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

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

Stroke is increasingly becoming a major cause of death and morbidity in African population among most of which the frequencies of hypertension are considerable, although hard data based on community surveys are lacking and most of the information available is from hospital data. The epidemiology of stroke in the Africans is reviewed. The frequencies in hospital populations varied from 0.9% to 4.0% and stroke accounted for 0.5% to 45% of neurological admissions. There is male predominance in published series. The main risk factors are hypertension, diabetes mellitus and homozygous sickle cell disease (in children only). Ischaemic stroke is by far the commonest clinical type encountered. These conclusions are further supported by experience at Ibadan, of over 1100 Africans seen over 18 years reported briefly in this communication. The results of the first community study over a 2-year period on the incidence of stroke in an African Urban (Ibadan) Community are presented. The study was carried out as part of a multinational multicentric study initiated and sponsored by the World Health Organization. The male to female ratio was five to two. Incidence rates reached peaks in the eighth decade in males and in seventh decade in females and were higher in males in all age groups, and the rates are comparable with those recorded in European populations, except in those under the age of 40 in Ibadan, in which age-specific incidence rates are considerably lower than in European and Japanese populations. Hypertension, diabetes mellitus constituted the main risk factors. Mortality and recurrence rates are described and are similar to experience in the Caucasians. Hypertension in the Nigerians predispose to a high frequency of cerebrovascular disease other than through mainly cerebral atherosclerosis. With increasing longevity of Nigerians and other Africans, the mortality and morbidity caused by cerebrovascular disease would probably become of enormous dimensions and adequate control of high blood pressure on a community basis may be the only way of preventing this: this would be desirable as myocardial infarction in contradistinction to hypertensive heart disease is an uncommon complication of high blood pressure in the Africans and prevention of hypertensive heart disease as shown by experience elsewhere can be achieved by control of high blood pressure, which does not seem to prevent ischaemic myocardial disease.
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PMID:Stroke in the Africans. 41 66

Patients with the clinical diagnosis of ischemic heart disease who were found to be free of significant coronary artery atherosclerotic disease (n = 150) underwent coronary vasodilator reserve testing, 2-dimensional echocardiography, and dipyridamole limited-stress thallium testing. After exclusions (predominantly for technically poor coronary artery Doppler signals or suboptimal echocardiography), 100 patients formed the study population. The purpose was to characterize typical cardiac and coronary artery findings in hypertensive patients with severe left ventricular (LV) hypertrophy (n = 15) and to investigate the evidence for myocardial ischemia unrelated to coronary atherosclerosis in early and advanced hypertensive heart disease. Normotensive and hypertensive control groups without LV hypertrophy (n = 12 and 34, respectively) were used for comparison. Severe LV hypertrophy was defined as LV mass index greater than or equal to 50% above established gender specific norms using 2-dimensional-directed M-mode echocardiography and the cube equation corrected to agree with necropsy estimates of mass. Clinical characteristics more often associated with severe LV hypertrophy were black race (67%), diabetes mellitus (33%), proteinuria (47%) and elevated creatinine (1.5 +/- 0.9 mg/dl). Baseline electrocardiograms and dipyridamole limited-stress thallium scans were highly likely to be abnormal (94 and 73%, respectively). Both eccentric and concentric cardiac hypertrophies were found in the severe group. Ejection fraction was significantly lower (0.51 vs 0.68, p = 0.002) and basal coronary flow velocity higher (12.0 vs 5.0 cm/s, p = 0.0004) among these patients when compared with normotensive control patients. Coronary flow reserve did not differ between control groups but was significantly depressed in patients with severe LV hypertrophy (2.5 vs 3.9, p = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Morphologic, hemodynamic and coronary perfusion characteristics in severe left ventricular hypertrophy secondary to systemic hypertension and evidence for nonatherosclerotic myocardial ischemia. 153 Sep 94

Cardiovascular disease is the third most common cause of death in Tshepong Hospital in the western Transvaal, and the most common cause of death in patients older than 35 years. A prospective study was undertaken which included limited necropsies in 90 of the 167 cardiovascular disease deaths over 1 year. A reliable mortality pattern for cardiovascular deaths is described. Additionally, attention is paid to co-existing conditions. Conditions relating to cardiovascular disease, such as hypertension, benign hypertensive nephrosclerosis, atherosclerosis and obesity, were also evaluated. Cerebrovascular conditions were found in 32% of cardiovascular deaths. Intracerebral haemorrhage was found in 50% and cerebral infarction in 29% of cases. Fifty-seven per cent of cardiovascular deaths were due to cardiac conditions, the most common being pulmonary hypertension (31%), dilated cardiomyopathy and chronic rheumatic valvular disease (17% each) and hypertensive heart disease (14%). Forty-nine per cent of subjects were hypertensive, while 40% exhibited benign nephrosclerosis and only 3% of the examined vessels had signs of severe atherosclerosis. Tuberculosis was present in 13% of cases. The clinical diagnosis was the same as the final necropsy diagnosis in 38% of cases. These results emphasise the importance of performing necropsies to obtain reliable mortality statistics.
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PMID:Cardiovascular causes of death at Tshepong Hospital in 1 year, 1989-1990. A necropsy study. 173 52

The manifestations of cardiac involvement in hypertension include: (1) the development of hypertensive heart disease characterized by left ventricular hypertrophy (LVH), and (2) the consequences of coronary atherosclerosis, as angina pectoris, myocardial infarction, and sudden cardiac death. Whereas the former is directly related to increased blood pressure, the latter are sequelae of atherosclerosis per se, and hypertension acts only as a risk factor in this regard. This can partially explain why antihypertensive treatment is effective in diminishing the incidence of congestive heart failure, which is the final consequence of LVH, but is not very effective in preventing coronary complications. It is generally accepted about LVH that increased arterial pressure is the major stimulus to cardiac hypertrophy in hypertension; however, there are a lot of both quantitative and qualitative events suggesting that other factors beside blood pressure levels can modulate the development of LVH, in particular neurohumoral influences. From a morphological point of view, hypertrophy of the cardiac muscle is defined as an increase in the size of existing myocardial fibers. In most experimental models, myocardial hypertrophy is associated with myosin isoenzymatic changes, consisting in a shift from the faster migrating isoenzyme V1 to V3, a form that migrates more slowly. However these changes do not occur in all animal species and particularly in humans. In the hypertrophied human ventricle, a decreased ATPase activity of myofibrils was observed, probably related to changes in myosin light chains. Presently the changes in ATPase activity and in ventricular contractility do not still have a clear molecular basis in humans.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heart and hypertension. 252 4

In an attempt to determine the importance of atherosclerosis in medium-sized coronary arteries, the hearts of 20 patients dying of cardiac disease, within 24 hours of the onset of symptoms, were compared with 19 controls. Post-mortem coronary angiograms were performed and the coronary arteries dissected in detail. Severe stenoses, or complete occlusions, were present in 34 of 80 major coronary arteries in the sudden cardiac death (SCD) group and 5 of 76 in the controls. Medium-sized branch vessels were severely stenosed or occluded in 20.5 per cent (37 of 180 vessels) in the SCD group and 6.4 per cent (11 of 171 vessels) in the controls. Forty of the 48 diseased branch vessels arose from the left anterior descending artery. In the SCD group, 18 patients died from major coronary artery atheroma, one from hypertensive heart disease and only one from disease of a branch vessel. We conclude that, in most cases of SCD, careful macroscopic examination of the major coronary vessels will provide an adequate explanation for death. Detailed dissection of all medium-sized branch vessels is unlikely to be of value as a routine procedure but, at the very least, pathologists should identify and dissect the first septal and diagonal branches of the left anterior descending artery in every post-mortem.
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PMID:Small coronary vessel disease and sudden coronary death. 274 67

Coronary artery spasm is the most frequent cause of ischemic heart disease without coronary atherosclerosis once other causes such as cardiomyopathy, arteritis, coronary ectasia, valvular heart disease or hypertensive heart disease are eliminated. We report 23 patients, 15 males and 8 females, whose ages ranged from 34 to 63 years, with a mean age of 47 years, with demonstrated angina pectoris and myocardial ischemia, whose cardiac cineangiography showed no signs of atherosclerosis. Nevertheless, a significant retardation in the progression speed of the contrast medium was observed, as indirect evidence of the increment in coronary resistance at the arteriole level. Coronary spasm was ruled out by administration of intracoronary ergonovine, and other causes of myocardial ischemia, such as muscular bridges, were also discarded. The clinical presentation of the ischemic heart disease was unstable angina (UA) in 21 patients and myocardial infarction (MI) in 2. In the UA group, 14 patients showed ischemic changes in the ECG while the pain lasted, and in 8 patients the changes were present during the stress test. In all of them, the stress test perfusion scan with thallium 201 showed myocardial ischemia. In the IM group, the diagnosis was based on the clinical findings, the ECG, the enzyme curve, and the technetium 99 cardiac scintigram. In the two-year follow-up the prognosis has been favorable with treatment based on calcium antagonists. Nowadays 18 patients are asymptomatic, four have stable angina and only one has unstable angina.
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PMID:[X syndrome. Angiographic findings]. 278 88

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

Management of patients with concomitant hypertension and angina pectoris mandates that the physician pay attention to the underlying pathophysiology. The heart, when exposed to years of hypertension, becomes "remodeled." Overall mass is enlarged, the walls are thickened, and initial cavity volume remains normal or relatively small. Left ventricular end-diastolic pressure rises in the setting of a hypertrophic noncompliant ventricle; coronary resistance and coronary perfusion pressure are increased; and coronary vascular reserve, even with widely patent coronary arteries, is decreased. Long-standing hypertension--a risk factor for coronary atherosclerosis--is often accompanied by epicardial coronary stenoses that aggravate these coronary abnormalities. In managing the patient with hypertension and angina pectoris, it is important to determine whether the angina occurs in the setting of hypertensive hypertrophic disease alone or coexists with coronary arterial stenoses. Also important to therapy is whether the ventricle is of normal size with good function or decompensated with dilatation and diminished function. The latter two anatomic considerations, namely, epicardial coronary patency and left ventricular cavity size, will influence the choice of an anti-ischemic regimen. For example, diuretic and nitrate therapy can be hazardous, and digitalis unnecessary, in the setting of a nondilated hypertrophic ventricle with hyperdynamic function. On the other hand, the combined use of beta blocking agents plus calcium antagonists is particularly effective in lowering blood pressure and in improving coronary blood flow. Finally, this combination has been shown to be rapidly effective and to have prolonged benefit in this setting. The choice of these latter agents is also affected by the underlying state of the ventricle. Calcium channel blocking agents without significant negative inotropic effect, such as nifedipine and nitrendipine, would be suitable in patients with decompensated ventricular function and dilated left ventricular cavities. Both of these drugs have been shown to increase cardiac output and contractility via a reflex effect and to have little or no direct negative inotropic effect. In contrast, verapamil has a direct negative inotropic effect. The final choice of agents must be tailored to the needs of the individual patient, and the physician also has to determine the role of specific agents in the natural history of hypertensive heart disease.
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PMID:Management of patients with hypertension and angina pectoris. 614 86

The biracial population of New Orleans has a high overall mortality rate, high coronary heart disease (CHD) mortality rate, and high autopsy rate. In the New Orleans Community Pathology Study we investigated atherosclerosis and CHD in all deceased males aged 25 to 44 years, with major focus on the 52% of subjects from whom heart and arterial specimens were collected and evaluated according to standardized procedures. Morphologic correlates of CHD are the same in young black and white males. CHD mortality and mortality from cerebral hemorrhage, hypertensive heart disease, chronic renal disease, and diabetes are greater in young black males than young white males. Age, serum cholesterol, and hypertension were identified as important associated factors in the atherosclerotic process, as well as in CHD. The extent of coronary lesions seems to have decreased between 1960-1964 and 1969-1978 in young white males but not in blacks. Racial differences in coronary lesion involvement in non-CHD deaths are smaller than in our earlier studies.
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PMID:Coronary heart disease in young black and white males in New Orleans: Community Pathology Study. 647 44


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