Integrated Reperfusion for Simultaneous Stemi and Large–vessel Occlusion: A Case Report

Introduction Simultaneous ST–elevation myocardial infarction (STEMI) and acute ischemic stroke (simultaneous cardio–cerebral infarction) is rare and challenging. Both are time–dependent and require rapid reperfusion, yet STEMI antithrombotic therapy may increase intracranial bleeding risk. Treatment sequencing should be individualized according to hemodynamic status, neurological severity, and local logistics. Case report A 75–year–old woman with hypertension and dyslipidemia, without known heart disease, presented with constrictive chest pain (∼55 min onset) followed 10–15 min later by aphasia and right upper–limb weakness. She was unstable: BP 88/58 mmHg, HR 125 bpm, SpO₂ 86% on room air, diffuse crackles (acute pulmonary edema), cold extremities; NIHSS 12. ECG showed anterior ST elevation (V1–V4 up to 4 mm) extending to I/aVL with reciprocal ST depression in II, III, aVF. hs–troponin I was 410 ng/L (URL ‹34) with peak ›30,000 ng/L at 12–18 h; NT–proBNP 5,600 pg/mL (URL ‹300). Non–contrast brain CT excluded hemorrhage; CT angiography revealed left MCA M1 occlusion with fronto–temporo–insular hypoperfusion. Decision making A multidisciplinary cardiology–stroke pathway was activated. Given hypotension, pulmonary edema, and extensive anterior STEMI with high risk of deterioration/cardiac arrest, a “heart–first” strategy was selected: immediate coronary angiography and primary PCI, followed by mechanical thrombectomy after stabilization. IV thrombolysis was deemed unfavorable due to bleeding risk and the anticipated need for dual antiplatelet therapy, with immediate endovascular stroke treatment available. Treatment and course Coronary angiography (radial access) showed proximal thrombotic LAD occlusion (TIMI 0) and no significant disease elsewhere. Primary PCI with DES achieved TIMI 3 flow and improved BP (110/70 mmHg) with relief of dyspnea. The patient then underwent thrombectomy with TICI 3 reperfusion. CT at 24 h showed no hemorrhagic transformation; NIHSS improved to 5. Echocardiography showed anteroseptal/apical akinesia, LVEF 35–40%, elevated filling pressures, and mild functional MR; no initial LV thrombus (serial reassessment planned). Antithrombotic therapy was initiated and reviewed daily, balancing coronary ischemic risk against cerebral bleeding risk.