A 29 year old African American male presented with non-radiating, mid-sternal chest pain, which was relieved by sitting up. His vital signs and physical examination were unremarkable. His initial EKG showed J point elevation in leads III, aVF, V2-V5, consistent with early repolarization changes. Overnight, his subsequent EKG showed diffuse ST elevation and PR segment depression suggestive of pericarditis, and he was started on colchicine and NSAIDs. However, his chest pain did not resolve. His CRP was 0.2 mg/dL and ESR was 2 mm/hr. Troponin levels gradually increased from 0.099 > 0.192 > 0.296 ng/mL. CK and CK-MB were 544 U/L and 49.5 ng/mL, respectively. He was started on aspirin and heparin drip. Later on, his EKG depicted T-wave inversions in III, aVF and ST segment elevation in II, V4-V6 (fig.1). Echocardiogram revealed a normal left ventricle size with EF of 65%, but there was one segment of apical hypokinesis, with no thrombus. Cardiac Catheterization was performed which showed acute total occlusion of the distal part of the LAD due to a thrombus (fig.2). No intervention was undertaken. Also, the patient had right coronary artery (RCA) dominance. He was medically managed with aspirin, clopidogrel, metoprolol, and atorvastatin.
Isolated apical MI is a rare condition. A history of chest pain with elevated cardiac enzymes in the setting of widespread ST changes should prompt further investigation with echocardiography and cardiac catheterization. Apical infarction also occurs as an extension of either anterior or inferolateral MI. It occurs mostly in patients with RCA dominance. Since a large area is involved, EKG changes are found in inferior leads II, III, aVF, lateral I and aVL, and precordial leads V2 to V6. This leads to a diagnostic dilemma as it can be confused with pericarditis or an aortic dissection that occludes the coronary ostia.
Apical MI should be considered when EKG illustrates widespread ST changes, especially in a clinical setting of chest pain, elevated cardiac enzymes, and echocardiographic apical wall motion abnormalities.