About: Aortic sinus is a research topic. Over the lifetime, 823 publications have been published within this topic receiving 19187 citations. The topic is also known as: sinus of Valsalva & sinus of Morgagni.
TL;DR: Coronary artery anomalies were found in 1,686 patients undergoing coronary arteriography at the Cleveland Clinic Foundation from 1960 to 1988 and usually were discovered as incidental findings at the time of catheterization.
Abstract: Coronary artery anomalies were found in 1,686 patients (13% incidence) undergoing coronary arteriography at the Cleveland Clinic Foundation from 1960 to 1988 Of the 1,686 patients, 1,461 (87%) had anomalies of origin and distribution, and 225 (13%) had coronary artery fistulae Most coronary anomalies did not result in signs, symptoms, or complications, and usually were discovered as incidental findings at the time of catheterization Eighty-one percent were “benign” anomalies: (1) separate origin of the left anerior descending and circumflex from the left sinus of Valsalva; (2) ectopic origin of the circumflex from the right sinus of Valsalva; (3) ectopic coronary origin from the posterior sinus of Valsalva; (4) anomalous coronary origin from the ascending aorta; (5) absent circumflex; (6) intercoronary communications; and (7) small coronary artery fistulae Other anomalies may be associated with potentially serious sequelae such as angina pectoris, myocardial infarction, syncope, cardiac arrhythmias, congestive heart failure, or sudden death Potentially serious anomalies include: (1) ectopic coronary origin from the pulmonary artery; (2) ectopic coronary origin from the opposite aortic sinus; (3) single coronary artery; and (4) large coronary fistulae Coronary artery anomalies require accurate recognition, and at times, surgical correction
TL;DR: Standard testing with ECG under resting or exercise conditions is unlikely to provide clinical evidence of myocardial ischemia and would not be reliable as screening tests in large athletic populations, and premonitory cardiac symptoms not uncommonly occurred shortly before sudden death, suggesting that a history of exertional syncope or chest pain requires exclusion of this anomaly.
TL;DR: The results show that the complexity of the atherosclerotic lesions that develop in these apo E deficient-mice are similar to those described in other species and therefore represent an important model for studies of genetic and environmental influences on the atheosclerotic process.
Abstract: Apolipoprotein E-deficient mice have spontaneous elevations of total plasma cholesterol and triglycerides and reduced high-density lipoprotein. The mice develop arterial lesions in a time-dependent manner. Lesional distribution was centered in the aortic sinus in young mice, and the lesions were widely distributed throughout the arterial tree in mice at 8 to 9 months of age. In young mice, subendothelial foam cell deposits were present in the aortic sinus adjacent to valve-attachment sites. By 5 months of age, foam cell deposits, free cholesterol, and admixed smooth muscle cells composed the developing atherosclerotic lesions. After 8 to 9 months of age, the arterial lesions showed increased complexity, and fibrous cap lesions were present. Transmission electron microscopy showed foam cells, smooth muscle cells (both contractile and synthetic varieties), cellular debris, and acicular cholesterol deposits within the plaques. By scanning electron microscopy, subendothelial collections of foam cells were present within the aortic sinus and ascending aorta. The results show that the complexity of the atherosclerotic lesions that develop in these apo E deficient-mice are similar to those described in other species and therefore represent an important model for studies of genetic and environmental influences on the atherosclerotic process.
TL;DR: Anomalies of origin are particularly common in hearts in which other major congenital cardiovascular malformations are present and will be limited to those anomalies of origin observed in hearts without other major mal Formations of the heart or great vessels.
TL;DR: The innominate artery, a small vessel connecting the aortic arch to the right subclavian and right carotid artery, exhibits a highly consistent rate of lesion progression and develops a narrowed vessel characterized by atrophic media and perivascular inflammation.
Abstract: Most previous studies of atherosclerosis in hyperlipidemic mouse models have focused their investigations on lesions within the aorta or aortic sinus in young animals. None of these studies has demonstrated clinically significant advanced lesions. We previously mapped the distribution of lesions throughout the arterial tree of apolipoprotein E knockout (apoE(-/-)) mice between the ages of 24 and 60 weeks. We found that the innominate artery, a small vessel connecting the aortic arch to the right subclavian and right carotid artery, exhibits a highly consistent rate of lesion progression and develops a narrowed vessel characterized by atrophic media and perivascular inflammation. The present study reports the characteristics of advanced lesions in the innominate artery of apoE(-/-) mice aged 42 to 60 weeks. In animals aged 42 to 54 weeks, there is a very high frequency of intraplaque hemorrhage and a fibrotic conversion of necrotic zones accompanied by loss of the fibrous cap. By 60 weeks of age, the lesions are characterized by the presence of collagen-rich fibrofatty nodules often flanked by lateral xanthomas. The processes underlying these changes in the innominate artery of older apoE(-/-) mice could well be a model for the critical processes leading to the breakdown and healing of the human atherosclerotic plaque.