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Internal Medicine
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Case Report
Abstract
Background: People living with HIV (PLWH) experience nearly double the risk of premature atherosclerotic cardiovascular disease and often present with acute coronary syndromes at younger ages [1]. Chronic inflammation, immune activation, and drug–drug interactions between antiretrovirals and antiplatelet agents further contribute to accelerated atherosclerosis and poor outcomes after percutaneous coronary intervention (PCI) [2,3]. Importantly, in-stent restenosis (ISR) remains disproportionately frequent in PLWH despite modern drug-eluting stents, with medication nonadherence compounding risk [4]. We present a young woman with HIV and recurrent myocardial infarction due to rapid ISR, underscoring the impact of inflammation, adherence, and pharmacologic interactions on secondary prevention.
Case Presentation: A 31-year-old woman with a history of methamphetamine use, poorly controlled diabetes, and prior LAD stenting for myocardial infarction in February 2025 presented with recurrent chest pain. At the time of her first PCI, she was newly diagnosed with HIV but had been nonadherent to dual antiplatelet therapy. Two days before this admission, she reportedly left another hospital against medical advice after being told to stop methamphetamine use. On arrival, she endorsed diaphoresis and headache but denied chest pain. Examination revealed a HEART score of 6, markedly elevated high-sensitivity troponin (15,436 pg/mL), and an ECG with mild ST elevation in V1–V2. Echocardiography showed an ejection fraction of 40–45% with anterior and anteroseptal hypokinesis. A diagnosis of NSTEMI was made, and she was started on aspirin and heparin. Cardiac catheterization demonstrated thrombus within the prior LAD stent, managed with balloon angioplasty, and a new 90% ostial diagonal lesion requiring PCI. She was discharged on DAPT, statin, lisinopril, empagliflozin, and Biktarvy.
Conclusions: Young people living with HIV carry a disproportionate burden of premature coronary disease, often experiencing myocardial infarction years earlier than the general population. Traditional risk factors do not fully explain this pattern: persistent immune activation, endothelial dysfunction, and chronic inflammation can accelerate atherosclerosis and may increase in-stent restenosis (ISR) even with contemporary drug-eluting stents. Consistent with this, post-PCI outcomes in PLWH are frequently complicated by recurrent ischemia and repeat revascularization. This case brings several real-world drivers into sharp focus. Rapid ISR in a young woman highlights the ongoing role of inflammation. Equally important, nonadherence to both antiretroviral therapy and dual antiplatelet therapy likely amplified thrombotic and restenosis risk. Finally, clinically relevant interactions between certain antiretroviral regimens and P2Y12 inhibitors may reduce platelet inhibition, undermining secondary prevention at the very moment it matters most. The key takeaway is that preventing recurrence after PCI in HIV demands more than technically successful revascularization. Clinicians should pair an interaction-aware antiplatelet strategy with structured adherence support and close coordination with HIV specialists. Addressing these factors early may reduce repeat events and improve long-term outcomes in this vulnerable population.
Recommended Citation
Loayza Pintado, Jose J.; Ajani, Taiwo; Lopez Jesus, Angelica; Calderon, Aura; and Pena, Jose, "The Triple Threat: HIV, Nonadherence, and Substance Use Driving Premature Coronary Events" (2026). Research Symposium. 9.
https://scholarworks.utrgv.edu/somrs/2026/posters/9
Included in
The Triple Threat: HIV, Nonadherence, and Substance Use Driving Premature Coronary Events
Background: People living with HIV (PLWH) experience nearly double the risk of premature atherosclerotic cardiovascular disease and often present with acute coronary syndromes at younger ages [1]. Chronic inflammation, immune activation, and drug–drug interactions between antiretrovirals and antiplatelet agents further contribute to accelerated atherosclerosis and poor outcomes after percutaneous coronary intervention (PCI) [2,3]. Importantly, in-stent restenosis (ISR) remains disproportionately frequent in PLWH despite modern drug-eluting stents, with medication nonadherence compounding risk [4]. We present a young woman with HIV and recurrent myocardial infarction due to rapid ISR, underscoring the impact of inflammation, adherence, and pharmacologic interactions on secondary prevention.
Case Presentation: A 31-year-old woman with a history of methamphetamine use, poorly controlled diabetes, and prior LAD stenting for myocardial infarction in February 2025 presented with recurrent chest pain. At the time of her first PCI, she was newly diagnosed with HIV but had been nonadherent to dual antiplatelet therapy. Two days before this admission, she reportedly left another hospital against medical advice after being told to stop methamphetamine use. On arrival, she endorsed diaphoresis and headache but denied chest pain. Examination revealed a HEART score of 6, markedly elevated high-sensitivity troponin (15,436 pg/mL), and an ECG with mild ST elevation in V1–V2. Echocardiography showed an ejection fraction of 40–45% with anterior and anteroseptal hypokinesis. A diagnosis of NSTEMI was made, and she was started on aspirin and heparin. Cardiac catheterization demonstrated thrombus within the prior LAD stent, managed with balloon angioplasty, and a new 90% ostial diagonal lesion requiring PCI. She was discharged on DAPT, statin, lisinopril, empagliflozin, and Biktarvy.
Conclusions: Young people living with HIV carry a disproportionate burden of premature coronary disease, often experiencing myocardial infarction years earlier than the general population. Traditional risk factors do not fully explain this pattern: persistent immune activation, endothelial dysfunction, and chronic inflammation can accelerate atherosclerosis and may increase in-stent restenosis (ISR) even with contemporary drug-eluting stents. Consistent with this, post-PCI outcomes in PLWH are frequently complicated by recurrent ischemia and repeat revascularization. This case brings several real-world drivers into sharp focus. Rapid ISR in a young woman highlights the ongoing role of inflammation. Equally important, nonadherence to both antiretroviral therapy and dual antiplatelet therapy likely amplified thrombotic and restenosis risk. Finally, clinically relevant interactions between certain antiretroviral regimens and P2Y12 inhibitors may reduce platelet inhibition, undermining secondary prevention at the very moment it matters most. The key takeaway is that preventing recurrence after PCI in HIV demands more than technically successful revascularization. Clinicians should pair an interaction-aware antiplatelet strategy with structured adherence support and close coordination with HIV specialists. Addressing these factors early may reduce repeat events and improve long-term outcomes in this vulnerable population.
