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

Coronary patients with heart failure (HF) stage I-III received captopril. The drug was found to attenuate symptoms of HF, to reduce the size of the left heart, to improve contractility. For stage HF I, kallikrein urinary excretion was similar to that of normal subjects, while in stage II-III patients it fell significantly. Captopril induced a drop in relevant secretion for stage I and a rise for stage II-III subjects. The drug administration did not influence the relations between the initial serum Na levels and kallikrein urinary excretion, nor it changed serum levels of Na and K. Alterations in morphofunctional characteristics of the heart and changes in diurnal urinary excretion of kallikrein demonstrated close relationships.
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PMID:[Morphofunctional state of the heart and activity of the kallikrein-kinin system in patients with chronic heart failure during treatment with captopril]. 183 24

We present preliminary data of a study comparing captopril, a short acting, with lisinopril, a long acting ACE-inhibitor in 8 of 12 projected patients with severe chronic heart failure (NYHA III-IV) and one additional risk factor (e.g. diabetes mellitus, renal failure). The 8 patients were treated in a cross over design for 12 weeks with either drug. While lisinopril improved NYHA-class in all patients, captopril reached this goal in only 3. Renal function was stable in all patients. Captopril influenced hormones (renin, aldosterone, norepinephrine, epinephrine) and microalbuminuria less than lisinopril. The number of adverse reactions was smaller in lisinopril treated patients. These preliminary data demonstrate at least an equal efficacy of lisinopril compared to captopril in high risk patients with severe chronic heart failure.
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PMID:[Comparison of lisinopril and captopril in treatment of severe heart failure (NYHA III-IV) in high risk patients. Preliminary results of the trial]. 185 Sep 42

Little is known concerning the long-term drug management of chronic heart failure (CHF) in old patients (greater than or equal to 75 years). Accordingly, this double-blind, placebo-controlled trial compared the long-term (over 6 months) effect of captopril (37.5-75 mg/day) and of ibopamine (150-300 mg/day) on exercise testing, symptoms and subjective feeling of well-being, in 150 CHF elderly patients (mean age 75 years) under treatment with digitalis and/or diuretics. During an additional open follow-up of approximately 1.5 years, morbid events and deaths were also recorded. Captopril and ibopamine performed better (p less than 0.01) than placebo, improving the 6-min walking distance (captopril from 300 to 404 m, ibopamine from 282 to 385 m; placebo from 283 to 299 m). NYHA status, symptom score and patients' global assessment. The difference between the active study drugs was not statistically significant (p greater than 0.05). Complicating events, including diuretic use, frequency of hospitalization, worsening of CHF and deaths, were grouped by patient-years. These events were significantly (p less than 0.01) lower (captopril: 28/75 patient-years; ibopamine 33/74 patient-years) in the active treatment groups with respect to placebo (58/96 patient-years). Captopril and ibopamine showed a different safety profile. Creatinine increase (2 patients), symptomatic hypotension (4 patients), hyperkalemia (2 patients) and upper respiratory symptoms were mostly associated with captopril treatment. Gastrointestinal adverse events were observed in 11 patients under ibopamine treatment. The study provides evidence of the clinical usefulness of both captopril or ibopamine in the long-term treatment of CHF in old patients. The safety profile of each drug will suggest the preferred therapeutic application.
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PMID:Comparative effects of long-term therapy with captopril and ibopamine in chronic congestive heart failure in old patients. 186 2

Angiotensin-converting enzyme inhibitors suppress plasma concentrations of the sodium retaining hormones angiotensin II and aldosterone. This action should potentiate the natriuretic and diuretic effects of loop diuretics. Some studies indicate, however, that the introduction of angiotensin-converting enzyme inhibitors for the treatment of cardiac failure is associated with transient weight gain and the development of oedema. We have compared the natriuretic and diuretic response to intravenous frusemide 40 mg alone with the natriuretic and diuretic response to intravenous frusemide 40 mg following the administration of a single dose of captopril in 12 supine male patients with stable chronic cardiac failure. Captopril lowered the 4 h diuretic response to frusemide from 1160 (60) to 685 (77) ml (P less than 0.05) and the natriuretic response from 120 (9.6) to 68 (11.7) mmol (P less than 0.05). Creatinine clearance fell after captopril from 91 (7.2) to 57 (7.7) ml min-1 (P less than 0.05). Systolic and diastolic blood pressures were lower after the administration of captopril but these changes were not significant. Plasma renin activity rose from 3.8 (1.04) to 12.34 (2.94) ng ml h-1 (P less than 0.05) and plasma angiotensin II was reduced from 24.9 (5.05) to 8.14 (1.8) pg ml-1 (P less than 0.05). Plasma aldosterone concentrations were not significantly lower following captopril. Angiotensin-converting enzyme inhibitors cause an acute fall in creatinine clearance which may reduce the effects of loop diuretics and attention must be paid to diuretic dosage when initiating angiotensin-converting enzyme inhibitors for the treatment of cardiac failure.
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PMID:Acute administration of captopril lowers the natriuretic and diuretic response to a loop diuretic in patients with chronic cardiac failure. 191 30

Captopril has attained widespread use as an effective agent in the treatment of heart failure and hypertension. Dermatological, renal and haematological toxicity associated with its use has been widely described and is usually well recognized. There have been comparatively few reports implicating it as causing hepatic drug reactions. Most descriptions have emphasized strongly cholestatic features, although a mixed hepatocellular cholestatic picture and predominant hepatocellular reactions have been reported. Between November 1972 and June 1990 only five cases of possible Captopril-associated hepatic dysfunction were reported to the Australian Adverse Drug Reaction Advisory Committee. Cases reported suggest equal sex distribution, latent period to development of abnormality between 1 week and 20 months, with slow resolution of jaundice and biochemical abnormality from 1 week to 6 months after withdrawal of the drug. One case of hepatic coma and death with massive acute hepatic necrosis on biopsy has been reported. Not uncommonly the accompanying systemic features suggest a syndrome of drug hypersensitivity. We report a case of Captopril-induced cholestatic jaundice in which the abnormality occurred 2 weeks after commencement of the drug and resolved slowly upon discontinuation. The case illustrates two important points: first, the importance of taking a full history, obtaining detailed information about previous drug administration in patients admitted with jaundice; and second, in the case of Captopril-induced liver disease, the jaundice may persist for many weeks after drug withdrawal.
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PMID:Cholestatic jaundice associated with captopril therapy. 193 74

Angiotensin converting enzyme inhibitor therapy decreases the production of the vasoconstrictive angiotensin II and reduces the degradation of certain kinines of vasodilatator action. Of captopril, enalapril, and lysinopril marketed abroad, only captopril of shorter action is available in Hungary. Angiotensin converting enzyme inhibitors are new means for the therapy of hypertension and congestive heart failure. Captopril seems to be effective at an early stage of heart failure. It slows down or even inhibits the progression of heart failure. New aspects of therapy have been revealed. It may be successfully used in angina pectoris, for the prevention of reperfusion arrhythmias accompanying myocardial infarction, for the treatment of renoparenchimal renal diseases, diabetic nephropathy. The side-effects, interactions, and dosage of angiotensin converting enzyme inhibitors have also been discussed.
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PMID:Angiotensin converting enzyme inhibitor therapy. 194 79

The effects of captopril and placebo were compared in 18 patients with chronic heart failure and angina pectoris with use of a double-blind crossover trial design. Symptoms were assessed by patient treatment preference, visual analogue scores and nitroglycerin consumption. Exercise performance was assessed using two different treadmill protocols of different work intensity with simultaneous measurement of oxygen consumption and by supine bicycle exercise and simultaneous radionuclide ventriculography. Arrhythmias were assessed by 48 h ambulatory electrocardiographic monitoring. Patients generally preferred placebo to captopril, and this appeared to be due to an increase in symptoms of angina with captopril. Treadmill exercise time on a high intensity protocol was shorter with captopril than with placebo; on a low intensity protocol, angina became a more frequent limiting symptom even though overall exercise performance was not changed. The heart rate-blood pressure product was reduced, but largely because of a reduction in blood pressure rather than in heart rate. During supine bicycle exercise, no differences in symptoms, exercise performance, ejection fraction or changes in blood pressure were noted and ventricular arrhythmias were reduced. Captopril does not appear to be clinically useful in alleviating angina pectoris in patients with heart failure, and this effect may be related to a decrease in coronary perfusion pressure. Nonetheless, desirable metabolic effects, a reduction in arrhythmias and potential effects on survival require further study of captopril in patients with both angina and heart failure.
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PMID:Effect of captopril, an angiotensin-converting enzyme inhibitor, in patients with angina pectoris and heart failure. 167 75

1. Fifty patients with symptoms due to chronic heart failure despite diuretic therapy were randomised to receive additional treatment with either hydralazine or captopril. The dose was titrated; 24 received hydralazine and 26 captopril up to a maximum daily dosage of 225 mg and 75 mg respectively. Forty-three patients had coronary heart disease and seven dilated cardiomyopathy. 2. Dyspnoea and tiredness were assessed using a visual analogue scale (0-100) before and during 12 weeks' treatment. Captopril produced a significantly greater reduction in breathlessness (F = 31.6, P less than 0.001) and tiredness (F = 65.8, P less than 0.001) compared with hydralazine. 3. There was an increase in treadmill exercise time during treatment with both hydralazine (from 5.5 (3.47-7.53) min to 6.9 (4.87-8.93) min), and captopril (from 5.0 (3.05-6.95) min to 7.8 (5.85-9.75) min), but the degree of improvement was significantly greater in the patients treated with captopril (F = 7.4, P less than 0.001). 4. There was no significant change in right ventricular ejection fraction (from 27.9 (19.3-36.5)% to 28.7 (20.1-37.3)%) or left ventricular ejection fraction (from 22.2 (14.2-30.2)% to 23.9 (15.9-31.9)%) during treatment with hydralazine. However, both right and left ventricular ejection fraction increased significantly during treatment with captopril (from 27.1 (18.9-35.3)% to 32.0 (23.8-40.2)%, P less than 0.05; and from 25.0 (17.2-32.8)% to 29.6 (21.8-37.4)%, P less than 0.05 respectively). 5. These results suggest that in patients with symptoms due to chronic heart failure despite diuretic therapy, treatment with captopril produces a greater symptomatic and haemodynamic improvement than treatment with hydralazine.
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PMID:Which vasodilator drug in patients with chronic heart failure? A randomised comparison of captopril and hydralazine. 201 67

The remodelling of the left ventricle after myocardial infarction results from the expansion of the infarcted zone in the acute phase and the dilation of the healthy zone of the left ventricle which complicates the initial expansion. It brings about an increase in the left ventricular volume which is a major pejorative prognosis factor after myocardial infarction. The expansion, defined by the dilation and parietal stricture of the infarcted zone, complicates about 30 p. cent of the infarctions and appears in the first hours of the infarction. It is favoured by the transmural nature of the infarction, by its extent and its previous topography, and by arterial hypertension. It is accompanied by a higher mortality rate, increases the risk of parietal rupture, exposes to post-infarction aneurysm and to intraventricular thrombi, and initializes the ventricular remodelling, factor of secondary cardiac failure. The dilation of the healthy zone of the left ventricle is observed mainly in case of initial expansion. Its importance increases with the size of the infarction. It corresponds to the volume overload secondary to the increase in the telediastolic parietal constraint of the left ventricle. The remodelling of the left ventricle after infarction is limited by captopril, and possibly by the restoration of the blood flow in the artery responsible for the infarction. Captopril, administered in the first weeks following the infarction, limits the dilation of the left ventricle in man as well as in animals. This beneficial effect is due to a decrease in the post-load of the left ventricle. Captopril improves the survival after infarction in animals, but its effect on the post-infarction mortality in man is still under study.
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PMID:[Expansion and remodelling of the left ventricle after myocardial infarction]. 214 11

The renin-angiotensin-aldosterone system (RAAS) has been implicated in the pathogenesis of congestive heart failure (CHF). Abnormal activation of the RAAS adversely affects cardiac performance and impairs functional status, increasing both afterload and preload through direct and indirect mechanisms. Conventional first-line therapy for CHF consists of diuretics and/or digitalis. Diuretics offer rapid relief of symptoms, effective volume control, and ease of administration, but are associated with a number of disadvantages, including further activation of neurohormonal systems resulting in augmented vasoconstriction. Angiotensin-converting enzyme (ACE) inhibitors, which block the RAAS by inhibiting production of angiotensin II from angiotensin I, are emerging as the vasodilators of choice in combination with diuretics with or without concomitant digitalis. Direct comparative studies have shown that ACE inhibitors provide acute and long-term symptomatic, hemodynamic, and exercise-related benefits as well as improved functional class and, possibly, slowed progression of disease with enhanced survival in specific subgroups. Captopril was the first orally effective ACE inhibitor associated with improved exercise tolerance and functional class in large multicenter trials of patients with severe heart failure and mild to moderate heart failure. Enalapril reduced the probability of death in patients with severe heart failure in the CONSENSUS trial. The new ACE inhibitor quinapril has been shown to improve hemodynamic status both acutely and chronically and to produce dose-related improvements in exercise tolerance. ACE inhibitors have a favorable safety profile, although hypotension can occur with initial doses, particularly in volume-depleted patients or at times when excessive initial doses are administered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:ACE inhibitors in the treatment of heart failure. 218 19


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