Anterior ST-Segment Elevation Myocardial Infarction With Coronary Thrombosis in a Young Man with Newly Diagnosed HIV Infection and Pneumocystis jirovecii Pneumonia.

Human immunodeficiency virus (HIV) infection is associated with an increased cardiovascular risk through chronic inflammation, immune dysregulation, endothelial dysfunction, and prothrombotic mechanisms. However, the mechanisms underlying acute coronary events in young patients with newly diagnosed advanced HIV infection remain incompletely understood. We report the case of a 36-year-old man with newly diagnosed HIV infection and severe immunosuppression who was initially evaluated for suspected systemic vasculitis and subsequently diagnosed with Pneumocystis jirovecii pneumonia. His initial CD4 cell count was 13.56 cells/mm³, and his HIV RNA level was 14,095,323 copies/mL. Twenty-five days after the initiation of antiretroviral therapy, he developed an acute anterior ST-segment elevation myocardial infarction. Peak high-sensitivity cardiac troponin T was 1051 ng/L. Coronary angiography demonstrated a 90-99% thrombotic lesion at the ostium of the left anterior descending artery with preserved TIMI 3 flow. Given his clinical stability, preserved coronary flow, and potential procedural risks, percutaneous coronary intervention was deferred, and treatment with abciximab, unfractionated heparin, aspirin, and ticagrelor was continued. Repeat angiography after 72 hours demonstrated marked regression of the thrombotic lesion without significant residual stenosis, and no coronary intervention was required. Antiphospholipid antibody testing was negative; however, a comprehensive evaluation for inherited and acquired thrombophilia was not performed. The coexistence of profound immunosuppression, active opportunistic infection, systemic inflammation, and acute coronary thrombosis raises the possibility of a multifactorial prothrombotic state. However, causality cannot be established based on a single case. This case highlights the importance of considering acute coronary thrombosis in young patients with severe HIV-related immunosuppression and active opportunistic infection while recognizing alternative thrombotic mechanisms.