Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the factors able to stimulate (hormones, drugs, fluid volume changes and prostaglandin precursors) or inhibit (NSAIDs) renal prostaglandin synthesis. We then assessed the effects of NSAIDs on: A) the efficacy of certain drugs (furosemide, ACE-inhibitors), whose action is mediated by a stimulation of prostaglandin synthesis; B) the physiopathology of cardiovascular diseases such as myocardial infarction and heart failure, in which renal and circulatory output is reduced; C) arterial hypertension.
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PMID:Changes in prostaglandin renal synthesis in cardiovascular disease. 267 7

Recent evidence suggests that the most common form of idiopathic cardiomyopathy in our altitudes, the dilated cardiomyopathy (DCM), is a post-infectious autoimmune disease which is triggered by virus infections. In animal experiments, the development of the coxsackie virus B3 myocarditis to a congestive cardiac insufficiency resembling the clinical picture of DCM was demonstrated. In mice, species-dependent varying disease courses could be observed, which point to a genetically different behaviour of the animals' immunological reactions, either humoral or T-cell mediated immune reactions being responsible. In comparison with non-DCM patients, patients with DCM and chronic myocarditis exhibit significantly higher coxsackie virus antibody titres. Obviously, also a differently long viral persistency in the cardiac muscle plays a role, as enterovirus-specific RNA was detected in myocardial biopsies from patients with DCM. Along with myocardial fibroses, endomyocardial biopsies in DCM frequently reveal mononuclear cellular infiltrates, which, however, only in 20-25% of the cases may be regarded as chronic persisting myocarditis. The clinical and paraclinical findings in DCM and in the so-called latent cardiomyopathy are presented. In congestive heart failure, the best therapeutic results are achieved by the ACE inhibitors, along with vasodilator agents, digitalis glycosides and diuretics. Ultima ratio is the orthotopic heart transplantation, as it is only this intervention that will be able to improve the primarily bad prognosis decisively. Whether the treatment with immunosuppressive drugs exerts an influence upon the prognosis, has thus far remained an open question.
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PMID:[Dilated cardiomyopathy--heart muscle disease of unknown origin or an autoimmune disease? New aspects of etiology, pathogenesis and clinical practice]. 268 30

CHF afflicts 15 million persons worldwide despite advances made in its diagnosis and treatment. A thorough physical examination and basic, noninvasive evaluation are essential for establishing the diagnosis of heart failure and for designing an optimal, individualized treatment regimen. Although digitalis and diuretics continue to be used commonly for the treatment of CHF of all severities, the use of vasodilators and ACE inhibitors has increased dramatically, as they are used more widely and earlier in the course of the illness. Because the RAA system contributes significantly to the altered cardiovascular hemodynamics and symptomatology characteristic of heart failure, the ACE inhibitors provide a rational approach to therapy for many patients. Results of controlled clinical trials have shown that selected vasodilators and ACE inhibitors can improve survival in patients with CHF and that patients receiving ACE inhibitors show sustained improvement in clinical class, exercise tolerance, and hemodynamics. Thus the therapeutic spectrum available to the clinician dealing with patients with CHF has broadened substantively over the past decade.
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PMID:Mild heart failure: diagnosis and treatment. 268 81

In the case of heart failure of any etiology, so common in the elderly, symptomatic treatment predominates; causal therapy is hardly ever possible. The aim of treatment is to improve myocardial contractility and influence secondary compensation mechanisms which, although associated with a favorable effect in the early stage, in the late stage lead to an unacceptable elevation of afterload and an overall uneconomical cardiac performance, thus producing a negative effect on cardiac failure and its prognosis. In contrast, suitable treatment improves the quality of the patient's life and prolongs life expectancy. In the aged, suitable therapy includes, where indicated, in particular digitalis (there is no alternative!), ACE-inhibitors and diuretics. The incidence and extent of adverse reactions and interactions in the elderly are greater than in the young and middle-aged patient.
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PMID:[Drug therapy of heart failure in the elderly]. 268 40

1. Myocyte loss, reactive hypertrophy, dynamic ischaemia with 'stunning', and ventricular wall remodelling are all involved in the initiation and progression of myocardial failure which is ischaemic in origin. 2. The effects of ACE inhibitors to reduce preload and afterload has potentially salutary effects in these settings. Moreover, sulphyl containing ACE inhibitors may have further actions in reducing free radicals and their damage in the acute phases of these events. 3. These promising initial studies warrant further exploration.
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PMID:ACE inhibitors in acute and chronic ischaemia: current status and future promise. 269 Sep 6

Since hypertension is an important risk factor for atherosclerosis, it is logical to assume that treatment to lower blood pressure will prevent atherosclerosis. However, the relationship between hypertension and atherosclerosis is indirect and complex. Drugs that lower pressure will prevent heart failure and arteriolar complications such as renal failure or strokes caused by lacunar infarction or brain haemorrhage due to rupture of microaneurysms. However, there is little evidence that atherosclerotic complications can be reduced by lowering pressure. It is important to understand the pathogenesis of atherosclerosis and its complications, which are related to lipoproteins and arterial flow disturbances, in order to develop an approach to selecting those antihypertensive drugs which may prevent atherosclerotic complications related not only to initiation and progression of atherosclerotic plaques, but to the embolisation of platelet clumps or atherosclerotic debris, or events such as intraplaque haemorrhages, that lead to myocardial or cerebral infarction. Antihypertensive drugs have different effects on lipoproteins and on arterial flow disturbances that may have important implications for prevention. Alpha-blockers and drugs with beta 2 agonist activity have beneficial effects on lipoprotein profiles, ACE inhibitors and calcium channel antagonists have some anti-atherosclerotic effects in animal models, while beta-blockers have beneficial effects on flow disturbances and are anti-atherosclerotic in animal models and man. Future studies to determine how to prevent atherosclerotic complications in hypertensive patients will require methods for noninvasive measurement of atherosclerosis.
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PMID:Pathogenesis of atherosclerosis and its complications: effects of antihypertensive drugs. 269 95

Plasma ADH, PA and PRA in patients with respiratory failure (RF) were studied. RF patients were divided into 4 groups, i.e. acute RF (ARF) and chronic RF (CRF), with or without hypercapnia. The levels of these hormones were significantly higher in RF than those in control subjects, moreover, they were markedly elevated in ARF than those in CRF. In multiple regression analysis, ADH correlated with PaO2, pH and PRA in RF patients, but correlated with serum osmolality in control subjects. It was considered that ADH in RF was affected by the direct effect of blood gases and circulatory disorder. The mechanism of elevated PA and PRA in RF probably was mediated through restriction of intake of water and Na, reduction of renal blood flow and decreased ACE often occurred in RF. Abnormally elevated hormones are more often recognized in edematous patients than in nonedematous patients. It was suggested that many patients with RF develop heart failure or edema due to hormonal abnormalities.
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PMID:[ADH (anti-diuretic hormone), aldosterone (PA) and renin activity (PRA) in patients with respiratory failure]. 269 88

1. Left ventricular myocardial infarction was induced in female Wistar rats by ligation of the left anterior descending coronary artery. 2. One month following operation, rats with infarcts developed marked cardiomegaly compared to sham operated rats, indicating the presence of chronic left ventricular failure. 3. The ratio of the noradrenaline metabolite 3,4-dihydroxyphenylethylene glycol (DHPG) to noradrenaline (NA) was elevated in the right ventricle of rats with heart failure one month following infarction, suggesting a chronic increase in cardiac sympathetic activity. 4. Perindopril therapy for one month commenced 4 weeks after infarction returned cardiac weights to normal and significantly reduced right ventricular DHPG/NA ratios. 5. The results suggest that ACE inhibition with perindopril reduces elevated levels of cardiac sympathetic activity in rats with chronic left ventricular failure and leads to regression of cardiomegaly.
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PMID:Cardiac 3,4-dihydroxyphenylethylene glycol (DHPG) and catecholamine levels during perindopril therapy of chronic left ventricular failure in rats. 272 98

The relationship between angiotensin converting enzyme inhibitors (ACE inhibitors) and the development of cough was studied in 80 patients. Cough developed in 25 (31%). Seventeen patients had detailed respiratory investigations of whom 12 developed a new cough. Five of the 12 patients had a remission on placebo and recurrence on rechallenge. Cough does occur with ACE inhibitors but there are other possible causes of cough such as asthma, bronchitis, smoking and heart failure. The true incidence of new cough with ACE inhibitors is uncertain at present.
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PMID:Angiotensin converting enzyme inhibitors and cough. 283 99

We have introduced enalapril, in doses equal to or less than the 2.5 mg currently recommended, as an adjuvant to digoxin and diuretics in 17 patients of mean (SD) age 83 (5) years with severe heart failure. Only eleven patients tolerated its introduction. Unlike those reported in younger patients, all but one of the adverse drug reactions occurred 8 h or more after the first dose. Aged patients started on ACE inhibitors should be observed in hospital until stabilized on a maintenance dose. Three patients had an adverse reaction which differed in nature from those previously reported: acute confusional state, ataxia and mesenteric ischaemia. Ten patients were discharged on 5 mg or 10 mg maintenance doses of enalapril. In nine of them improvement on triple therapy was sustained for a minimum of three months. ACE inhibition was lost in the other patient when her compliance with enalapril therapy fell to around 75%: monitoring compliance is essential when ACE inhibitors are used in low dosages. Enalapril was withdrawn during follow up in three patients because of symptoms of mesenteric ischaemia and in four because of dramatic deterioration of renal function. One of the latter was found subsequently to have severe bilateral atheromatous renal artery stenosis. When isosorbide dinitrate was substituted for enalapril, symptoms of mesenteric ischaemia resolved and renal function returned to baseline. Continuing surveillance for adverse effects is essential in patients of this age group with severe heart failure, and the risk of occult renal artery stenosis requires regular biochemical screening during follow up.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of the safety of enalapril in the treatment of heart failure in the very old. 284 29


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