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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiovascular disease is a major cause of morbidity and mortality in the U.K. and other developed countries. In the U.K., mortality from coronary heart disease has increased progressively over the past 25 years, particularly in males. This paper examines the possible role of trace metals in the development of cardiovascular disease, with particular reference to the effects of cobalt, cadmium and lead in myocardial disease, atherosclerosis and hypertension. It is concluded that cobalt is an unimportant factor in community levels of cardiovascular disease, that cadmium has striking effects on blood pressure in animals and that there is some evidence for an association between environmental lead and high blood pressure.
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PMID:Cardiovascular disease and trace metals. 4 Feb 34

Clinical, experimental and pathologic studies strongly indicate that hypertension is a major factor in coronary heart disease, sudden death, stroke congestive heart failure and renal insufficiency. The deleterious effect of the elevated blood pressure on the cardiovascular system appears to be due mainly to the mechanical stress placed on the heart and blood vessels. Humoral factors and vasoactive hormones such as angiotensin, catecholamines and prostaglandins may play a role in the pathogenesis of hypertensive cardiovascular disease but this role has not yet been defined and is probably secondary. Hypertension and the resulting increase in tangential tension on the myocardial and arterial walls, leads to the development of hypertensive heart disease and congestive heart failure as well as hypertensive vascular disease that affects not only the kidneys but also the heart and brain. Hypertensive vascular disease involves both large and small arteries as well as arterioles and is characterized by fibromuscular thickening of the intima and media with luminal narrowing of the small arteries and arterioles. The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis. Thus the patient with hypertension is a candidate for both hypertensive and atherosclerotic vascular disease of the coronary and cerebral vessels leading to occlusive disease of both the large and small arteries and resulting in myocardial infarction and stroke. Other major complications of hypertensive vascular disease include rupture and thrombotic occlusion of blood vessels, especially in the brain. Disease of the arterial media, which begins in childhood with the deposition of calcium in the vessels, may be an important cause of arterial hypertension. This form of hypertension may manifest itself in adults as arteriosclerotic hypertension and lead to cardiovascular complications very similar to those of essential hypertension. The relation of arteriosclerotic hypertension to nutritional factors, including dietary salt intake, deserves study.
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PMID:Role of hypertension in atherosclerosis and cardiovascular disease. 13 91

1. To determine lipoprotein (LP) abnormalities, clinical characteristics and preclinical signs of atherosclerosis in asymptomatic subjects with hyperlipidaemia serum cholesterol and triglyceride (TG) concentrations were determined in 20,000 subjects attending a health control centre linked to their employment. 2. Three hundred and fourteen asymptomatic subjects with serum cholesterol larger than or equal to 350 mg/100 ml and/or TG larger than or equal to 3.50 mmol/l in the screening test but without signs or symptoms of secondary hyperlipideaemia or history of cardiovascular disease were examined further. 3. LP analysis with preparative ultracentrifugation separating very lof cholestrol and TG concentrations in each fraction was performed. LP paper electrophoresis was run on while serum and on top and bottom fractions after separation in the ultracentrifuge at d=1.006. Typing of hyperlipoproteinaemia (HLP) was performed according to WO based upon the values of for VLDL and LDL. Exercise ECG was performed on a heart rate controlled bicycle ergometer. The subjects worked at constant predetermined heart rates. ECG at rest and furing exercise was interpreted without knowledge of whether or not the subject has HLP and coded according to the Minnesota criteria. Digital pulse plethysmography was performed on the lower limbs....
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PMID:Studies in asymptomatic primary hyperlipidaemia. Clinical, biochemical and physiological investigations. 17 Aug

There is a growing number of lipoprotein markers recognized by immunological, electrophoretic, and other biochemical methods, and a beginning has been made on studying their modes of inheritance and linkage relations. Suggestive but inconclusive evidence of a relation between the cerumen polymorphism and arteriosclerosis has been published. Associations of the ABO blood groups with cardiovascular disease and serum lipid levels have been established, but the exact relation to lipoproteins and atherosclerosis remains to be determined.
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PMID:Genetic markers in atherosclerosis: a review. 18 Feb 92

The influence of daily oral cyclical estrogen therapy on the plasma lipid and lipoprotein levels in postmenopausal women was determined. Included were 39 women with distressing postmenopausal vasomotor symptoms. Ethinyl estradiol (EE2) .05 mg was given to 20 women and estradiol valerinate (EV) to 19 others. The drugs were given as tablets once daily for 3-week cycles with 1-week intervals. After overnight fasts, blood samples were taken before and during treatment at 1, 3, and 6 months. During EV therapy, the HDL-TC and the HDL-phosphlipid concentrations increased 10-15% after 6 cycles. The net effect on the risk of development of ischemic cardiovascular disease due to the change in plasma lipids induced by EE2 is uncertain. The plasma lipid changes during EV therapy might possibly retard the development of atherosclerosis. However, the lipid metabolism of postmenopausal women may be different from that of fertile women.
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PMID:Metabolic and hormonal effects of post-menopausal oestrogen replacement treatment. II. Plasma lipids. 20 45

Studies on the pathogenic potential of the human cardiotropic enterovirus, coxsackievirus B5, show that this agent localizes and replicates in the aorta of mice. Nutritionally-induced hypercholesterolemia leads to an increased replication and persistence of virus in tissues, specifically the aorta. Coxsackievirus B cardiopathy is markedly augmented in the hypercholesterolemic host, resulting in a persistent cardiomyolysis which is not evident in virus-infected animals with normal cholesterol levels. Pathological changes in the aorta become evident only months after the acute infection, and only in hypercholesterolemic animals previously infected with coxsackievirus B5. Our findings of coxsackievirus B-induced angiopathy and cardiopathy in the hypercholesterolemic host extend the known pathogenic range of these human viruses, and further emphasizes their potential as etiological agents of cardiovascular disease.
Atherosclerosis 1978 Nov
PMID:Coxsackievirus B cardiopathy and angiopathy in the hypercholesterolemic host. 21 92

Six highly trained marathon runners developed myocardial infarction. One of the two cases of clinically diagnosed myocardial infarction was fatal, and there were four cases of angiographically-proven infarction. Two athletes had significant arterial disease of two major coronary arteries, a third had stenosis of the anterior descending and the fourth of the right coronary artery. All these athletes had warning symptoms. Three of them completed marathon races despite symptoms, one athlete running more than 20 miles after the onset of exertional discomfort to complete the 56 mile Comrades Marathon. In spite of developing chest pain, another athlete who died had continued training for three weeks, including a 40 mile run. Two other athletes also continued to train with chest pain. We conclude that the marathon runners studied were not immune to coronary heart disease, nor to coronary atherosclerosis and that high levels of physical fitness did not guarantee the absence of significant cardiovascular disease. In addition, the relationship of exercise and myocardial infarction was complex because two athletes developed myocardial infarction during marathon running in the absence of complete coronary artery occlusion. We stress that marathon runners, like other sportsmen, should be warned of the serious significance of the development of exertional symptoms. Our conclusions do not reflect on the possible value of exercise in the prevention of coronary heart disease. Rather we refute exaggerated claims that marathon running provides complete immunity from coronary heart disease.
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PMID:Coronary heart disease in marathon runners. 27 Sep 40

This relatively young man with a host of medical problems including polycystic kidneys. chronic renal failure, long-standing hypertension, and premature atherosclerosis, died of cardiovascular disease; not, as might be expected, from his severe coronary artery disease but rather from purulent pericarditis. The latter was an unusual and unexpected consequence of the entire complex of his illnesses and because of its confinement to the posterior pericardium by postoperative adhesions produced an asymmetric cardiac tamponade.
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PMID:Clinical pathologic conference. Purulent pericarditis with asymmetric cardiac tamponade: a cause of death months after coronary artery bypass surgery. 30 Sep 84

Heart disease continues to be a major cause of disablement and death in Canada. Elevated serum cholesterol concentrations, hypertension and cigarette smoking are among the standard risk factors associated with ischemic heart disease. Research attention has also been directed at the role of behavioural factors in the development of atherosclerosis and myocardial infarction. Experimental findings support a conceptual approach to the interplay of psychologic stress, the type A "coronary"-prone behaviour pattern and pathophysiologic mechanisms that have been implicated in the development of coronary artery disease. It is concluded that type A behaviour and stress contribute substantially to the pathogenesis of cardiovascular disease. However, assessment of the manner in which these two variables influence the pathophysiology of ischemic heart disease requires further research, with systematic examination of physiologic and biochemical processes. Potential strategies for modifying type A behaviour are reviewed. However, unequivocal support for the preventive efficacy of behavioural approaches must await future research.
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PMID:Behavioural prevention of ischemic heart disease. 36 Nov 91

A vasomotor (nitritoid) reaction occurred following an initial injection of gold sodium thiomalate (GST; Myochrysine) in a 69-year-old man with rheumatoid arthritis (RA). An acute anterior wall myocardial infarction, documented by serial electrocardiographic and serum enzyme changes, developed immediately thereafter. A second patient, a 49-year-old man with RA and a history of GST-associated vasomotor reactions, was monitored clinically and electrocardiographically after GST administration. Sinus tachycardia developed and peripheral blood pressure fell within 2 minutes of injection, simultaneous with the onset of vasomotor symptoms. Vasomotor reactions from GST may compromise myocardial perfusion by their action on arteriolar smooth muscle, and thus result in peripheral vasodilatation, or they may act by adrenergic discharge initiated by such a reaction, and thus increase myocardial work and oxygen demand. Aurothioglucose (Solganal), rarely produces vasomotor reactions, and may be preferred to GST in elderly RA patients with concomitant cardiovascular disease or atherosclerosis.
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PMID:Acute myocardial infarction following gold sodium thiomalate induced vasomotor (nitritoid) reaction. 40 17


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