Abstract 15243: Incidence and Predictors of Chemotherapy-Induced Cardiomyopathy in African Americans: A Single-Center Experience

Abstract

Introduction: African Americans (AA) have largely been under-represented in randomized clinical trials investigating chemotherapy-induced cardiomyopathy (CICM) associated with doxorubicin and trastuzumab. Limited and conflicting evidence has linked higher incidence of CICM among AA patients to a higher prevalence of underlying co-morbidities. Hypothesis: African Americans have a higher incidence of CICM which is associated with higher prevalence of underlying co-morbidities in these patients. Methods: We retrospectively identified and included AA patients who underwent treatment with doxorubicin and trastuzumab at our institution. CICM was defined as a decline in ejection fraction (EF) to <50% OR >/=10% decline in baseline EF post-treatment. A univariate analysis was performed to study the association of common co-morbidities with CICM. JMP software (SAS v 9.4) was used for statistical analysis. Results: A total of 121 patients were included for analysis, out of which, 52.1% (63/121) and 47.9% (58/121) were treated with trastuzumab and doxorubicin respectively. Majority (85.1%, 103/121) were females and the mean age was 62.4±5.2 years. Median EF pre- and post-treatment were 65% (IQR 60%,65%) and 60% (IQR 55%,65%) respectively. The cumulative incidence of CICM in our cohort was 24% (29/121). There was no statistically significant association of CICM with female sex [OR=0.79 (0.25-2.99), p=0.68], age [OR=0.99 (0.96-1.02), p=0.88], pre-treatment EF [OR=1.09 (0.96-1.94), p=0.27], hypertension [OR=1.27 (0.51-3.18), p=0.60], diabetes [OR=1.91 (0.89-4.95), p=0.13], hyperlipidemia [OR=1.19 (0.44-2.92), p=0.78] or coronary artery disease [OR=1.93 (0.68-5.93), p=0.21]. Conclusions: Per existing literature, the incidence of CICM in our cohort of AA patients is higher than general population. As historically postulated, CICM was not found to be associated with pre-existing co-morbidities. Further clinical and translational research is needed to study genetic and pathophysiological mechanisms driving CICM in AA patients.