Uncommon association of coronary artery ectasia and myocardial bridge presenting as non–ST-segment elevation myocardial infarction: a case report

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/m 2 ). 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.