Coronary artery ectasia as a culprit for acute myocardial infarction: review of pathophysiology and management

Abstract

Coronary artery ectasia (CAE) is defined as localized coronary dilatation, which exceeds the diameter of normal adjacent segments or the diameter of the patient's largest coronary vessel by 1.5 times. The pathophysiology of CAE remains unclear as its relationship with atherosclerosis remains only modestly established. The histological variances and conflicting reports of the role of traditional cardiovascular risk factors, also, weakens the significance of such association. The slow coronary flow (CSF) of CAE may lead to ischemic and thrombotic events, a mechanism that has never been fully elucidated, but may play a fundamental role in its pathogenesis. While pure, non-atherosclerotic, CAE is believed to have better prognosis when compared to atherosclerotic obstructive CAE, it is thought that CAE is not a simple condition but rather has an adverse clinical course. Nevertheless, long-term prognosis and outcome of CAE is similar to atherosclerotic-non-CAE. Since CAE was first described, oral anticoagulants have been considered as a valid treatment option. Dual antiplatelet therapy is widely employed in acute coronary syndrome (ACS), which also applies to CAE patients presenting with ACS. However, there is a significant uncertainty about the best treatment strategy for CAE in acute myocardial infarction. We hereby report a variety of presentations of CAE complicated with ST elevation myocardial infarction (STEMI). Pathophysiological and anatomical varieties of ectatic coronary culprit lesions represent clinical challenges in uniformly managing this condition. Our review is unique in critically showing the pathophysiology, available controversial evidence upon management and prognostic features of CAE with STEMI. (Anadolu Kardiyol Derg 2013; 13: 695-701)

Elevated Plasma Level of Pentraxin-3 Predicts In-Hospital and 30-Day Clinical Outcomes in Patients with Non-ST-Segment Elevation Myocardial Infarction Who Have Undergone Percutaneous Coronary Intervention

“…The most common cause of ACS is the rupture of a ‘vulnerable' atherosclerotic coronary plaque. Other coronary events, such as coronary embolism, coronary vasospasm, drug ingestion or spontaneous coronary artery dissection, also contribute to a reduction in coronary blood flow, causing myocardial ischemia [21,22]. If the episode of myocardial ischemia is temporary, cardiac symptoms are present transiently and serologic evidence of myonecrosis is absent, leading to a diagnosis of unstable angina.…”

Is Anticoagulant Necessary in Patients with Coronary Artery Ectasia Presenting with Acute Coronary Syndrome? A Systematic Review of Case Reports

“…Unfortunately, these issues cannot be managed by anticoagulation alone due to the increased platelet activity that occurs in CAE. 2 With the increased platelet activation that occurs in patients with CAE, and the increased procoagulant activity, the combined role of antiplatelet þ anticoagulant is of paramount importance. This is further supported by results of a study by Erden et al that favors triple anticoagulation therapy in CAE to reduce the thrombus burden in MI related cases.…”

“…We collected 13 cases from 11 reports. 1,2,[9][10][11][12][13][14][15][16] Ten patients (76.9%) were male, and three (23.1%) were female. Mean age was 54.92 AE 4.17 years.…”

Impact of insulin like growth factor-1 in development of coronary artery ectasia

“…In most cases, CAE is found to coexist with CAD, whereas in 10-20 of cases, it is associated with cocaine abuse, toxins, infl ammation, infections, infl ammatory diseases, cardiac lymphoma and connective tissue disorders such as Kawasaki disease, systemic lupus erythematosus, Marfan syndrome, and Ehlers-Danlos syndrome [6][7][8][9][10]. In histopathological appearance of the disease, marked destruction and reduction of the medial elastic fi bers with disruption of the internal and external elastic lamina, smooth muscle hyalinization of the coronary fi bro-muscular media, excessive nitric oxide (NO) production which leads to hyalinization by indirect acetylcholine production have been found [6][7][8][9][10]. Severe coronary wall infl ammation may play a role in CAE pathogenesis [10,11].…”