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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the elderly, drug treatment is used for the prevention and control of cardiovascular disease. Prevention of cardiovascular disease includes management of hypercholesterolemia to reduce risk of myocardial infarction, treatment of acute myocardial infarction to reduce the risk of recurrence, and treatment of hypertension to reduce the risk of hypertensive heart disease and stroke. Management of chronic cardiovascular disease with permanent disability is the major therapeutic goal. The most commonly treated disorders of the heart and peripheral vascular system include congestive heart failure, arrhythmias, angina, and thromboses. Reduction of plasma lipid levels may be undertaken by drug therapy as a means of preventing myocardial infarction.
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PMID:Drug and nutrient interactions in elderly cardiac patients. 307 53

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

This paper discusses the possible pathogenesis of the cerebral atrophy (CA) observed in a large percentage of uraemic patients, taking the form of prevalently cortical damage (cortical atrophy) and/or subcortical enlargement of ventricular cavities (subcortical atrophy). This central nervous system pathology seems to share very little either with the better known 'dialysis encephalopathy' or with the 'acute encephalopathy syndrome', even though sporadic cases of both these forms have shown concomitant CA. Histopathologically it offers the picture of loss of neurons and nerve fibres and can thus be compared with uraemic peripheral nervous system damage. CA is unquestionably important because of its implications in terms of impairment of superior cortical functions, just as in CA of non-uraemic aetiology. A first aetiopathogenic hypothesis might include endogenous uraemic intoxication to the nerve tissue, believed responsible for peripheral uraemic neuropathy, but other possibilities merit consideration: vascular calcification secondary to hyperparathyroidism, blood lipid disorders, and systemic hypertension--factors that contribute to impairing the brain vasculature, with cascade effects on brain tissue oxygenation, neuronal metabolism, and energy exchanges. Tissue oxygenation is already jeopardized in the uraemic patient by the concomitant chronic anaemia and by cardiac insufficiency in cases with hypertensive heart disease. In dialysis patients with volume-dependent hypertension the brain may be further damaged by abrupt pressure changes produced by dialytic ultrafiltration; these constitute a severe challenge to cerebral blood flow autoregulation. Cyclic variations of brain tissue hydration connected with regular dialysis treatment may have adverse effects on neurotransmitter functions, particularly those mediated by neuropeptidergic systems. Chronic intoxication may result from oral Al(OH)3 of phosphorus-chelating agents: in animal studies and clinical observations in non-uraemic populations the neurotoxic potential of Al is indicated by a significant correlation between histological neuronal damage, impaired function, and Al concentration in brain tissues. In addition, a concausal role of malnutrition in central nervous system damage in the uraemic patient cannot be overlooked, since malnutrition is known to give rise to functional and structural alterations in non-uraemic human pathology. In the light of these clinical observations and experimental findings, it would appear that the prevention of CA in uraemia is today feasible.
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PMID:Pathogenesis of cerebral atrophy in uraemia. State of the art. 328 91

Heart morphology and function in hypertension is viewed as a continuum between the following types as land marks: concentric/septal hypertrophy and increased systolic function. slightly dilated left ventricle, no hypertrophy, increased systolic function. eccentric hypertrophy, slightly reduced systolic function. dilated cardiomyopathy without signs of ischaemic heart disease. dilated cardiomyopathy with signs of ischaemic heart disease. The time course of the development of hypertensive heart disease is suggested.
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PMID:The natural history of hypertensive heart disease as suggested by echocardiography. 347 40

To confirm the reported association of body fat distribution with cardiovascular disease, diabetes, blood pressure and serum cholesterol, data from the 1960-62 Health Examination Survey were analyzed. In this sample drawn from the noninstitutionalized population of the United States aged 18-79, mean values of two indices of upper versus lower body fat distribution increased steadily with age. Men had higher values than women, and black women had higher values than white women. Higher values of the indices were significantly associated with higher blood pressure, post-load serum glucose and greater prevalence of definite hypertension and definite hypertensive heart disease independent of multiple confounders. Associations with higher serum cholesterol and definite coronary heart disease prevalence were independent of overall ponderosity but not of age and multiple other confounders. Greater abdominal relative to lower body fat deposits were independently associated with increased cardiovascular risk in men and women, blacks and whites.
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PMID:The association of body fat distribution with hypertension, hypertensive heart disease, coronary heart disease, diabetes and cardiovascular risk factors in men and women aged 18-79 years. 349 34

In a randomly selected population of 9067 individuals, 32-64 years of age in 1967-1970, 25 (0.28%) had chronic atrial fibrillation (CAF). Eight had lone atrial fibrillation. In 1984 the cases were compared with an age- and sex-matched control group of 50 and found to have more cerebrovascular accidents (6 versus 2; P less than 0.05), congestive heart failure (9 versus 1; P less than 0.001), and valvular rheumatic heart disease (3 versus 0) or history consistent with rheumatic fever (6 versus 0; P less than 0.01). The mortality in the CAF group was 60% higher due to an excess in cardiovascular (relative risk 6.1; P less than 0.05) and cerebrovascular (relative risk 12.2; P less than 0.05) causes. The prevalence or incidence of ischaemic or hypertensive heart disease or the presence of coronary risk factors did not significantly differ in the two groups. By M-mode echocardiography the left atrial size, left ventricular enddiastolic dimension and left ventricular mass were increased in the CAF patients, while the systolic left ventricular shortening was significantly less. Thus, the prevalence of CAF is low in a randomly selected population 32-64 years of age and CAF is not strongly associated with ischaemic heart disease or hypertension. The CAF patients have an increased risk of dying prematurely particularly from cerebrovascular causes, even in the absence of valve disease.
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PMID:Chronic atrial fibrillation--epidemiologic features and 14 year follow-up: a case control study. 349 34

The pattern of cardiac admissions to a rural district general hospital has been analysed. Coronary artery disease is the major disorder, both as an acute and chronic problem. Other forms of heart disease are relatively uncommon. The absence of hypertension and hypertensive heart disease is striking. The deaths were mainly related to coronary artery disease.
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PMID:Inpatient cardiology in a rural district general hospital. 356 70

To elucidate recent trends in the mortality and morbidity of myocardial infarction (MI), we investigated death certificates and changes in the survival rate of MI patients at coronary care units (CCUs), which may affect the death rates. For all cases of MI, acute heart failure (AHF), heart failure (HF) as underlying cause, and hypertension as underlying cause with HF or AHF (categorized as hypertensive heart disease) on death certificates in two rural and two urban populations between 1981 and 1984, medical records were reviewed and case histories obtained from interviews with patients' families to validate the diagnosis. The number of MI deaths on the death certificates was not underestimated because some MI deaths were misdiagnosed as AHF, HF and hypertensive heart disease and some MI death certificates were misdiagnosed. Survival of MI patients at CCUs improved in several major cities, Tokyo, Osaka, Wakayama and Asahikawa between 1978 and 1984; a total of 4318 MI deaths were estimated to be averted by CCUs in 1984 compared with the number of deaths in 1978. Therefore, improvement of MI cases at CCUs may be one of the factors attenuating the rise in death rates in all of Japan.
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PMID:Recent morbidity trends in myocardial infarction in Japan: investigation of death certificates and the survival rates at coronary care units. 359 73

A cohort of 1,804 residents of Rochester, Minnesota, who were at least 50 years old, free of stroke, and who underwent examination at the Mayo Clinic in 1960, was followed for 13 years. During this period, there were 110 first ischemic strokes and 616 deaths without stroke. The time of onset, if available, or the time of diagnosis of potential risk factors was determined for all patients during the study and was used to construct a proportional hazards model of time to occurrence of stroke with time-dependent risk factors. The model included 8 risk factors (2 fixed and 6 time-dependent). For these, the individual relative risks are: 1.6 for age (per 10 years), 2.0 for males, 4.0 for definite hypertension, 3.9 for transient ischemic attacks, 2.2 for hypertensive heart disease, 2.2 for coronary heart disease, 1.7 for congestive heart failure, and 1.7 for diabetes mellitus. Atrial fibrillation was not a significant risk factor using time-dependent multivariate analysis.
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PMID:Risk factors for ischemic stroke: a prospective study in Rochester, Minnesota. 367 97

The distribution of fibrosis was studied quantitatively in the entire left ventricular wall of a transverse slice of the heart from 10 necropsy cases of hypertrophic cardiomyopathy, 10 cases of hypertensive heart disease, and 20 normal adults. The percentage area (mean (SD)) of fibrosis in the left ventricular wall in hypertrophic cardiomyopathy (10.5 (4.3)%) was significantly greater than that in hypertensive heart disease (2.6 (1.5)%) or in normal hearts (1.1 (0.5)%). In hypertrophic cardiomyopathy the percentage area of fibrosis was greater (13.1 (4.8)%) in the ventricular septum than in the left ventricular free wall (7.7 (4.2)%) whereas in hypertensive heart disease and normal hearts values in these two areas were similar. The percentage area of fibrosis in the left ventricular free wall (where myocardial fibre disarray was not extensive even in hypertrophic cardiomyopathy) was greater in hypertrophic cardiomyopathy than in hypertensive heart disease. The percentage area of fibrosis correlated with heart weight in hypertensive heart disease, but not in hypertrophic cardiomyopathy. These results suggest that widespread fibrosis in hypertrophic cardiomyopathy cannot be explained by cardiac hypertrophy alone, and that disarray and other factors are also important in pathogenesis. The increase in the percentage area of fibrosis from the outer to the inner third of the left ventricular free wall in hypertrophic cardiomyopathy and in hypertension probably reflected transmural gradients of wall stress and myocardial fibre diameter. Although fibrosis is not specific to hypertrophic cardiomyopathy, its quantification and analysis of its regional distribution provide information that is useful in investigating the pathophysiology of the disorder.
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PMID:Quantitative analysis of myocardial fibrosis in normals, hypertensive hearts, and hypertrophic cardiomyopathy. 371 96


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