Patterns of coronary artery ectasia and short-term outcome in acute myocardial infarction.

OBJECTIVE: To assess the relationship between hematological inflammatory signs, cardiovascular risk (CV) factors and prognosis in patients presenting with acute myocardial infarction (AMI) and coronary artery ectasia (CAE). DESIGN: We investigated 3321 AMI patients who required urgent primary percutaneous intervention in two centres in the United Kingdom between January 2009 and August 2012. Thirty patients with CAE were compared with 60 age- and gender-matched controls. Blood was collected within 2 h of the onset of chest pain. CV risk factors were assessed from the records. Major acute cardiac events and/or mortality (MACE) over 2 years were documented. RESULTS: CAE occurred in 2.7% and more often affected the right (RCA) (p = 0.001) and left circumflex artery (LCx) (0.0001). Culprit lesions were more frequently related to atherosclerosis in non-CAE patients (p = 0.001). Yet, CV risk factors failed to differentiate between the groups, except diabetes, which was less frequent in CAE (p = 0.02). CRP was higher in CAE (p = 0.006), whereas total leucocyte, neutrophil counts and neutrophil/lymphocyte ratio (N/L ratio) were lower (p = 0.002, 0.002 and 0.032, respectively) than among non-CAE. This also was the case in diffuse versus localised CAE (p = 0.02, 0.008 and 0.03, respectively). The MACE incidence did not differ between CAE and non-CAE (p = 0.083) patients, and clinical management and MACE were unrelated to the inflammatory markers. CONCLUSION: In AMI, patients with CAE commonly have aneurysmal changes in RCA and LCx, and their inflammatory responses differ from those with non-CAE. These differences did not have prognostic relevance, and do not suggest different management.

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

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.