PMID- 24084147 OWN - NLM STAT- MEDLINE DCOM- 20150828 LR - 20220311 IS - 1308-0032 (Electronic) IS - 1302-8723 (Linking) VI - 13 IP - 7 DP - 2013 Nov TI - Coronary artery ectasia as a culprit for acute myocardial infarction: review of pathophysiology and management. PG - 695-701 LID - 10.5152/akd.2013.227 [doi] AB - 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. FAU - Boles, Usama AU - Boles U AD - Department of Public Health and Medicine, Heart Centre, Umea University, Utmea-Sweden. bolesu@tcd.ie. FAU - Rakhit, Roby AU - Rakhit R FAU - Shiu, Man Fi AU - Shiu MF FAU - Patel, Ketna AU - Patel K FAU - Henein, Michael AU - Henein M LA - eng PT - Journal Article PT - Review DEP - 20130926 PL - Turkey TA - Anadolu Kardiyol Derg JT - Anadolu kardiyoloji dergisi : AKD = the Anatolian journal of cardiology JID - 101095069 SB - IM MH - Coronary Artery Disease/complications/*physiopathology/prevention & control MH - Dilatation, Pathologic MH - Humans MH - Myocardial Infarction/complications/*physiopathology/prevention & control EDAT- 2013/10/03 06:00 MHDA- 2015/09/01 06:00 CRDT- 2013/10/03 06:00 PHST- 2013/10/03 06:00 [entrez] PHST- 2013/10/03 06:00 [pubmed] PHST- 2015/09/01 06:00 [medline] AID - 10.5152/akd.2013.227 [doi] PST - ppublish SO - Anadolu Kardiyol Derg. 2013 Nov;13(7):695-701. doi: 10.5152/akd.2013.227. Epub 2013 Sep 26.