Patient with ST-elevation myocardial infarction, coronary artery embolism and no signs of coronary atherosclerosis in angiography

Case report

A 43-year-old male patient with arterial hypertension and hypercholesterolemia, body mass index 39 kg/m², with no previous history of heart disease, was admitted due to sudden onset of chest pain 6 h prior to seeking medical help. ECG showed normal sinus rhythm with ST-segment elevation in leads aVR and V1–V3 and corresponding ST wave depression in leads I, II, III, aVL, and V5–V6. ST-elevation myocardial infarction (STEMI) was diagnosed in the patient.
Due to loud crescendo/decrescendo systolic murmur with punctum maximum at the aortic valve position, transthoracic echocardiography (TTE) was performed, confirming severe aortic stenosis (maximal pressure gradient (max PG) = 91 mm Hg, mean PG = 65 mm Hg, aortic valve area (AVA) = 0.6 cm²). Furthermore, TTE showed apical akinesia. The left atrium size was moderately enlarged with diameter values of 4.0 × 4.6 cm.
After administration of 300 mg of acetylsalicylic acid, 600 mg of clopidogrel, and 100 mg of enoxaparin, the patient was referred to the catheterization laboratory for primary percutaneous coronary intervention (pPCI). Coronary angiography showed no angiographic signs of atherosclerosis in coronary arteries, but the presence of thrombus in the mid segment of the left anterior descending artery (LAD) was detected (Figure 1).
Intracoronary bolus of eptifibatide (18 mg) followed by intravenous infusion (12 mg/h) was administered to the patient. Then coronary aspiration thrombectomy was performed in the LAD using a 6F Export AP Aspiration Catheter (Medtronic, Santa Clara, CA, USA). After successful thrombus removal, no residual stenosis was visible in the LAD (Figure 2). As there were no accompanying angiographic signs of atherosclerosis in other coronary arteries, we concluded that the thrombus was an embolus arising from a heart structure, most likely the left atrial appendage (LAA). Therefore no stent was implanted, the patient received optimal medical treatment, and further diagnostics to identify the potential source of the embolization were scheduled.
Transesophageal echocardiography carried out the next day confirmed severe aortic stenosis (tricuspid aortic valve), and no other heart defects (e.g. patent foramen ovale, atrial septal defect) as a potential mechanism of paradoxical embolism were detected. The left atrium was moderately enlarged with a thrombus-free LAA, but the presence of echogenic blood was confirmed. Short...


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