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

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

In 33 patients with heart failure (NYHA II-III) 24-h blood pressure was examined during the titration of two ACE-inhibitors. Blood pressure was measured by the oscillometric method using the blood pressure monitor 90202 from SpaceLabs, Inc. The measurements were taken from 06.00 to 22.00 hours every 20 min, and from 22.00 to 06.00 hours every 1 h. All patients received an additional therapy, either with captopril (group 1, n = 17) or enalapril (group 2, n = 16) in random order. Serum-electrolytes, serum-creatinine, and plasma-renin activity were measured before and during therapy with both ACE-inhibitors. 24-h blood pressure measurements were taken before and on the first and fifth day of the treatment with ACE-inhibitors. The groups did not different in respect to the degree of heart failure, the concomitant medication, or the 24-h profiles of blood pressure and heart rate. The mean initial doses of captopril was 9.2 +/- 1.2 mg. Each patient of group 2 received an initial dose of 2.5 mg enalapril. The maximal decrease of diastolic blood pressure occurred after 1 h in group 1 and after 4 h in group 2 and was similar in both groups (8 vs, 7 mmHg). The 24-h blood pressure values on day 5 were consistently below the pretreatment values (p less than 0.005). Heart rate was not affected by either ACE-inhibitor. The groups did not differ significantly during ACE-inhibition in their 24-h blood pressure and heart rate profiles. Before treatment, serum-sodium, -potassium and -creatinine were within the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[24-hour blood pressure and renal function in cardiac failure during the titration phase of captopril and enalapril]. 227 66

Apart from their established use in the treatment of hypertension and heart failure, ACE inhibitors have been suggested to exert anti-ischemic effects. This article reviews the mechanisms of systemic and intracardiac angiotensin formation, as well as its interaction with the bradykinin, the prostaglandin, and the sympathetic nervous system. While high doses of angiotensin can precipitate myocardial ischemia. experimental data on a potential beneficial effect of ACE inhibitors on ischemic myocardial blood flow and function are inconsistent and controversial. Pooling the few available clinical data, several ACE inhibitors may attenuate myocardial ischemia at rest and during exercise. However, a significant fraction of patients does not benefit or even deteriorates. Recent experimental studies suggest a beneficial role of ACE inhibitors in attenuating reperfusion arrhythmias and postinfarction left ventricular remodeling. Unless the mechanisms and determinants of potential anti-ischemic actions of ACE inhibitors can be better defined, their use for treatment of myocardial ischemia cannot be recommended at present.
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PMID:ACE inhibitors for the treatment of myocardial ischemia? 227 72

Perindopril is a non-sulphydryl, pro-drug, ACE inhibitor. Following oral dosing, peak concentrations of the active moiety, perindoprilat, are achieved after 2-3 hours and perindoprilat is barely detectable by 24 hours. In contrast, maximal ACE inhibition is observed 4-6 hours after oral dosing and substantial inhibition persists beyond 24 hours. Inhibition of ACE is dose-dependent over the range 1-16 mg perindopril orally, and is mirrored by elevation of plasma renin activity and falls in aldosterone concentrations. Blood pressure reductions have been confirmed in normotensive and hypertensive subjects with maximal effect 6-10 hours after dosing and adequate antihypertensive activity at 24 hours. Blood pressure reductions are greater in the elderly than in young subjects due to pharmacokinetic differences. Dose reduction is required in elderly subjects and those with renal impairment. The antihypertensive efficacy of perindopril 4-8 mg once daily, is comparable to that of atenolol 50-100 mg once daily, captopril 25-50 mg twice daily or a hydrochlorothiazide/amiloride combination. Reduction in heart failure severity has also been reported. Perindopril appears to be a safe and effective agent for use in hypertension.
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PMID:Clinical pharmacology of perindopril. 228 58

ACE inhibitors have provided a major advance in cardiovascular therapeutics. The rationale for their use in hypertension and heart failure, and their cardiac effects are well documented. Further information is required on the relevance of their direct myocardial and other tissue effects, and it is likely that their use in hypertension and heart failure will increase further over the next several years.
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PMID:Cardiac effects of angiotensin converting enzyme inhibitors. 228 17

There are several indications that the oxygen supply to the myocardium is inadequate in chronic heart failure. This is due to an increased intramyocardial vascular resistance, elevated filling pressures, and a shortened diastolic perfusion time. In parallel, the myocardial oxygen demand is heightened due to elevated wall stress, heart rate and contractility. This imbalance between myocardial oxygen supply and demand might be the cause of the adaptive metabolic changes seen in severe chronic heart failure. We showed increased LDH 5, decreased LDH 1 and increased ADP/ATP-carrier concentration in the myocardium from patients with chronic heart failure. After ACE-inhibitor treatment in 33 patients with chronic heart failure, LDH 1 increased from 38.7 +/- 6.7% to 42.3 +/- 5.5% (P less than 0.005) paralleled by a decrease in LDH 5 from 20.8 +/- 7.0% to 15.8 +/- 4.7% (P less than 0.001). The ADP/ATP-carrier concentration also decreased significantly within the normal range. This shift in the LDH isoenzyme pattern and decrease in the ADP/ATP-concentration can be interpreted as an indication for an improvement of myocardial energy balance in chronic heart failure under ACE-inhibitor therapy. This might help interrupt the self-perpetuation of chronic heart failure which is partially caused by a progressive subendocardial perfusion deficit.
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PMID:The effect of ACE inhibition on myocardial energy metabolism. 236 54


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