Major adverse cardiovascular events among prostate cancer patients in the VA, stratified by HIV status and androgen deprivation therapy.

12157 Background: Despite the rapidly increasing trend in incidence of prostate cancer among persons with HIV (PWH), comprehensive data outlining outcomes and treatment toxicities of prostate cancer in this population remain sparse. Notably, both HIV infection and prostate cancer treatment independently increase the risk of cardiovascular disease. We sought to quantify the risk of major cardiovascular adverse events (MACE) among a large Veterans Affairs (VA) cohort of PWH and people without HIV (PWoH). Methods: We used patient data from the VA Corporate Data Warehouse and the VA Central Cancer Registry, including demographics, laboratory data, medications administered in inpatient/outpatient pharmacies, International Classification of Diseases 9 th Edition and 10 th edition diagnoses and procedure codes. Patients were included if they had diagnosis of prostate adenocarcinoma between 1/1/2008 and 12/31/2020. Patients were excluded if they had a diagnosis with any prior invasive cancer on or prior to prostate cancer diagnosis, diagnosis with prostate cancer prior to HIV positive diagnosis, or MACE within 6 months prior to prostate cancer diagnosis. MACE was defined as having a diagnosis code of myocardial infarction, stroke, or arrhythmia, within five years of start of treatment approach for prostate cancer (defined as androgen deprivation therapy (ADT) or active surveillance). We conducted a time-to-event analysis using the Cox proportional hazards model to examine the time to first occurrence of MACE, accounting for censoring and varying follow-up times. Results: A total of 87,144 prostate cancer patients were included (654 PWH and 86,490 PWoH). About 37.5% of PWH were < 60-years-old at time of prostate cancer diagnosis (compared with 19.6% of PWoH). Among 62,259 patients with low-risk or intermediate-risk localized prostate cancer, the risk of MACE was 24% greater among PWH compared with PWoH (HR 1.24, 95% CI 1.02-1.51, p = 0.03) after controlling for age, race, and cardiovascular risk factors at time of cancer diagnosis. Among PWH with prostate cancer, receiving ADT was associated with a 3.5 fold increased risk of developing MACE vs. those not receiving ADT (HR 3.51, 95% CI 2.25-5.49, p < 0.01). Among PWoH with prostate cancer, receiving ADT had a 2.7-fold increased risk of developing MACE vs. those not receiving ADT (HR 2.72, 95% CI 2.61-2.84). Conclusions: Both HIV infection and ADT increase the risk of MACE among prostate cancer patients. Future studies are warranted to explore the mechanistic links between HIV infection, ADT, and cardiovascular health.