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Coronary artery ectasia (CAE) is well-recognized, angiographic finding of abnormal coronary dilatation, and detected in 0.3-5.3% of angiographic studies. The gold standard for diagnosis this type of aneurysm is coronary angiography, which provides information about the size, sample, location and number of aneurysms. Despite growing prevalence in recent years, controversy still exists as to the pathogenetic mechanisms that underlie this entity. An increased incidence of CAE has been reported in several disorders. Examples include atherosclerotic vascular disease, heterozygous familial hypercholesterolemia, usage of substances including herbicide spray, acetylcholinesterase inhibitors and nitrates, previous arterial balloon angioplasty, polyarteritis nodosa and Kawasaki syndrome. In addition, possible factors contributing to CAE are imbalance between matrix metalloproteinase and tissue inhibitor of metalloproteinase, angiotensin converting enzyme genotype, elevated homocysteine levels, cocaine user, smoking, vascular trauma, nitrate use and diabetes. Emerging investigations have pinpointed inflammation as a central process in all stages of atherosclerosis. This inflammatory process culminates in acute thrombotic complications and clinical events, which is involved in different clinical settings of atherosclerotic diseases. Recent data have also showed that CAE is associated with inflammatory response presented as elevated inflammatory cytokines and C-reactive protein. Accordingly, more complete understanding of the pro- and anti-inflammatory circuits that operate during CAE in particular may foster the development of novel therapeutic approaches.
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PMID:Is any link between inflammation and coronary artery ectasia? 1722 19

Coronary artery ectasia (CAE) is defined as a localized or diffuse non-obstructive lesion of the epicardial coronary arteries with a luminal dilation exceeding 1.5-fold the diameter of the normal adjacent arterial segment. The incidence of CAE has been reported to range between 2% and 4%, which might be an overestimation of the true frequency. The coincidence of CAE with other systemic vascular dilatations has suggested that the mechanism underlying CAE is not only localized to coronary arteries, but also to other vascular compartments such as aorta or peripheral veins. Although the pathophysiology of CAE remains largely unknown, it was supposed to represent a variant of coronary atherosclerosis. This review focuses on this controversy of whether CAE and coronary artery disease (CAD) are two manifestations of the same underlying process. There are clear differences between CAD and CAE with respect to cardiovascular risk factors such as diabetes mellitus, and pathogenic steps in disease progress such as inflammation or extracellular matrix remodeling. As this review will underscore, the current knowledge of the field is insufficient to finally clarify the causative interrelation between CAE and CAD. The clinical course and treatment of CAE mainly depends on its coexistence with CAD. When coexisting with CAD, the prognosis and treatment of CAE are the same as for CAD alone. In isolated CAE, prognosis is better and anti-platelet drugs are the mainstay of treatment. Surgical treatment can be considered in selected patients. For clarifying the mechanism underlying CAE, additional clinical, histopathological and pathophysiological investigations are required. In fact, every patient with CAE should be evaluated systematically for pathological changes in other vascular territories, both in the arterial system as well as in the venous system, which might occur in the disease process.
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PMID:Novel insights into an old controversy: is coronary artery ectasia a variant of coronary atherosclerosis? 1787 34

Coronary artery ectasia (CAE) is frequently considered as a form of coronary artery disease. Cardiovascular risk factors were determined in a patient population with CAE. The 51 patients with isolated CAE (group 1), 61 patients with CAE coexisting with significant coronary stenosis (group 2), and 62 subjects with significant coronary stenosis (group 3) were included in the study, and the distribution of cardiovascular risk factors was compared. Thirty of 51 patients with isolated CAE had presented with typical angina pectoris, 8 patients with unstable angina pectoris, and 13 patients had atypical chest pain or palpitation. The 21 of 51 patients with isolated CAE had definitive positive treadmill exercise test results. Positive family history was similar in each group. The history of smoking was similar in group 1 and group 2 but higher than group 3. Frequency of hypertension was similar in group 1 and group 2 but higher than that in group 3. Frequency of diabetes mellitus was similar in group 1 and group 2 but lower than group 3. Plasma lipid levels and the number of patients with lipid disturbances were also similar in each group. In addition, C-reactive protein (CRP) levels were above the normal limits and there was no difference among groups with respect to plasma CRP levels. CAE appears to be associated with traditional cardiovascular risk factors such as hypertension, smoking, and hyperlipidemia. In addition, elevated CRP level in patients with CAE may suggest the role of inflammatory process in development of CAE.
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PMID:Identifying cardiovascular risk factors in a patient population with coronary artery ectasia. 1821 79

Coronary artery ectasia (CAE) is a well-recognized angiographic finding, characterized by abnormal dilatation of the coronary arteries. We reviewed the current concepts of the condition including etiology, pathogenesis, flow alterations, clinical implications, prognosis and treatment. CAE is often viewed as a variant of obstructive coronary atherosclerosis. Exaggerated positive vascular remodeling due to inflammation, and chronic overstimulation of the endothelium by nitric oxide are potential causative mechanisms. The condition is associated with cardiovascular risk factors such as smoking and hypertension, while it appears to be inversely associated with age and diabetes mellitus. Patients with CAE typically present with angina, and are at risk for myocardial infarctions and sudden cardiac death due to slow flow, coronary vasospasm, dissection, and/or intracoronary thrombosis. CAE may be a diffuse disease associated with dilatation in other parts of the vasculature. As the incidence of this not so benign condition is expected to rise, the optimal treatment options remain undefined. Medical therapy with anticoagulants, nitrates and calcium channel blockers has been proposed and seems rational; however prospective studies with proof of efficacy are needed.
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PMID:Coronary artery ectasia: current concepts and interventions. 2220 72