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

The long-term prognosis in severe congestive heart failure is very poor. Therapeutic regimens, in order to improve prognosis, should directly or indirectly influence the compensatory systems that are activated, ACE-inhibitor therapy has emerged as an important regimen in this context. In the CONSENSUS-trial (3), we could demonstrate that the addition of enalapril to conventional therapy in severe CHF significantly improved survival. The experience from this study forms the background for the recommendations in this work. 253 patients with severe heart failure (New York Heart Association (NYHA) Classification functional class IV) were randomized at 35 Scandinavian centers to placebo (n = 126) or enalapril (n = 127), in addition to their conventional therapy. The treatment dose of enalapril varied between 2.5 and 40 mg daily (man 18.3 mg). Blood samples for measurement of serum electrolytes and serum creatinine were taken repeatedly during follow-up. There seems to be about a 10% increase in creatinine within 2 weeks of initiating enalapril therapy. This increase seems to be independent of baseline creatinine level. Adverse experience regarding serum creatinine was reported in 22 placebo-treated patients and in 51 patients in the enalapril group. This reporting was based upon the investigators' feelings of significant importance of the observation and not on symptomatology. This was the main reason for permanent withdrawal in 2 and 7 patients, respectively. During initiation of enalapril therapy the blood pressure response is important after the very first dose, but for renal function the response may not appear until several days later. However, in most patients there are no problems with starting enalapril.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of ACE-inhibition on renal function in severe congestive heart failure. 202 43

Infectious heart diseases in childhood are--with less than 1% of hospital admissions--rare, but serious diseases. Among several causes of myocarditis in our region virus myocarditis plays the most important role. Besides of the acute course an autoimmune mediated chronic myocarditis and the transition to dilated cardiomyopathy are observed. The patho-histological assessment depends also on subjective influences. Clinical diagnosis is based on cardiac symptoms (Adams-Stokes, congestive heart failure, LV-dilatation), ECG-changes with increased enzyme levels and positive virus-serology or endomyocardial biopsy. Immunoserology and -histology as well as in-situ-hybridization can support diagnosis, echocardiography and eventually heart catheterization exclude other causes. In respect to therapy, ACE-inhibitors are a substantial improvement of conventional therapy of heart failure, while immunosuppressive therapy of chronic myocarditis has to assessed.
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PMID:[Myocarditis in childhood]. 202 60

A prospective study was carried out to investigate the effects of the ACE inhibitor captopril on glucose tolerance in 14 elderly patients, aged 76 to 89 years, who had co-incident cardiac failure and stable Type II diabetes mellitus. Patients were maintained on their diet and diabetic therapy and were given 12.5 mg captopril twice daily. Clinical findings, including signs of cardiac failure, body weight and blood pressure, biochemical profile and chest X-ray appearance were documented at each visit. Blood glucose tolerance testing was carried out immediately before starting captopril and again 28 days later. A reduction in symptoms of heart failure occurred in all patients and 5 of them reduced their New York Heart Association grade of heart failure. Significant improvement in glucose tolerance occurred in all patients. Four were able to reduce hypoglycaemic therapy and 1 was able to stop his hypoglycaemic agents. This potentially valuable additional benefit of captopril in improving glucose tolerance has not yet been shown to occur with other ACE inhibitors.
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PMID:Effects of captopril on glucose tolerance in elderly patients with congestive cardiac failure. 204 97

It is now established that ACE-inhibitors are effective in the treatment of severe chronic heart failure; in addition to digitalis and diuretics. Furthermore, recent studies suggest, that beneficial effects of ACE-inhibitors can be expected in patients with moderate heart failure: when combined with diuretics. In atrial fibrillation, the combination with digitalis is recommended. Up to now, there is no clear evidence that monotherapy with ACE-inhibitors is superior to first line therapy with diuretics or digitalis. Nevertheless, initial (and limited) experience favors the use of ACE-inhibitors to prevent progressive LV-dysfunction following myocardial infarction. Based on experimental data, several additional mechanisms of action (besides unloading the heart) have been proposed; which may open up new indications for ACE-inhibition, such as antiarrhythmic, antiischemic or antiproliferative effects (including decreased incidence of coronary restenosis following angioplasty). If confirmed by clinical studies, the indications for ACE-inhibitors will expand considerably, putting emphasis on prevention of occurrence and progression of heart failure rather than treatment of very late stages of chronic heart failure. Yet, the Consensus trial demonstrated a significant impact of these agents on mortality in the latter patient population.
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PMID:[The role of ACE-inhibition in the therapy of chronic heart insufficiency]. 213 55

Sudden death has been shown to be due in the majority of cases to ventricular arrhythmia. Left ventricular hypertrophy (LVH) may be implicated in the aetiology of some arrhythmia and sudden death. Recent evidence suggests that the relationship between LVH and arrhythmia may be complex and that there may be an interaction with serum potassium levels. ACE inhibitors have been shown to be anti-arrhythmic in heart failure. Although other vasodilators have been shown to be anti-arrhythmic, ACE inhibitors also raise serum potassium levels and this may therefore be of importance to their anti-arrhythmic activity. In LVH, their antiarrhythmic potential may be greatest in those who are potassium depleted.
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PMID:ACE inhibitors and the heart: hypertrophy reversal and antiarrhythmic effects. 214 90

The effect of a single oral dose (50 mg) of captopril was studied in 12 hypertensive patients divided into 2 groups: 6 had a normal hemodynamic profile; the other 6 had NYHA class III or IV heart failure. Medical history and clinical and laboratory investigation showed that the heart failure was due exclusively to arterial hypertension. Mean arterial pressure (MAP), aldosterone, plasma renin activity (PRA) and atrial natriuretic factor (ANF) were followed for 4 hours after administration of captopril. MAP values showed a similar decrease in the 2 groups but the variations in the 3 hormones were much greater in the second group. This group showed higher basal levels of PRA, aldosterone and ANF; after stimulation PRA increased sharply preceded by a substantial decrease in aldosterone and ANF. To explain this phenomenon, the Authors propose that the liver of the patients with heart failure is unable to rapidly compensate the reduction in synthesis of angiotensin II caused by the drug with a corresponding increase in angiotensinogen production; the consequent sharp drop in plasma aldosterone would lead to a rise in renin production by the kidney. The arteriolar and venous vasodilatation induced by the ACE-inhibitor, would explain the drop in intra-atrial pressure with reduced plasma levels of ANF. The decrease in ANF could also be caused by the inhibition of the renin-angiotensin system of the heart leading to improved blood supply and hence myocardial contractility.
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PMID:[Captopril and hypertensive cardiopathy : therapeutic effects and hormonal changes]. 215 Mar 43

ACE-inhibitors have been shown to have considerable therapeutic effectiveness in the treatment of heart failure and to be able to significantly prolong the survival of treated patients. The benefits of these drugs when used in the treatment of heart failure are due to their vasodilator action on both arterial and venous vessels. An even more relevant mechanism might be the modulation of some neuro-endocrine responses induced by heart failure, such as angiotensin-aldosterone production, which are sometimes excessive or harmful. The molecules presently available in Italy are four (captopril, enalapril, lisinopril, quinapril), endowed with considerably different pharmacological characteristics, but substantially similar as far as effectiveness and tolerability are concerned. Although general guidelines cannot be suggested on the basis of the pharmacological profile alone, the choice of the drug to be used in every single patient with heart failure should be made taking into account the adequacy of the pharmacological properties for the specific situation.
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PMID:[ACE inhibitors and heart failure]. 215 9

Cardiac insufficiency is a clinical syndrome which presents several distinctive findings but is nevertheless difficult to define both clinically and in the scientific literature. In this article we maintain that cardiac insufficiency is a clinical condition characterized by symptomatic fluid retention on a cardiac basis, combined with signs of impaired pumping in the form of reduced capacity and/or other organic effects such as reduced renal function. The renin-angiotensin system is of cardinal importance once cardiac insufficiency is established and ACE inhibition is of essential significance for the treatment. It is not yet clear whether it is possible to prevent the onset of cardiac insufficiency in patients at high risk thereof. Current studies may answer this question.
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PMID:[ACE inhibitors in the treatment of heart failure]. 221 86

The pathogenesis of heart failure is not yet fully understood. In animal models there is some evidence to suggest a role for free radicals (FRs). We have investigated malondialdehyde - LM in plasma of patients with heart failure and found it to be raised when compared to controls. We present data to show that Captopril, a drug with an ACE inhibitory effect is a FR scavenger both in vitro and ex-vivo in patients with heart failure.
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PMID:Oxidative damage in chronic heart failure: protection by captopril through free radical scavenging? 224 3

Angiotensin converting enzyme inhibitors are now firmly established in the treatment of patients with chronic heart failure (CHF). Their beneficial acute and chronic hemodynamic effects are not associated with reflex tachycardia or drug tolerance. Angiotensin converting enzyme inhibitors produce symptomatic improvement and improve exercise capacity in all grades of heart failure. They also improve the prognosis of patients with severe heart failure. Quinapril is a recently introduced, nonsulfhydryl ACE inhibitor, whose intermediate half-life makes it well-suited for the treatment of patients with CHF. The acute and chronic hemodynamic effects of quinapril are similar to those of other ACE inhibitors. In a large, multicenter, randomized, placebo-controlled study of 225 patients with mild to moderate CHF, 10 to 40 mg/day quinapril significantly improved clinical status and exercise capacity in a dose-related manner. The incidence of side effects did not differ significantly from that of placebo. The initial studies with quinapril are promising and warrant further clinical investigation of this compound.
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PMID:Quinapril in chronic heart failure. 226 Nov 47


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