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Acute Inferior Wall Myocardial Infarction due to Occlusion of the Wrapped Left Anterior Descending Coronary Artery

DOI: 10.1155/2013/983943

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Abstract:

Acute occlusion of the left anterior descending coronary artery (LAD) generally results in ST segment elevations in precordial leads and reciprocal ST segment depression in inferior leads. The occurrence of isolated inferior myocardial infarction due to occlusion of LAD is very rare. We describe an isolated acute inferior myocardial infarction due to occlusion of a wrapped LAD at the apex which continues as the large posterior descending coronary artery (PDA) beyond the occlusion. 1. Introduction Acute occlusion of the left anterior descending coronary artery (LAD) generally results in ST segment elevations in precordial leads and reciprocal ST segment depression in inferior leads. When ST segment elevation occurs in inferior leads, the culprit artery is either the right coronary artery (RCA) or left circumflex coronary artery (LCX). Simultaneous anterior and inferior myocardial infarction has been described due to occlusion of “wrapped LAD” [1]. The occurrence of isolated inferior myocardial infarction due to occlusion of LAD is unknown. Here we describe an isolated acute inferior myocardial infarction due to occlusion of LAD which continues as the posterior descending coronary artery (PDA). 2. Case Report A 41-year-old previously healthy male presented to our emergency department with severe crushing chest pain of 2-hour duration. The pain was retrosternal, was crushing, and was associated with profuse sweating. There was no radiation of pain, breathlessness, nausea, or vomiting. He is a known hypertensive on telmisartan. He did not have any other risk factors for coronary artery disease. He was not a smoker, and there was no family history of coronary artery disease. Initial ECG in the emergency room showed ST segment elevation in leads II, III, AVF, V5, and V6. There was reciprocal ST depression in lead AVL, and there was no right ventricular involvement or any conduction disturbances (Figure 1). On physical examination, his blood pressure was 120/80?mm of Hg and heart rate was 52/minute, and there were no abnormal findings on physical examination. Figure 1: 12-lead ECG showing hyperacute phase of inferior wall myocardial infarction. ST segment elevation is seen in leads II, III, and AVF with upright T wave merging with the ST segment. ST elevation is also noticed in V5 and V6. The patient was administered Aspirin 300?mg orally and clopidogrel 300?mg orally, and thrombolytic therapy was given with intravenous bolus tenecteplase 9000 units followed by enoxaparin 30?mg intravenously and 80?mg subcutaneously twice daily on the subsequent days. Chest

References

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