Frontiers in cardiovascular medicine · 2025
Uncommon association of coronary artery ectasia and myocardial bridge presenting as non-ST-segment elevation myocardial infarction: a case report.
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Rojas-Cadena Marlon, Rodríguez-Arcentales Felipe, Arteaga Colon, Davila Sylvia, Gaibor Juan Carlos, Izquierdo-Condoy Juan S
Аннотация
INTRODUCTION: Coronary artery ectasia (CAE)-diffuse dilatation ≥1.5× the adjacent segments is uncommon and lacks standardized management. Its coexistence with a hemodynamically significant myocardial bridge (MB) is unusual and may create competing disturbances in coronary flow that complicate diagnosis and treatment.
CASE PRESENTATION: An 80-year-old man with hypothyroidism, epilepsy, benign prostatic hyperplasia, and paroxysmal atrial fibrillation on rivaroxaban presented with acute precordial pain consistent with non-ST-segment elevation myocardial infarction (NSTEMI). He was hemodynamically stable; ECG showed inferior ST depression with T-wave inversion in V3-V4, and high-sensitivity troponin was elevated (Killip I, GRACE 177, CRUSADE 49). Early diagnostic angiography (<24 h) revealed diffuse three-vessel ectasia (Markis I) with slow TIMI-2 flow and a prominent mid-LAD MB (∼75% systolic "milking"); the intermediate branch had an ostial lesion with downstream aneurysmal dilatation and was not amenable to PCI. Echocardiography showed LVEF >65% with basal inferior/inferoseptal hypokinesia and severe left-atrial enlargement (57 ml/m2). A diagnosis of type 2 NSTEMI due to supply-demand mismatch in the setting of diffuse CAE and MB was established. He was treated with clopidogrel (single antiplatelet therapy) (INR 2.0-3.0), high-intensity statin, and beta-blocker, with symptomatic improvement and remained asymptomatic without recurrent ischemic events over a 4-month follow-up.
CONCLUSIONS: Diffuse CAE with significant MB can precipitate NSTEMI without discrete obstructive lesions and challenges standard revascularization. In such anatomy, individualized conservative therapy-rate control and tailored antithrombotic management-may be preferable, while advanced imaging and diastolic physiology can refine diagnosis and selection for invasive strategies.
CASE PRESENTATION: An 80-year-old man with hypothyroidism, epilepsy, benign prostatic hyperplasia, and paroxysmal atrial fibrillation on rivaroxaban presented with acute precordial pain consistent with non-ST-segment elevation myocardial infarction (NSTEMI). He was hemodynamically stable; ECG showed inferior ST depression with T-wave inversion in V3-V4, and high-sensitivity troponin was elevated (Killip I, GRACE 177, CRUSADE 49). Early diagnostic angiography (<24 h) revealed diffuse three-vessel ectasia (Markis I) with slow TIMI-2 flow and a prominent mid-LAD MB (∼75% systolic "milking"); the intermediate branch had an ostial lesion with downstream aneurysmal dilatation and was not amenable to PCI. Echocardiography showed LVEF >65% with basal inferior/inferoseptal hypokinesia and severe left-atrial enlargement (57 ml/m2). A diagnosis of type 2 NSTEMI due to supply-demand mismatch in the setting of diffuse CAE and MB was established. He was treated with clopidogrel (single antiplatelet therapy) (INR 2.0-3.0), high-intensity statin, and beta-blocker, with symptomatic improvement and remained asymptomatic without recurrent ischemic events over a 4-month follow-up.
CONCLUSIONS: Diffuse CAE with significant MB can precipitate NSTEMI without discrete obstructive lesions and challenges standard revascularization. In such anatomy, individualized conservative therapy-rate control and tailored antithrombotic management-may be preferable, while advanced imaging and diastolic physiology can refine diagnosis and selection for invasive strategies.