Case Report Open Access Aksoy et al., J Clin Exp Cardiolog 2013, 4:2 DOI: 10.4172/2155-9880.1000233 Volume 4 • Issue 2 • 1000233 J Clin Exp Cardiolog ISSN:2155-9880 JCEC, an open access journal *Corresponding author: Fatih Aksoy, Suleyman Demirel Univesitesi Tıp Fakültesi, Kardiyoloji AD, Türkiye, Tel: +90 5052313661; Fax: +90 2462324510; E-mail: dr.aksoy@hotmail.com Received December 09, 2012; Accepted January 07, 2013; Published January 09, 2013 Citation: Aksoy F, Arslan A, Uysal Md BA, Altinbas A (2013) A Rare Cause of Acute Myocardial Infarction: The Coronary Artery Ectasia. J Clin Exp Cardiolog 4: 233. doi:10.4172/2155-9880.1000233 Copyright: © 2013 Aksoy F, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. A Rare Cause of Acute Myocardial Infarction: The Coronary Artery Ectasia Fatih Aksoy*, Akif Arslan, Bayram Ali Uysal Md and Ahmet Altinbas Faculty of Medicine, Department of Cardiology, Suleyman Demirel University, Isparta, Turkey Introduction Coronary artery ectasia (CAE) is characterized by an abnormal dilatation of coronary arteries. More than half of CAE is due to atherosclerosis, and thus it has been considered as a variant of atherosclerotic coronary artery disease (CAD). It may result in angina pectoris, even in myocardial infarction due to impaired coronary blood fow [1-3]. In this report, we present a patient who developed ST elevation myocardial infarction due to multivessel ectasia. Case Report A 46 year-old male patient presented with severe, squeezing chest pain of an hour onset. ST-segment elevation was detected in DII, DIII, aVF, V5 and V6 and ST-segment depression was detected in V1, V2 and D1, aVL. Age, obesity and smoking were present as risk factors for coronary heart disease. On physical examination, heart rate was 77/min and arterial blood pressure was 140/80 mmHg. Tere were no pathologic fndings except for a 2/6 degree systolic murmur on the mitral auscultation area. On his electrocardiogram, ST-segment elevation detected in DII, DIII, aVF, V5 and V6 derivations (Figure 1). Cardiac enzymes levels were elevated. Transthoracic echocardiography revealed a lef ventricular ejection fraction of 50% and hypokinesia in inferior, posterior and lateral ventricle free walls. Te patient was admitted to the coronary intensive care unit with the diagnosis of acute coronary syndrome. He underwent primer coronary angiography with the diagnosis of acute ST elevation myocardial infarction. Coronary angiography revealed coronary artery ectasia involving lef main coronary artery, lef anterior descending artery and circumfex coronary artery. Right common artery was normal. Tere was no stenotic lesion in coronary arteries (Figure 2). He underwent subcutaneous enoxaparin, oral aspirin, clopidogrel, atorvastatin metoprolol and ramipril. His chest pain did not recur following medical therapy in the coronary intensive care unit. Patient’s symptoms rebounded signifcantly afer anticoagulant, antiaggregant, and ant ischemic therapies . Ten, ECG gradually showed the resolution of ST-segment elevation with Q-wave in the inferior leads (Figure 3). Creatine kinase (CK)-MB fraction of CK (CK-MB) and Troponin T values rose to 661 IU/L (normal range: 0-171 U/L), 37 U/L (normal range: <24 U/L) and 1,29 ng/mL (normal range: <0.04 ng/mL), respectively. Other hematological and biochemical tests revealed the following: prothrombin time 11 second (normal range: 10-14 second), and activated partial thromboplastin time 29 second (normal range: 25-36 second). Total cholesterol 221 mg/dL (normal range: 110-200 mg/dL), triglyceride 252 mg/dL (normal range: 0-200 mg/dL). Discussion CAE, or aneurysmal coronary artery disease, is defned as dilatation of an arterial segment to a diameter at least 1.5 times that of the adjacent normal coronary artery. CAE can be found in up to 5% of angio-graphic and in 0.22% to 1.4% of autopsy series [4-7]. It can be either difuse, by afecting the entire length of a coronary artery, or localized. When the dilatation involves the entire vessel the word “ectasia” is used in- stead of aneurismatic disease. Coronary artery ectasia or aneurysm is attributed to atherosclerosis in 50% of cases, whereas 20-30% has been considered to be congenital in origin. In the great majority of these patients ectasia coexists with coronary artery disease. Only 10% to 20% of cases of CAE have been described in as-sociation with infammatory or connective tissue diseases [1,5,6]. Te presence of aneurysmal segments produces sluggish or turbulent blood fow, with increased incidence of typical exercise induced angina pectoris and myocardial infarction, regardless of the severity of coexisting stenotic coronary disease. Tis is due to the repeated dissemination of microemboli to segments distal to the ectasia, or to thrombotic occlusion of the dilated vessel [7,8]. Slow blood fow in the coronary artery may also be a causative factor [9]. Patients with pure ectasia [15% of the total population with CAE] have a more benign course, but 39% of them still present signs of previous myocardial infarction [9]. Tere is a higher incidence of adverse events in this population compared to people with normal coronary arteries [5]. Markis et al. [5] classifed CAE in four types: type 1 includes difuse ectasia involving two or three vessels, type 2 includes difuse ectasia involving one vessel and discrete ectasia in another, type 3 includes difuse ectasia in only one vessel, and type 4 includes localized or segmental ectasia in only one vessel. When our case was considered, the patient had presence of multiple ectasia in two major epicardial coronary arteries without any obstructive lesion. Based on these fndings, he was accepted as having type 2 CAE. Te clinical spectrum of CAE is variable, including stable angina pectoris, unstable angina pectoris, vasospastic angina, and myocardial infarction. Te most common symptom is exertional angina [5,10]. Tendency to thrombosis due to diminished coronary fow and vasospasm due to structural changes in the vessel wall may cause chest pain and even myocardial infarction [11]. In our case, collagen tissue diseases and malignancy, which are known to cause in situ coronary thrombosis, were excluded. No abnormality in blood coagulation tests was detected, as well. Te patient was asymptomatic before the diagnosis of ST elevation myocardial infarction, which was understandable with the advanced age and diminished physical activity of the patient. Afer the diag-nosis of ST elevation myocardial infarction, he was treated with anticoagulant, antiaggregant, and antiischemic therapies: β-blocker therapy was was applied for antiischemic therapy. An angiotensin converting enzyme inhibitor and a statin were added to treatment due to their therapeutic efects on the endothelial dysfunction. Afer discharge, he described no acute chest pain or chronic exertional angina under medical therapy for three months. Journal of Clinical & Experimental Cardiology J o u r n a l o f C l i n ic a l & E x p e r i m e n t a l C a r d i o l o g y ISSN: 2155-9880