Case Report

ST-segment Elevation Myocardial Infarction in Severe Coronary Artery Stenosis: A Case Series

Mayank Agrawal, MD, Barry Uretsky, MD, Rajesh Sachdeva, MD
Mayank Agrawal, MD, Barry Uretsky, MD, Rajesh Sachdeva, MD
ABSTRACT: Recently, it has been reported that acute ST-segment elevation myocardial infarction (STEMI) frequently develops at the site of severe stenosis. This impression was derived from the observation of stenosis severity after aspiration of the thrombus leading to the event. In the past, STEMI was considered as a thrombotic event on a non-flow limiting coronary plaque mainly. We report a case series of patients who developed STEMI within hours to days of initial angiography, all of whom demonstrated severe flow limiting coronary artery stenosis. J INVASIVE CARDIOL 2010;22:E34–E36 Acute ST-segment elevation myocardial infarction (STEMI) has been attributed to plaque rupture primarily in non-obstructive lesions.1–5 More recently, there have been reports strongly pointing to the possibility that STEMIs more frequently develop at the site of severe stenoses.6,7 These latter studies have evaluated the stenosis severity after the myocardial infarction had occurred. We report 3 cases of patients who developed STEMI within hours to days of initial angiography, all of whom demonstrated severe flow limiting coronary artery stenosis. Case 1. A 66-year-old male diabetic with known coronary artery disease (CAD) and exertional angina underwent a dipyridamole stress test that revealed anteroseptal and distal anterior wall ischemia. Angiography demonstrated a chronic total obstruction (CTO) of the mid-left anterior descending artery (LAD), 80% stenosis of the proximal circumflex (CX) and first obtuse marginal (OM) branch (Figure 1A). Based on the patient’s symptoms and positive stress test results and treatment preference, an attempt was made to cross the CTO which was unsuccessful. The patient’s blood pressure began to fall with development of ST elevation in the lateral leads. Angiography demonstrated occlusion of the CX and OM branch (Figure 1B), which was successfully treated with deployment of three bare metal stents (Figure 1C). Case 2. A 77-year-old male with hypertension, hyperlipidemia and carotid artery stenosis was admitted with non-exertional chest pain without ECG changes and negative cardiac biomarkers. Coronary CT angiography showed a CTO of the right coronary artery (RCA) and large atheromatous plaque causing near complete occlusion of the proximal LAD. Angiography demonstrated severe 3-vessel CAD with 99% stenosis in the mid LAD (Figure 2A), 90% stenosis in the distal CX and 100% occlusion of the proximal RCA. Coronary artery bypass graft surgery was scheduled for 3 days later. One day prior to surgery, the patient developed severe chest pain with ST-segment elevation in the anterior precordial leads. Angiography demonstrated 100% occlusion of the mid-LAD (Figure 2B). This was successfully treated with deployment of a bare metal stent.(Figure 2C). Case 3. A 58-year-old male with hypertension, hyperlipidemia, type 2 diabetes mellitus and CAD with previous stenting to the mid-LAD 4 years prior to admission presented with chest pain without electrocardiographic changes and normal cardiac biomarkers. Angiography showed 100% in-stent restenosis in the mid LAD with filling of the distal vessel by collaterals, 90% ostial stenosis of the first diagonal and 99% stenosis in the distal RCA (Figure 3A). Coronary artery bypass graft surgery was recommended. Immediately after angiography, the patient started to complain of increasing chest pain and became diaphoretic. An ECG showed inferior ST-segment elevation. Emergent angiography showed total RCA occlusion (Figure 3B). The patient then underwent a successful implantation of a drug-eluting stent (Figure 3C). Discussion. STEMI has been considered a thrombotic complication of non-flow limiting coronary plaque either due to plaque rupture (60–75%), plaque erosion (25–40%), calcified nodule (2–7%) and possibly other undefined pathways.1–5 In studies suggesting that modest lesions are responsible for STEMI in most cases, the time intervals between the index event and previous angiography ranged from 6 weeks to 11 years, with an average of 3.3 years.3–5 This relatively long time interval and the well known phenomenon of rapid progression of coronary artery disease in some patients make such extrapolations questionable. More recent data strongly implicate more severe stenosis as frequent sites of thrombotic occlusion causing STEMI.6,7 In a study by Manoharan et al7 in a consecutive series of STEMI patients undergoing aspiration thrombectomy prior to angioplasty and intervention, the average stenosis was approximately 70%. Most of the occlusions occurred at sites with angiographic stenosis > 50%. Only 10% of the patients with STEMI had diameter stenosis 0.75) were randomized to stenting or medical treatment only9 further suggests that physiologically nonsignificant stenoses have a lower risk for death or acute myocardial infarction within the next 5 years (________________________________________________
From the Division of Cardiovascular Medicine, Department of Internal Medicine, University of Arkansas for Medical Sciences, and Central Arkansas Veterans Healthcare System, Little Rock, Arkansas. The authors report no conflicts of interest regarding the content herein. Manuscript submitted August 6, 2009 and accepted August 14, 2009. Address for correspondence: Rajesh Sachdeva, MD, Central Arkansas Veterans Healthcare System, 4300 West 7th Street, Little Rock, AR 72205. E-mail:



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