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)

The inhibitor of angiotensin converting enzyme played in recent years a significant role in the treatment of cardiac failure. Captopril administration to patients after myocardial infarction prevents enlargement of the left ventricle and its dysfunction. This leads to a reduced mortality and fewer relapses of infarction even in patients with asymptomatic left ventricular dysfunction.
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PMID:[Captopril in the treatment of heart failure]. 776 68

Angiotensin converting enzyme (ACE) inhibitors are now widely used for the treatment of hypertension and heart failure. They are of particular value in treating hypertensive patients with left ventricular dysfunction, and in diabetics where they have been shown to delay the progression of diabetic nephropathy. Differences in the metabolism, pharmacokinetics, and pharmacodynamics between the various ACE inhibitors generally do not translate into significant clinical differences in the majority of patients. However, fosinopril may be the preferred ACE inhibitor in patients with significant renal dysfunction because of a reduced requirement for dosage reduction. The duration of action of ACE inhibitors is determined by two properties, the plasma half-life and the affinity of binding to tissue ACE. All of the ACE inhibitors (with the possible exception of captopril) can provide satisfactory 24-hour blood pressure control in the majority of patients with mild to moderate hypertension when given once daily. Lisinopril provides consistently better 24-hour control of blood pressure than either captopril or enalapril. Evidence for superior 24-hour blood pressure control over enalapril has not been as well established for the other ACE inhibitors. Captopril may be preferred for initiating therapy in patients with severe heart failure who are at risk of first dose hypertension because of its rapid onset of action and relatively short duration of action. There is evidence, however, that perindopril may have a low risk of first dose hypertension in heart failure because of its gradual onset of action. Long-acting ACE inhibitors may be preferable for chronic therapy of heart failure. All of the ACE inhibitors have a low incidence of adverse effects in both young and elderly patients, and there is no convincing evidence of differences in tolerability between the drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Critical assessment of ACE inhibitors. Part 2. 777 72

Captopril, furosemide, and a sodium-restricted diet were administered to 6 normal dogs and 10 dogs with congestive heart failure. Serum electrolyte concentrations and renal function were monitored in both groups. In the normal dogs, no clinically meaningful changes in serum electrolyte, urea nitrogen, or creatinine concentrations developed during therapy with a sodium-restricted diet and 4 weeks each of furosemide alone, captopril alone, or furosemide plus captopril. Three of 6 normal dogs on furosemide and a sodium-restricted diet had at least one serum potassium concentration above the reference range during the 4 weeks of observation. One normal dog on captopril, furosemide, and a sodium-restricted diet developed azotemia, and 2 dogs had serum potassium concentrations above the reference range during the 4 weeks of observation. Ten dogs with congestive heart failure were treated with captopril, furosemide, a sodium-restricted diet, and digoxin. Etiopathogenesis of the heart failure included valvular insufficiency (n = 6), dilated cardiomyopathy (n = 3), and dilated cardiomyopathy and dirofilariasis (n = 1). Serum electrolyte concentrations and renal function were monitored for 5 consecutive weeks in 7 of the 10 dogs and for 17 weeks or longer in 6. Two dogs were euthanized after 4 weeks because of acute decompensation of heart failure, and one dog developed severe azotemia and uremia. Six of 10 dogs with congestive heart failure had at least one serum potassium concentration above the reference range sometime during the 5 weeks of observation, although the changes in the mean serum potassium concentrations were not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of combined therapy with captopril, furosemide, and a sodium-restricted diet on serum electrolyte concentrations and renal function in normal dogs and dogs with congestive heart failure. 783 9

Angiotensin converting enzyme inhibitors (ACEIs) are a cornerstone of treatment of hypertension and heart failure yet their mechanism of action is still debated. This study was designed to test whether the ACEI captopril increases skin microvascular blood flow by a bradykinin-dependent mechanism. Local changes in microvascular blood flow were measured in the skin of rabbits and of human volunteers using a laser Doppler flow probe. Captopril injected intradermally increased skin blood flow over the dose range of 10(-12)-10(-8) mol site in rabbits and humans. In both species the response was abolished by coinjecting either a nitric oxide synthase (NOS) inhibitor or a cyclooxygenase inhibitor. Intradermal bradykinin also increased rabbit skin microvascular blood flow; at 10(-11) mol site it increased mean +/- SE basal blood flow by 88 +/- 12%. The responses to bradykinin or captopril were abolished by coinjecting a bradykinin antagonist, a specific bradykinin B2 receptor antagonist, or inhibitors of NOS or cyclooxygenase. Injecting a specific angiotensin II receptor antagonist at a dose that antagonized the constrictor effects of exogenous angiotensin II did not cause a significant increase in rabbit skin blood flow. This suggests that endogenous angiotensin II does not influence microvascular blood flow in this model. The results indicate that captopril increases skin microvascular blood flow in rabbits and humans secondary to an increase in endogenous tissue bradykinin; this stimulates B2 receptors with subsequent release of prostaglandins and nitric oxide. ACEIs may increase microvascular perfusion by a bradykinin-dependent mechanism.
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PMID:Captopril increases skin microvascular blood flow secondary to bradykinin, nitric oxide, and prostaglandins. 789 12

The influence of angiotensin converting enzyme inhibitor therapy on elevated plasma endothelin concentrations in chronic heart failure was investigated by measuring plasma endothelin immunoreactivity in 22 patients with severe but stable chronic heart failure before and after 16 weeks of therapy with quinapril (n = 12) or captopril (n = 10). Plasma endothelin immunoreactivity in the patients (10.2 +/- 34 pg/ml) was significantly higher than a control group (5.9 +/- 1.8 pg/ml). Quinapril improved symptoms and haemodynamics but did not affect plasma endothelin immunoreactivity (11.9 +/- 2.9 pg/ml at baseline and 12.3 +/- 3.4 pg/ml after 16 weeks of quinapril). Captopril also had no effect on endothelin levels (8.1 +/- 2.9 at baseline and 8.1 +/- 3.8 pg/ml after 16 weeks of captopril). The vasodilatory effects of angiotensin converting enzyme inhibitors in heart failure are not mediated by, or associated with, changes in plasma endothelin immunoreactivity.
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PMID:Effect of angiotensin converting enzyme inhibition on plasma endothelin in congestive heart failure. 818 87

The efficacy of captopril (capoten) and digoxin was comparatively studied in long-term randomized, double blind trials of 22 male patients with postinfarction cardiosclerosis, functional classes I-III and preserved sinus rhythm. The optimal doses of the drugs proved to be small (0.31 and 35 mg/day of digoxin and capoten, respectively). No adverse effects were noted. The mortality rate was 10 and 16.7% with digoxin and captopril, respectively. The drugs equally improved the functional class by 0.51 and 0.45 and VO2 max by 1.5 and 1.7 ml/min. Digoxin had a mild effect on heart rate (-8.4%) and ejection fraction (+5.7%) and deteriorated diastolic relaxation, by slowing down the early peak of transmitral Doppler spectrum by 16.2%. Captopril significantly improved diastolic function by increasing the early peak by 17.2%. No significant changes in left ventricular sizes were recorded. The clinical efficacy of captopril was explained by a significant decrease in angiotension II (70%) and norepinephrine (40%) levels and by associated normalization of baroreflex regulation. Digoxin insignificantly affected the levels of angiotensin II and norepinephrine, but improved the baroreceptor regulation of sympathetic control impaired in chronic heart failure. It is concluded that extracardiac mechanisms play a major role in the action of not only captopril, but digoxin in the treatment of patients with postinfarct cardiosclerosis and chronic heart failure with sinus rhythm.
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PMID:[Comparative study on use of angiotensin-converting enzyme inhibitors and cardiac glycosides in the treatment of cardiac insufficiency]. 819 54

This study examined the effects of conventional doses of oral captopril on the renal responses to oral furosemide in ambulant patients with stable chronic heart failure. Twenty-five men (mean age 63 years) were randomized to one of two groups. Group 1 received placebo on days 1 and 2 before furosemide. Group 2 received placebo on day 1 before furosemide and captopril thereafter (i.e., captopril before furosemide on day 2). Urine was collected after either placebo or captopril and after furosemide (taken after placebo or captopril pretreatment). Captopril by itself did not affect renal function. Captopril did, however, significantly affect the renal response to furosemide. The increase in urine flow rate after furosemide in group 2 was decreased from 225% with placebo to 128% with captopril (p < 0.02). The increase in sodium excretion after furosemide was decreased from 623% with placebo to 242% with captopril (p < 0.001). Pretreatment with captopril abolished the increase in creatine clearance after furosemide. The increase in urinary albumin excretion (used as a marker of glomerular function) after furosemide was also significantly blunted by captopril. Conventional doses of captopril acutely inhibit the natriuretic and diuretic responses to furosemide at the glomerular level in ambulant patients with stable chronic heart failure.
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PMID:Acute effects of captopril on the renal actions of furosemide in patients with chronic heart failure. 821 45

Captopril was administered to 50 carefully selected patients with severe circulatory failure (18 patients classified as class III and 32 as class IV according to NYHA) in daily dose of 37.5-75 mg for two years. Patients were also given digoxin, diuretic agents and iso-dinitrosorbide. Clinical improvement increased with duration of captopril therapy. A significant improvement following the correction of therapy was achieved in 15% of patients, following one month in 28%, three months--in 70%, and after 1 and 2 years in 84% of the treated patients. All patients survived for one year, and 44--for two years (88%). Clinical improvement was manifested by: diminished of dyspnoea, edema, pulmonary and liver congestion, increase in left ventricle ejection fraction, change of disease staging by one or two NYHA classes, and reduced ventricular rate during atrial fibrillation (in 30% of patients within one year). More noticeable improvement was seen in patients with baseline ejection fraction > 40% than those with EF < 30%, in hypertensive patients than normotensive, and in patients classified to III NYHA class. Ejection fraction increased from 37.9 +/- 9.2% before the treatment to 54.6 +/- 7.7% after a two-year captopril therapy (p < .01). Captopril greatly contributes to the successful therapy of the chronic severe heart failure.
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PMID:[Captopril treatment--2-year period of observation]. 841 45

Captopril is an angiotensin converting enzyme (ACE) inhibitor which has been used extensively in the treatment of patients with hypertension and congestive heart failure. In recent years, animal and human studies have demonstrated that captopril attenuates left ventricular remodelling (structural changes and enlargement) which occurs after myocardial infarction, and can lead to left ventricular dysfunction and increased risk of death. Subsequently, large clinical trials have shown reduced mortality and morbidity in patients receiving captopril or other ACE inhibitors (in addition to standard therapy) after acute myocardial infarction. Results of the 4th International Study of Infarct Survival (ISIS-4), a factorial trial which randomised more than 58,000 patients, indicate that captopril, initiated within 24 hours of myocardial infarction and titrated to 50 mg twice daily for 1 month, significantly reduced overall mortality at 5 weeks after randomisation compared with placebo (7.19 vs 7.69%; p = 0.02). This corresponds to an absolute benefit of 5 lives saved per 1000 patients treated with captopril over this period. Furthermore, the survival advantage appeared to be maintained at 1 year post-infarction. Although both high- and low-risk patients were included in the ISIS-4 trial, the greatest survival benefit of captopril occurred in patients at greater risk of mortality, such as those with signs of heart failure or previous infarction. A significant relative reduction in overall mortality of 19% was seen in patients with left ventricular dysfunction (but not overt heart failure or ongoing ischaemia) after acute myocardial infarction treated with captopril in the Survival and Ventricular Enlargement (SAVE) study. Captopril was started within 3 to 16 days after myocardial infarction and titrated to 50 mg 3 times daily for a mean duration of 42 months. In this high-risk group of patients, approximately 40 to 50 lives were saved per 1000 patients treated with captopril over this period. This was similar to survival benefits demonstrated with other ACE inhibitors following acute myocardial infarction in high-risk patients in other large randomised trials. Cost-effectiveness analyses using data from the SAVE trial indicate that captopril compares favourably with other interventions used for survivors of myocardial infarction. In general, captopril was well tolerated by patients in SAVE, ISIS-4 and other studies in this clinical setting. Thus, when added to standard therapy after acute myocardial infarction, early or late administration of captopril improves survival and reduces cardiovascular morbidity, particularly in selected high-risk patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Captopril. A review of its pharmacology and therapeutic efficacy after myocardial infarction and in ischaemic heart disease. 853 52

Angiotensin converting enzyme inhibitors (CEI) are logically proposed for the treatment of hypertension and heart failure because of their effect on reducing arteriol resistance. When administered early after myocardial infarction, CEI reduce mortality, particularly patients with severely deteriorated myocardium. Up to 74 lives can be saved for every 1000 patients treated. This beneficial effect is additive with that resulting from aspirin, beta-blockers and fibrinolysis. The effect occurs within the first month of treatment if initiated within the first 24 hours following the infarction, and persists even if treatment is discontinued. Tolerance is generally good, but dosage must be adapted in case of hypotension or temporary renal failure. Macroproteinuric nephropathy in insulin-dependent-diabetes is another indication for CEI. Captopril and enalapril have been shown to slow progression of renal failure and decrease the risk of death and of chronic dialysis. Further studies are being conducted to determine the effect of CEI in non-insulin-dependent diabetes. Finally, experimental arguments suggest that atherosclerosis is partly dependent on the renin/angiotensin system and that CEI might inhibit its development. Most clinical trials evaluating the action of CEI on atheromatosis have studied the effect in the carotid and coronary arteries.
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PMID:[Enzyme converting inhibitors. Current knowledge and perspectives]. 854 40


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