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Query: UMLS:C0018801 (heart failure)
72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four Black South African patients, representative of a larger group, are described in detail. The common features were long periods of observation, multiple hospital admissions in both normotensive and hypertensive cardiac failure, hypertensive retinopathy and good renal function. All had been diagnosed as having cardiomyopathy. Two of the patients in a normotensive phase became hypertensive after responding to therapy for heart failure. One patient with malignant hypertension showed the features of idiopathic cardiomyopathy at necropsy. These cases are regarded as evidence in favour of the hypothesis that many cases of cryptogenic heart disease (cardiomyopathy, congestive cardiomyopathy, idiopathic cardiomegaly) are in fact cases of hypertension presenting with normotensive cardiac failure.
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PMID:Hypertensive heart disease and cardiomyopathy in blacks. Diagnostic confusion. 45 82

The pathological changes in blood vessels observed in primary (essential hypertension) are similar to those seen in secondary hypertension due to renal disease or other causes. In benign hypertension, the major changes are in the small arteries and arterioles especially in the kidney. Interlobular arteries exhibit intimal thickening and duplication of the elastic lamina (elastosis) and there is hyaline change in the media of many arterioles. In some respects these changes are an accentuation of vessel ageing. Malignant hypertension usually presents in a younger age group (35--50 years) and is characterized pathologically by fibrous endarteritis in the interlobular arteries of the kidney and fibrinoid necrosis in the walls of a proportion of the efferent glomerular arterioles. Similar vessel changes are seen in other organs but many of the pathological changes in the heart and brain of patients with benign hypertension are related to the accentuation of arterosclerosis. There is an increased mortality from cardiac failure, myocardial infarction, cerebral haemorrhage and subarachnoid haemorrhage due to ruptured berry aneurysms in patients with benign hypertension. Although there is ischaemic damage to the kidneys in benign hypertension, death from renal failure is uncommon. Severe ischaemic damage to renal glomeruli and renal failure does, however, occur in malignant hypertension.
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PMID:Vascular pathology in hypertension. 46 85

The early diagnosis of heart disease during or better before pregnancy is one of the most important problems, as cardiac diseases are the most common cause for maternal deaths throughout the world. The knowledge of hemodynamic alterations in circulatory and respiratory physiology during pregnancy complicated by heart disease is a prerequisite for their management. The following indications for therapeutic abortion of pregnancy complicated by heart disease can be concluded according to our own observations: 1. history of significant heart failure (more than grade IV according to the classification of the New York Heart Association), frequent attacks of angina pectoris and longstanding cyanosis: 2. in spite of the most careful heart treatment with digitalis, diuretics and salftree diet cardiac-thorax-rate of more than 55% in congenital heart disease, cardiac-thorax-rate of more than 60% in acquired heart disease, significant signs of heart failure, namely more severe than grade III, tachycardic atrial fibrillation, pulse deficit of more than 30/min, active inflammatory processes of the heart (rheumatic fever, subacute bacterial endocarditis, Takayasu's disease); 3. especially severe metabolic disorders, i.e. diabetes mellitus, malignant hypertension, kidney diseases; 4. primiparae of an age of more than 35 years with any heart disease. Commissurotomy can be accomplished during pregnancy if it is too late for therapeutic abortion. Pregnancy in case of artificial valves is not recommended in general because of impending hemorrhagic diathesis.
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PMID:[Indication for pregnancy interruption in patients with heart diseases]. 85 89

Whether a person is medically fit to engage in sports depends not only on his or her present state of health but also on his or her previous medical history, age, personality, and of course, the nature of the particular sport in question. Anyone that feels fit, is physically in good condition, abstains from tobacco, alcohol and other intoxicant stimulants, and passes a thorough medical examination is healthy and fully capable of taking part in any sport whatever. Participation in any form of sport, on the other hand, is absolutely contra-indicated for persons suffering from severe or malignant hypertension, inflammatory or bacterial heart disease, severe angina pectoris - especially with an attendant risk of myocardial infarction - or haemodynamically significant arrhythmias that manifest themselves during, or are aggravated by, physical exertion. Physical activity is generally deleterious in patients with advanced pulmonary disease and chronic cor pulmonale, severe decompensated heart failure or severe renal insufficiency. Severe intercurrent infections also constitute an absolute contra-indication for sport. Between these two extremes of absolute fitness and absolute unfitness there are many intermediate states, e.g. diseases like essential hypertension (WHO Stages I and II), coronary disease and peripheral arterial circulatory disorders, in which patients can derive considerable benefit from properly chosen and carefully graded sporting activity.
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PMID:[Medical fitness for sports, with particular reference to cardiovascular conditions]. 102 Apr 74

1. This study includes 1038 patients (325 men and 713 women) who consulted the medical out-patient clinic, Rigshospitalet, Copenhagen, during the years 1932-38. All these patients had a blood pressure of 160/100 mmHg or 180 mmHg or more. 2. The average age at the first examination was 54 years; 97% were followed at intervals of 10 years until 1975, when sixty patients were still alive. Treatment was minimal until 1970. 3. Sixty percent of the men and 76% of the women reached an age of 65 years or more. Nine percent of the total patients lived to 85 years or more. Excess mortality was far higher in men than in women. 4. Causes of death were stroke in 17%, heart failure in 24%, coronary occlusion in 16%, uraemia in 4% and other diseases in 39%. At the first examination, thirteen cases of malignant hypertension were registered, none at later sessions.
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PMID:A 40 years' follow-up study of 1000 untreated hypertensive patients. 107 6

In rats with unilateral renal artery stenosis, the malignant phase of hypertension is characterized by: systolic blood pressure above 180-190 mm Hg; sodium and water loss; polyuria and polydipsia; markedly activated renin-angiotensin-aldosterone system; impairment of renal function and malignant nephrosclerosis in the contralateral kidney; some rats exhibit signs of cerebral hemorrhage, heart failure, acute renal failure, and some rats die. After such a phase of malignant hypertension, a period of remission may occur, which is followed by another malignant phase, etc. When malignant hypertensive rats are offered, in addition to water, saline as drinking fluid, they compulsively drink the saline, BP falls transiently, and all signs of malignant hypertension nearly or completely disappear. These observations indicate that, at a critically high BP level, it is salt and water loss which, by activating the renin-angiotensin system, trigger the vicious circle of malignant renal hypertension in rats.
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PMID:Pathogenesis of malignant hypertension: experimental evidence from the renal hypertensive rat. 119 18

Renal hypertension can usually be recognized only by examining all the features of the hypertensive illness. On the other hand, the investigation of a case of hypertension whose genesis was previously unclear can lead to the diagnosis of a hitherto unrecognized renal disease. The blood pressure values found in patients with renal hypertension are of widely differing degrees of severity. Slight rises in blood pressure (e.g. 140/90 mm Hg), can be a sign of renal disease in adolescent patients. 10-15% of the cases of chronic renal hypertension develop into malignant hypertension. High diastolic values above 120 mm Hg without renal symptomatology and without reduced renal function speak against a primary renal cause of the rise in blood pressure. The finding of hypertension developing during the course of renal disease is, with respect to the hypertensive cardiovascular complications, just as important as in the case of essential hypertension. Complications which can occur during renal hypertension include cardiac insufficiency, hypertensive encephalopathy, retinopathy, hypertensive crises and acceleration of the renal disease.
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PMID:The clinical picture of renal hypertension. 119 21

Angiotensin-converting enzyme (ACE) inhibitors act by lowering the level of angiotensin II. The therapeutic benefits of these drugs and their potential side-effects therefore result from suppression of the physiological effects of angiotensin II. It is rational to prescribe an ACE inhibitor when the renin-angiotensin system is activated, as in renin-dependent essential hypertension, malignant hypertension and hypertension associated with heart failure. The beneficial effects of ACE inhibitor must be weighed against the special risks of renovascular hypertension: risk of renal artery thrombosis in case of unilateral stenosis and risk of renal failure if the stenosis is bilateral or affects a solitary kidney. In some situations the renin-angiotensin system is not directly involved in hypertension but may play a local haemodynamic role, as in some cases of primary or diabetic nephropathy. In such case the ACE inhibitors are thought to exert a protective effect. ACE inhibitors were reputed to be less effective in the elderly than in younger patients, but we now know that they can be prescribed with equal success in both instances to reduce peripheral resistance and improve regional blood flow as well as arterial compliance. Finally, ACE inhibitors can be prescribed, albeit with limited effectiveness, when the renin-angiotensin system is not activated, as in low renin hypertension and idiopathic hyperaldosteronism due to adrenal hyperplasia. They are ineffective in case of Conn's adenoma and contra-indicated in pregnant women.
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PMID:[For which hypertensive patient should angiotensin-converting enzyme inhibitor be prescribed or forbidden?]. 129 38

The three approaches (physiopathological, epidemiological and pharmacological) to the management of hypertension should converge to provide a personalized prescription of the most appropriate treatment to prevent and/or cure the cardiovascular complications of hypertension: hypertensive left ventricular hypertrophy and the risks directly related to it (haemodynamic, arrhythmic, ischaemic) may be corrected by certain antihypertensive agents (methyldopa, ACE inhibitors, some calcium antagonists) although there is no proof as yet of the benefits of this intervention (which could suppress the adaptation to the increased wall stress of the left ventricle); malignant hypertension and its cardiovascular complications have almost disappeared with modern antihypertensive therapy. Cardiac failure can be effectively prevented and cured when exclusively related to hypertension. When diastolic pressures are lowered by 8-10 mmHg cerebrovascular risk is reduced by a half and coronary risk by a quarter. Cardiovascular mortality related to hypertension is thus reduced by 20% and total mortality is thereby significantly decreased; the large scale clinical trials which provided these data were performed in the years 1965-1985 with diuretic therapy relayed by (or compared with) betablockers from 1980 onwards. These two families remain the drugs of reference in the prevention and treatment of the cardiovascular complications of hypertension. Personalized description of antihypertensive therapy should take into account the degree of risk and previous cardiovascular complications of the hypertensive patient: betablockers eventually associated with calcium antagonists are to be preferred in cases of hypertension with coronary artery disease and/or arrhythmias, severe hypertension and hypertension complicated by cardiac failure are good indications for ACE inhibitors without prejudicing other therapeutic options necessary in certain contexts, in particular aspirin therapy in patients with previous transient ischemic cerebral attacks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Treatment of hypertension and cardiovascular complications]. 168 21

To assess the hemodynamic characteristics in malignant hypertension, echocardiography was performed in 18 patients with malignant essential hypertension (MH-I, n = 9) and secondary hypertension (MH-II, n = 9). Patients with benign hypertension with or without left ventricular hypertrophy (n = 8 and 7, respectively), patients with hypertensive heart failure (n = 7) and normotensive volunteers (n = 10) were subjected to controls. Plasma noradrenaline (NA) and renin activity (PRA) were also measured prior to the antihypertensive therapy. There were no significant differences in the durations of hypertension before the malignant phase, and the mean arterial pressure between MH-I and MH-II. Although posterior wall thickness (PWTd) in MH-II was similar to that in MH-I, interventricular septal thickness (IVSTd) was less marked in MH-II. The plasma NA and PRA were markedly increased in both MH-I and MH-II. End-diastolic dimension (Dd) of the left ventricle was within normal range, but end-systolic dimension (Ds) was significantly increased in MH-I, MH-II and hypertensive heart failure. The moderate decreases in ejection fraction (EF) and mean velocity of circumferential fiber shortening (mVcf) were observed in both MH-I and MH-II. Marked decreases in EF and mVcf were also observed in patients with hypertensive heart failure. The relationship between systolic blood pressure and Dd/PWTd was shifted toward the right and upper portion of the normal relation in MH-I and MH-II. The present study demonstrated that the hemodynamic characteristics in malignant hypertension are an inappropriate left ventricular hypertrophy due to a marked increase in systolic stress; dilatation of the left ventricle in systole; and a moderate decrease in ventricular systolic function. It is suggested that a decrease in left ventricular systolic function in malignant hypertension might be due in part to a marked increase in the influence of neurohumoral factors on hemodynamics.
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PMID:[Echocardiographic features of left ventricular hypertrophy and contractility in malignant hypertension]. 253 Mar 33


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