death compared to White women; cardiomyopathy is a leading cause of maternal mortality. Objectives: This study examined racial disparities in health outcomes among women with peripartum cardiomyopathy. Study design: Retrospective cohort of women with peripartum cardiomyopathy per the National Heart, Lung, and Blood Institute definition from January 2000 to November 2017 from a single referral center. Selected health outcomes among Black and White women were compared; primary outcome was ejection fraction at diagnosis. Secondary outcomes included cardiovascular outcomes, markers of maternal morbidity, resource utilization, and subsequent pregnancy outcomes. Results: Ninety-five women met inclusion criteria: 48% Black, 52% White. Nearly all peripartum cardiomyopathy diagnoses were postpartum (95.4% Black, 93% White, p=.11). Ejection fraction at diagnosis was not different between Black and White women (26.8 ± 12.5 vs. 28.7 ± 9.9, p=.41). Though non-significant, fewer Black women had myocardial recovery to EF ≥55% (35 vs. 53%, p=.07); however, 11 (24%) of Black women vs. 1 (2%) White woman had an ejection fraction ≤35% at 6–12 months postpartum (p<.01). More Black women underwent implantable cardioverter defibrillator placement: n = 15 (33%) vs. n = 7 (14%), p=.03. Eight women (8.4%) died in the study period, not different by race (p=.48). Black women had higher rates of healthcare utilization. In the subsequent pregnancy, Black women had a lower initial ejection fraction (40 vs. 55%, p=.007) and were less likely to recover postpartum (37.5 vs. 55%, p=.02). Conclusions: Black and White women have similar mean ejection fraction at diagnosis of peripartum cardiomyopathy, but Black women have more severe left ventricular systolic dysfunction leading to worse outcomes, increased resource use, and lower ejection fraction entering the subsequent pregnancy.

Dual antiplatelet therapy with aspirin and a P2Y12 receptor antagonist remains a mainstay in the prevention of ischemic events following coronary stent placement. Significant controversy exists regarding the optimal management of high platelet reactivity despite antiplatelet therapy; however this finding has been consistently associated with poor clinical outcomes including greater risk of stent thrombosis and myocardial infarction. Variability in antiplatelet effects of clopidogrel and prasugrel has been linked to genetic polymorphisms and potential drug–drug interactions. Both of these factors have significant influence on the cytochrome P-450 enzyme system activity of the liver responsible for their biotransformation to the active form of both drugs. Very little has been publicized regarding differences in antiplatelet effects which may be associated with conditions in which the functional capacity of the liver may be temporarily compromised. Patients who present with cardiogenic shock due to acute coronary syndromes have evidence of multiorgan dysfunction including liver dysfunction that may affect the activity of these drugs. This review aims to explore existing evidence and propose additional considerations to the selection of antiplatelet therapy in patients with cardiogenic shock who receive catheter-based revascularization and stent placement.