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)

Mitral annulus calcification (MAC) is a chronic, non-inflammatory, degenerative process of the fibrous support structure of the mitral valve. It occurs more often in women and the elderly. MAC is associated with known atherosclerotic risk factors such as diabetes mellitus, hypertension and hypercholesterolemia. It is also known that patient with MAC have higher prevalence of left atrial and left ventricular enlargement, hypertrophic cardiomyopathy, atrial fibrillation, aortic valve calcification and stenosis, various cardiac conduction defects, bacterial endocarditis, cardiovascular events and stroke, though the etiological basis is unknown. Pathological studies from the 80s present a theory that MAC is a form of atherosclerosis. In order to test this theory we conducted during the last years a few clinical studies to examine the association of MAC and known atherosclerotic phenomena. We found higher prevalence of aortic atheroma in patients with MAC and atheroma thickness. We also found in MAC patients higher prevalence of carotid artery stenosis, coronary artery stenosis, peripheral artery stenosis and higher levels of beta2-Glycoprotein I antibodies in patients with MAC thickness equal or greater than 5 mm. These studies support the theory that MAC is a form of atherosclerosis and define a group of patients with higher prevalence of atherosclerotic disease in multiple blood vessels. The purpose of this review is to summarize the data concerning MAC and atherosclerotic processes, emphasizing that MAC in itself may be an atherosclerotic process.
Atherosclerosis 2001 Mar
PMID:Mitral annulus calcification--a window to diffuse atherosclerosis of the vascular system. 1122 20

Sudden death is rare in the young athlete. The causes may vary. In the US, hypertrophic cardiomyopathy plays the predominant role whereas in Europe right ventricular arrhythmogenic dysplasia and atherosclerosis of the coronary arteries are more frequent. Other causes such as congenital anomalies of the coronary vessels, myocarditis, Marfan's disease, the long QT, the Brugada and the Wollf-Parkinson-White syndromes exist, but are rare. Attentive preparticipation screening (clinical history and medical examination) is mandatory in all future young athletes.
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PMID:[Sudden death in athletes]. 1147 27

Mitral annulus calcification (MAC) is best diagnosed by transthoracic echocardiography. MAC is associated with known atherosclerotic risk factors such as diabetes mellitus, hypertension and hypercholesterolemia. It is also known from the literature that patients with MAC have higher prevalence of left atrial and left ventricular enlargement, hypertrophic cardiomyopathy, atrial fibrillation, aortic valve calcification and stenosis, various cardiac conduction defects, bacterial endocarditis, cardiovascular events and stroke, though the etiological basis is unknown. Pathological studies from the 80's present a theory that MAC is a form of atherosclerosis. During the past few years we conducted a few clinical studies in order to test this theory and to examine the association between MAC and known atherosclerotic phenomena. We found higher prevalence of aortic atheroma in patients with MAC, especially complex atheroma, and we also found a continuous correlation between the MAC and atheroma thickness. We also noted that MAC patients have a higher prevalence of carotid artery stenosis, coronary artery stenosis, peripheral artery stenosis and higher levels of anti beta 2-Glycoprotein I antibodies in patients with MAC thickness equal or greater than 5 mm. These studies support the theory that MAC is a form of atherosclerosis and define a group of patients with higher prevalence of atherosclerotic disease in multiple blood vessels.
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PMID:[Association between mitral annulus calcification and atherosclerosis]. 1157 35

The rate of cardiac deaths that are sudden is approximately 50%, and decreases with age. The causes of sudden cardiac death are diverse, and are a function of age. In children and adolescents, coronary anomalies, hypertrophic cardiomyopathy and myocarditis are frequent substrates for lethal arrhythmias; in adults, coronary atherosclerosis and acquired forms of cardiomyopathy are the most common findings at autopsies of sudden cardiac death. This review focuses on coronary causes of sudden cardiac death, especially congenital coronary artery anomalies, which result in sudden death almost exclusively in adults younger than age 35, and coronary thrombosis. The most lethal coronary artery anomaly is the left coronary artery arising from the right sinus of Valsalva; this anomaly often results in fatal arrhythmias, often with exercise. The right coronary artery arising from the left sinus of Valsalva may also be lethal in adolescents and young adults, but, unlike the anomalous left, is more often an incidental finding at autopsy. Approximately 60% of sudden coronary death is caused by coronary thrombosis, the rest die with severe coronary disease in the absence of thrombosis. The two major substrates of coronary thrombosis are plaque rupture and plaque erosion, and are not only different pathologically, but are seen in patients with divergent risk factor profiles. Plaque rupture is the most common cause of fatal coronary thrombus, and is characterized by necrotic core with a thin fibrous cap, infiltrated by macrophages. The factors that result in plaque instability and rupture are largely unknown, and are under intense scrutiny; morphologic studies have identified serum lipid abnormalities as a key risk factor in the development of plaque rupture. Plaque erosion, in contrast to plaque rupture, is seen in younger men and women, is not associated with lipid abnormalities, and does not result from exposure of the lipid core to the lumen. The heterogeneity of the atherosclerotic plaque and the diverse mechanics of plaque progression and thrombosis have only been relatively recently explored, and are largely elucidated by autopsy studies of victims of sudden coronary death.
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PMID:Sudden cardiac death. 1167 58

Angina pectoris is a clinical syndrome of discomfort in the chest, jaw, arm, or other sites which is associated with myocardial ischaemia. The nature of angina has many individual variations, and it is easier first to consider the typical syndrome. It is hard to better the descriptions of William Heberden: There is a disorder of the breast, marked with strong and peculiar symptoms, considerable for the danger belonging to it.... Those who are afflicted with it are seized, while they are walking, and more particularly when they walk soon after eating, with a painful and most disagreeable sensation in the breast.... the moment they stand still all this uneasiness vanishes. After it has continued some months, it will not cease so instantaneous upon standing still ... (most) whom I have seen, who are at least twenty, were men, and almost all above 50 years old, and most of them with a short neck, and inclining to be fat.... But the natural tendency of this illness be to kill the patients suddenly.... The os sterni is usually pointed to as the seat of this malady ... and sometimes there is with it a pain about the middle of the left arm. The usual cause of myocardial ischaemia is coronary atherosclerosis. Other diseases of the coronary arteries (emboli, spasm, vasculitis, Kawasaki disease, congenital anomalies), other cardiac diseases (hypertrophic cardiomyopathy, severe hypertension, severe aortic valve disease), and high output states (severe anaemia, thyrotoxicosis) are all uncommon or rare causes of angina. However, while angina is usually associated with atherosclerotic coronary artery disease, the converse is not always true. The condition of coronary atherosclerosis is very common (fatty streaks and more advanced plaques are almost universal in adults in industrialised countries) but it does not always cause myocardial ischaemia. Furthermore, myocardial ischaemia may present other than with angina - for each presentation there is a wide differential diagnosis.
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PMID:Clinical presentation and diagnosis of coronary artery disease: stable angina. 1175 1

The prevalence and severity of coronary atherosclerosis increase dramatically with age, so that more than half of all deaths in persons aged over 65 are due to coronary arterial disease (CAD) and about three fourths of all deaths from CAD occur in the elderly. The aims of our study were, first, to detect myocardial ischemia development in elderly versus younger patients undergoing treatment for known CAD through the use of both conventional treadmill testing and 201T1 scintigraphy, and second, to determine the relationship between the above non-invasive tests and angiographically confirmed important coronary artery disease (iCAD). A database of 606 patients (355 men and 251 women) who had undergone coronary angiography, exercise ECG testing (ETT) using the treadmill Bruce protocol, and 201T1 scintigraphy, was reviewed retrospectively. All patients had displayed clinical expression of CAD with or without the existence of an old myocardial infarction (MI). The patients were from both sexes (440 men and 252 women) and divided into two groups, according to age. Group A was composed of 265 patients aged over 65 (170 men, 95 women, mean age = 70.3 +/- 5.3 years). Group B was composed of 341 patients aged under 65 (185 men, 156 women, mean age 54.4 +/- 9.1 years). Patients with uncontrolled arterial hypertension, hypertrophic cardiomyopathy, severe valve diseases, severe chronic obstructive lung diseases, severe anemia, peripheral atherosclerosis, orthopedic problems, or Parkinson's disease were excluded from the study. The term "important coronary artery disease" (iCAD) covers the following patterns of coronary anatomy: (a) left main stem stenosis > or = 50% with or without disease elsewhere, (b) proximal three-vessel disease, (c) three-vessel disease including the proximal left anterior descending artery (LAD), (d) proximal two-vessel disease including LAD, and (e) two-vessel disease including the proximal LAD. Biostatistical characteristics such as sensitivity, specificity, and predictive values of ETT-201T1 were estimated. Analyzing our results we concluded that: the biostatistical parameters in predicting important CAD in elderly and younger patients by means of exercise test and thallium scintigraphy need to be redefined through more closely scheduled and prospective studies; in elderly coronary patients, the appearance of positive results in both parameters of ETT-201T1 indicates a significant possibility of iCAD existence; in coronary patients younger than 65 years, the appearance of negative results in both parameters of ETT-201T1 almost excludes iCAD, in contrast to elderly patients, who display a significant proportion of iCAD; in elderly coronary patients, the appearance of equivocal results in both tests indicates a significant possibility of the existence of iCAD, in contrast to younger patients.
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PMID:Detection of myocardial ischemia in the elderly versus the young by stress thallium-201 scintigraphy and its relation to important coronary artery disease. 1222 83

Until recently, transgenic rabbits were produced exclusively by pronuclear microinjection which results in additive random insertional transgenesis; however, progress in somatic cell cloning based on nuclear transfer will soon make it possible to produce rabbits with modifications to specific genes by the combination of homologous recombination and subsequent prescreening of nuclear donor cells. Transgenic rabbits have been found to be excellent animal models for inherited and acquired human diseases including hypertrophic cardiomyopathy, perturbed lipoprotein metabolism and atherosclerosis. Transgenic rabbits have also proved to be suitable bioreactors for the production of recombinant protein both on an experimental and a commercial scale. This review summarizes recent research based on the transgenic rabbit model.
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PMID:The transgenic rabbit as model for human diseases and as a source of biologically active recombinant proteins. 1460 53

The microvascular involvement in systemic sclerosis (SSc) is characterized by endothelial damage and smooth muscle cell migration in the intima. The vascular pathologic modifications in SSc are strikingly similar to those of atherosclerosis. SSc also is characterized by an accelerated macrovascular disease. The gene encoding for angiotensin-converting enzyme (ACE) is a 21-kb, 26-exon gene, localized on chromosome 17 (17q23). Polymorphic sites are an insertion/deletion (I/D) that consists of three genotypes: DD and II homozygotes, and ID heterozygote. ACE gene polymorphisms have been linked to vascular disorders (coronary artery disease, hypertension, cerebrovascular disease, hypertrophic cardiomyopathy, and diabetic or nondiabetic nephropathy). In particular, the possession of ACE D allele was associated with an increased risk of developing malignant vascular injury. ACE D allele frequency of the I/D polymorphism was associated with an increased risk of SSc, suggesting a genetic contribution to the disease. The discrepancy between the high prevalence of D allele and reduced ACE plasma levels in SSc demonstrate the lack of knowledge on the regulation and function of renin-angiotensin system in SSc.
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PMID:Vascular injury in systemic sclerosis: angiotensin-converting enzyme insertion/deletion polymorphism. 1501 46

The causes of sudden cardiac death are diverse and are function of age. In young people, coronary anomalies, hypertrophic cardiomyopathy are the most common findings at autopsies; in adults, coronary atherosclerosis and acquired forms of cardiomyopathy are frequent findings. In many of non-ischemia related cases autopsies are unrevealing. One of the most frustrating challenges is the inability to determine the cause of death in a person previously healthy. The majority of such sudden deaths are caused by acute ventricular tachyarrhythmias, but unfortunately unassociated with structural injury to the heart. The present work evaluates incidence, clinical data, and laboratory tests. Biochemical studies on serum, pericardial fluid, vitreous humour and pathological characteristics of 38 cases of sudden cardiac death from 2003 were investigated by us. Also, non-cardiac natural causes of death must be excluded.
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PMID:Sudden death: correlation histopathological and biochemical. 1563 80

We describe an unusual case of coronary artery-left ventricular fistulae associated with apical hypertrophic cardiomyopathy in a 63-year-old man who had a 2-year history of angina pectoris without significant coronary atherosclerosis. It is important to recognize this anomaly as it may be the source of angina in patients without angiographic evidence of major atherosclerotic coronary artery disease.
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PMID:Coronary artery-left ventricular fistulae associated with apical hypertrophic cardiomyopathy. 1599 29


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