Abstract Body (Do not enter title and authors here): Background Those living with HIV are at an increased risk for cardiac dysfunction and clinical heart failure compared to people without HIV. Persons with HIV are also at an increased risk for cancer. There are limited data on the cardiotoxicity post anthracycline-based chemotherapy in cancer patients with HIV.

Hypothesis Cancer patients with HIV have a higher risk of cardiotoxicity post anthracycline-based chemotherapy than HIV negative controls.

Methods We included consecutive adult patients who underwent anthracycline-based chemotherapy from 2016 to 2019 for any type of cancer and who had a HIV testing. Patients with preexisting heart failure were excluded from the analysis. The endpoint was the development of cardiotoxicity (defined as clinical heart failure or a drop in left ventricular ejection fraction (LVEF)≥10% to LVEF<50%).

Results Among the 662 cancer patients who had a HIV testing (19% non-Hispanic White, 26% non-Hispanic Black, 34% Hispanic), 49 were positive (7.4%). More male (12% vs 5%) and non-Hispanic Black (15% vs 0-8% in other race and ethnicity) patients were HIV positive. The rate of cardiotoxicity was 13% overall during a median follow-up of 21 months and it was not different between patients with and without HIV (14% with HIV and 13% without HIV, p=0.75). Mean baseline CD4 count was 294±249 cells/mm3 and it was similar between patients with and without cardiotoxicity. Baseline HIV virus load was undetectable or <40/mL in 53% of patients and antiretroviral therapy was used in 88% of patients, and these rates were not different between patients with and without cardiotoxicity. In the unadjusted and adjusted (age, sex, race and ethnicity, baseline LVEF, anthracycline dose) Cox proportional hazards models, HIV status and HIV viral control (among those with HIV) were not associated with the development of cardiotoxicity.

Conclusions Based on a small cohort of cancer patients, HIV status, and HIV viral control among those with HIV, were not associated with the development of short-term cardiotoxicity.