A 43-year-old male presenting with atypical symptoms and STEMI ECG changes was diagnosed with SCAD after initial PCI failed to restore flow, highlighting the diagnostic challenge of SCAD in men.
Case Report (n=1)
This case highlights the diagnostic challenges of spontaneous coronary artery dissection in men presenting with atypical symptoms mimicking STEMI, emphasizing the need for high clinical suspicion to avoid inappropriate invasive interventions.
Abstract Background Spontaneous coronary artery dissection (SCAD) is an uncommon cause of acute coronary syndrome, distinct from atherosclerotic, traumatic, or iatrogenic etiologies. It predominantly affects middle-aged women, and its occurrence in men remains rare and diagnostically challenging. Angiographically, SCAD may mimic acute myocardial infarction due to plaque rupture, often leading to misdiagnosis and inappropriate interventions. Recognizing this condition early is critical, as management strategies differ substantially from traditional revascularization approaches. Case A 43-year-old Asian male with hypertension presented with a 12-hour history of headache, dizziness, and bilateral upper extremity numbness, accompanied by hypertensive urgency (202/120 mmHg). Despite the absence of chest pain, the ECG revealed ST-segment elevations in leads II, III, and aVF. Initial management included nicardipine and hydralazine for blood pressure control and serial cardiac biomarkers, which showed an upward trend, prompting urgent coronary angiography. Angiography demonstrated a 99% filling defect in the mid-right coronary artery and aneurysmal changes in both coronary systems, raising suspicion for thrombus versus SCAD Type III (Image-1). Following aspiration thrombectomy, three drug-eluting stents were deployed; however, TIMI 3 flow was not achieved. The patient was treated with intravenous eptifibatide, and repeat angiography the next day revealed complete RCA occlusion with collateral filling, confirming SCAD (Image-2). Intravascular imaging was deferred to avoid propagation of the dissection. During hospitalization, he developed atrial fibrillation and ventricular fibrillation requiring defibrillation. Echocardiography revealed an ejection fraction of 40% with reduced right ventricular function. He was discharged on dual antiplatelet therapy, apixaban, amiodarone, and antihypertensives, with plans for follow-up echocardiography, renal angiography, and autoimmune evaluation to assess for underlying connective tissue or vasculitic disorders. Discussion SCAD occurs from an intimal tear or intramural hematoma that separates the coronary wall layers, leading to ischemia. Risk factors include hypertension, connective tissue disease, and aneurysmal or tortuous arteries. Differentiating SCAD from plaque rupture-related STEMI can be extremely difficult, especially when angiography shows focal stenosis. In this case, atypical non-anginal symptoms, aneurysmal vessels, and delayed presentation complicated the diagnosis. Conservative management is preferred in stable patients, while invasive procedures may worsen the dissection. Conclusion This case underscores the importance of maintaining high clinical suspicion for SCAD even in atypical male presentations mimicking STEMI. It emphasizes the value of repeat angiography, multidisciplinary evaluation, and cautious use of intracoronary imaging to confirm diagnosis while minimizing procedural risk. This abstract is funded by: None
Sarraf et al. (Fri,) conducted a case report in Spontaneous coronary artery dissection (SCAD) (n=1). Aspiration thrombectomy, drug-eluting stents, and medical therapy was evaluated. A 43-year-old male presenting with atypical symptoms and STEMI ECG changes was diagnosed with SCAD after initial PCI failed to restore flow, highlighting the diagnostic challenge of SCAD in men.