Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coronary artery ectasia (CAE) is the saccular or fusiform dilatation of a coronary artery. CAE is found in 1.2% to 4.9% of patients at autopsy or during angiographic studies, with a similar prevalence of CAE found in patients with atherosclerotic peripheral vascular disease (PVD). Abdominal aortic aneurysm (AAA) and CAE are similar in pathogenesis and histology. To determine whether CAE occurs more frequently in patients with AAA than in occlusive forms of atherosclerotic PVD, a review of coronary angiograms was performed in patients who underwent cardiac catheterization and vascular reconstruction for AAA or occlusive atherosclerotic PVD of the lower extremities. Of 72 patients with AAA, 15 had CAE (20.8%) compared with only 2 of 69 patients with atherosclerotic PVD (2.9%) (p < 0.003). CAE was predominantly discrete, located in the left coronary system, and associated with significant coronary atherosclerosis. CAE may be more prevalent in patients with AAA resulting from a similar pathogenetic process.
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PMID:Coronary arterial ectasia: increased prevalence in patients with abdominal aortic aneurysm as compared to occlusive atherosclerotic peripheral vascular disease. 841 47

Coronary artery ectasia is an uncommon expression of coronary artery atherosclerosis and other diseases. It occurs in about 1.4 percent of the adult population. It is not distinguishable from obstructive coronary artery disease in severity of angina, clinical presentation, electrocardiograms, mortality, or outcome of coronary artery surgery. Although there is debate, treatment is indicated in the form of chronic warfarin anticoagulation to prevent coronary thrombus formation and its sequelae. Aspirin therapy may suffice in asymptomatic individuals.
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PMID:Coronary artery ectasia. 960 23

Coronary artery ectasia (CAE) is an abnormal dilatation of the coronary artery wall. The growing number of coronary angiographies and other invasive cardiologic procedures increased the documented incidence of CAE. There is no consensus about the etiology, prognostic significance and morbidity related to this phenomenon. Atherosclerosis is most probably the main cause of primary or idiopathic ectasia. In addition, it is postulated that chronic exposure to vasodilatatory substances, and therapeutic angioplastic procedures may mediate secondary ectasia. CAE is associated with increased coronary morbidity such as coronary spasm, dissection and thrombus formation. However, its relative contribution to coronary morbidity remains unclear. This uncertainty underlies the current dispute regarding the appropriate management and treatment of patients with CAE. Further studies including prospective therapeutic trials are needed to provide answers to these pending complex questions.
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PMID:[Coronary artery ectasia: a therapeutic dilemma]. 1253 4

Coronary artery ectasia, a variant of coronary atherosclerosis, is a relatively rare entity. Review of literature did not reveal an exclusive study on isolated ectasia. We decided to analyse the clinical presentation and angiographic prevalence of this subset. A retrospective study of patients who underwent coronary angiogram in our institute over the past six years was carried out and the epidemiological, clinical and angiographic characteristics of patients with isolated ectasia were analysed. Distribution of ectasia was with a modification of the Markis classification. Among 6938 angiograms analysed, 134 (2%) had isolated ectasia. Of the 118 symptomatic patients, 34 (25%) had a history of or presented with infarction, with correlation between the territory of infarction and the ectatic vessel in 32 patients. Of 62 patients with lipid abnormality, Hypertriglyceridemia in 42 (65%) was the most common. The left anterior descending artery was the most common vessel involved. Diffuse ectasia most commonly involved the right coronary artery. One patient had spontaneous coronary dissection. There is a relatively high prevalence of isolated coronary ectasia with predominant involvement of the right coronary vessel when diffuse and the left anterior descending artery when discrete. This entity is not innocuous and warrants a detailed study on the available management options.
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PMID:The prevalence and clinical profile of angiographic coronary ectasia. 1287 58

Coronary artery ectasia (CAE) is characterised by irregular, diffuse, saccular, or fusiform dilatation of the coronary arteries. Although the underlying mechanisms are not fully understood, CAE is considered to be an original form of vascular remodelling in response to atherosclerosis. However, it is not clear why some patients develop CAE while most do not. Experimental data suggest that activation of the renin angiotensin system may lead to an increased inflammatory response in the vessel wall or to an activation of matrix metalloproteinases. In addition, an insertion/deletion (ID) polymorphism of angiotensin converting enzyme (ACE) has been associated with coronary vascular tone and the development of aneurysms. Accordingly, we hypothesised that the gene polymorphism of ACE may be a potential factor influencing the genesis of CAE. We retrospectively evaluated 112 patients who underwent coronary angiography. ACE ID genotype was determined in two groups of patients. Group 1 consisted of 56 patients who were found to have CAE. Group 2 consisted of 56 patients with significant coronary artery disease (CAD) (> 50% stenosis in any of the major epicardial coronary arteries or their branches) but without any evidence of coronary ectasia. Polymerase Chain Reaction (PCR) was used to detect ACE genotype. The ratio of DD genotype was found to be greater in group 1 than group in 2 (39% versus 18%, respectively, P < 0.05). When assessed according to the presence of the I allele, it was greater was greater in group 2 than in group 1 (82.1% versus 60.7%, respectively, P < 0.05). The results indicate that an ACE DD genotype may be a risk factor for CAE.
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PMID:The role of angiotensin converting enzyme genotype in coronary artery ectasia. 1585 40

Coronary artery ectasia is defined as a > 1.5-fold dilation of the coronary artery compared to the diameter of adjacent normal segments. It must be distinguished from discrete aneurysms that appear in areas adjacent to coronary artery stenosis. It is usually considered a variant of coronary atherosclerosis. Dilated segments are thought to modify the rheology of blood, sluggish or turbulent flow predisposing to myocardial ischemia and its sequelae, including myocardial infarction and sudden death. We report the case of a 52-year-old man, light smoker, with arterial hypertension and family history of coronary artery disease, who was referred to our coronary care unit for an inferior ST-elevation acute myocardial infarction and presented with severe and diffuse vessel ectasia and right coronary thrombosis at coronary angiography.
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PMID:An unpleasant surprise in the setting of primary percutaneous coronary intervention: diffuse and severe vessel ectasia with acute thrombosis of the distal right coronary artery in a patient with acute inferior myocardial infarction. 1590 37

Coronary artery ectasia (CAE) is found in 0.3-5% of patients undergoing coronary angiography. Atherosclerosis is the main cause, followed by Kawasaki disease and infectious emboli. The exact pathogenesis has not been diagnosed as yet, but an inflammatory process is underlying. Symptoms, if present, are usually related to myocardial ischemia. Angiography is the mainstay for diagnosis. The prognosis is generally favorable. Thromboembolic complications are rare with antiplatelet therapy, and spontaneous rupture generally is rare but occurs more commonly in Kawasaki disease. Management varies from antithrombotic therapy to surgical ligation. Controlling coronary heart disease risk factors sharply affects the prognosis in patients with CAE.
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PMID:Coronary artery aneurysm: a review. 1706 47

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 a well recognized clinical entity encountered during diagnostic cardiac catheterization. The etiopathogenesis of this condition is poorly understood. Due to the frequent presence of associated obstructive coronary artery disease it is considered to be a maladaptive process of atherosclerosis. Based on its association with aortic aneurysm, coronary ectasia is considered to be caused by genetic abnormalities. It is usually not a benign condition, as normal smooth laminar flow is disrupted with a potential of thrombus formation. The role of long-term anticoagulation in this condition has not been well established. It is speculated that with increasing use of newer, noninvasive modalities the incidence of ectasia may rise, therefore necessitating this review.
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PMID:Coronary artery ectasia--is it time for a reappraisal? 1792 87


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