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)

Captopril, an inhibitor of the conversion enzyme, is a medication with a known efficacy in the treatment of arterial hypertension and congestive cardiac insufficiency. Its side-effects are few. Among them, agranulocytosis is a severe complication, all the more severe and frequent as it occurs in patients with chronic renal insufficiency, collagen disease, or patient treated with medication having a leucopenic potential. Our case reports an agranulocytosis secondary to captopril in a patient with cardiac insufficiency presenting none of these aggravating factors. The mechanism of agranulocytosis secondary to captopril remains currently debatable, but does not seem, in the present case, to be dose related. Thus, a captopril prescription must comply with certain rules; decrease of the dosage in case of renal insufficiency, usual precautions in patients with collagene diseases. The association to a medication with leucopenic potential is to be avoided. Hematologic monitoring will be adapted to each particular case.
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PMID:[Agranulocytosis caused by captopril]. 354 68

Several investigators have reported that hepatic metabolism of renin can be altered in pathophysiological states (e.g., high-output heart failure, cirrhosis, acute metal toxicity). The hypothesis that circulating angiotensin II may play a role in regulating renin metabolism by the liver was tested in anesthetized dogs. Captopril (SQ 14255) or an angiotensin II-competitive antagonist [( Sar1-Ile8]angiotensin II) was used for blockade of the renin-angiotensin system in two separate groups of dogs. The administration of captopril resulted in a significant fall in the percent extraction of renin by the liver (P less than 0.01) and in the clearance of renin (P less than 0.05). The group receiving the competitive antagonist and time-control animals showed no significant change in renin extraction or renin clearance by the liver. Our data do not support a role for angiotensin II in the regulation of hepatic metabolism of renin, since experiments utilizing the antagonist failed to produce a change. The mechanism by which captopril alters renin metabolism appears to be independent of its blockade of angiotensin II.
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PMID:Hepatic clearance of renin after angiotensin blockade. 388 84

The present study examined the regional vascular effects (radioactive microspheres) of converting-enzyme inhibition (captopril, 1 mg/kg) and calcium-antagonism (diltiazem, 1 mg/kg) in a rat model of cardiac failure due to large myocardial infarction (n = 18, infarct size 40% of the left ventricle) both at rest and during submaximal treadmill exercise. Diltiazem increased renal, gastrointestinal, coronary and cutaneous blood flow at rest by 29%, 28%, 26% and 37% (p less than 0.05 each) and enhanced skeletal muscle blood flow during exercise by 16% (p less than 0.05). Captopril improved primarily renal and coronary blood flow at rest (by 59% and 23%, respectively, p less than 0.05) and reduced vascular resistance in the gastrointestinal bed by 25% (p less than 0.05) without significant effects in other circulatory beds. We conclude that the regional vascular effects elicited by converting-enzyme inhibition and calcium antagonism differ considerably in this animal model of congestive heart failure and may be clinically important. The favourable regional vascular profile of diltiazem deserves further clinical investigation.
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PMID:[Modification of organ perfusion by calcium blocker and converting enzyme inhibitor in the conscious rat with heart failure]. 388 15

We compared the short-term hemodynamic effects of isosorbide dinitrate (40 mg orally) and captopril (25 mg orally) in 18 patients with severe chronic heart failure in a randomized, crossover study conducted on consecutive days. Captopril and isosorbide dinitrate produced similar decreases in systemic vascular resistance, but whereas nitrate therapy decreased pulmonary arteriolar resistance significantly, captopril did not; the difference between the two drugs was highly significant (-25% vs -5%, p less than 0.001). Left ventricular filling pressures declined similarly with both captopril (-10.5 mm Hg) and with isosorbide dinitrate (-9.3 mm Hg), but because pulmonary arteriolar resistance fell significantly with nitrate therapy, mean right atrial pressure decreased more with isosorbide dinitrate than with captopril (-5.4 vs -2.8 mm Hg, respectively; p less than 0.001). Although systemic resistance declined similarly with both drugs, cardiac index increased more with nitrate therapy than during converting-enzyme inhibition (+0.47 vs +0.23 L/min/m2) (p less than 0.01), and therefore mean arterial pressure fell less with isosorbide dinitrate than with captopril (-10.5 mm Hg vs -16.7 mm Hg); p less than 0.05); two patients developed symptomatic hypotension with captopril, whereas none did so with the nitrate. The difference in the effects of the two drugs on cardiac index was not due to differences in their effects on heart rate, since heart rate fell similarly with both drugs, and thus both drugs produced similar increases in stroke volume index. These data indicate that, in patients with severe chronic heart failure, nitrates exert favorable dilating effects on the pulmonary circulation not shared by captopril.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparative effects of captopril and isosorbide dinitrate on pulmonary arteriolar resistance and right ventricular function in patients with severe left ventricular failure: results of a randomized crossover study. 389 May 6

Captopril, the first orally effective converting enzyme inhibitor, was administered to 14 patients with chronic heart failure for 6 week periods, in a double-blind crossover comparison with placebo. Captopril improved symptoms and exercise performance, while left ventricular internal dimensions were reduced. The fall in blood pressure induced by captopril was well tolerated. Glomerular filtration rate was reduced and effective renal plasma flow increased on captopril. No decline in body weight or total body sodium was seen, suggesting that a natriuresis had not occurred. Serum and total body potassium rose. Ventricular arrhythmias declined.
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PMID:Angiotensin converting enzyme inhibition in heart failure. 609 32

The acute haemodynamic effects of low doses of the oral converting-enzyme inhibitor, captopril, were studied in 18 patients with severe chronic heart failure. The effects of long-term therapy were also evaluated. Increasing doses (1 mg, 2.5 mg, 6.25 mg, 12.5 mg, and 25 mg) of captopril were given at 2 h intervals with haemodynamic monitoring. Graded haemodynamic improvement (increased stroke-volume index and reduced mean pulmonary capillary wedge pressure) was noted from 1 hand was closely associated with reduction of blood pressure. Maximal haemodynamic improvement for the group was seen at 6 h and 7 h after the 6.25 mg and 12.5 mg doses, when stroke-volume index had risen 35% and mean pulmonary capillary wedge pressure had fallen 40% from control. Captopril 12.5-50 mg every 8 h was continued long term but was withdrawn in 2 patients with symptomatic hypotension and 1 patient with altered taste. 4 patients died and 1 was noncompliant with therapy. At 3 months, 10 patients showed significant improvement in symptoms, treadmill-exercise duration, and echocardiographic indices of left-ventricular size and function. Repeat haemodynamic measurements were similar to optimum measurements obtained during the initial study.
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PMID:Low-dose captopril in chronic heart failure: acute haemodynamic effects and long-term treatment. 610 67

In five patients with resistant heart failure treated with the oral converting-enzyme inhibitor, captopril, standardised and intensive haemodynamic, hormone, and electrolyte monitoring showed significantly raised cardiac output and reduced arterial, pulmonary-wedge, and pulmonary-artery pressures which correlated closely with concomitant alterations in the activity of the renin-angiotensin system. These changes occurred in the absence of a natriuresis or diuresis. Clinical improvement was dramatic and paralleled the objective haemodynamic changes. Hyponatraemia and a rise in plasma-potassium were noted. Captopril is a major advance in the treatment of resistant heart failure, and its beneficial haemodynamic effects relate primarily to a blockade of the renin-angiotensin system, the activity of which is increased by conventional drug therapy.
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PMID:Haemodynamic, hormonal, and electrolyte responses to captopril in resistant heart failure. 610 21

To determine whether temporary cessation of captopril therapy compromises cardiac performance, haemodynamic, hormonal, and electrolyte indices were measured for 2 days before, and 4 days after discontinuation of long-term captopril treatment in 5 patients with heart failure. Captopril withdrawal resulted in a four-fold rise in plasma angiotensin II, higher levels of noradrenaline, and a 13.5mmHg increase in mean arterial pressure. Despite there changes, cardiac output at rest and during exercise was well maintained, and right-heart pressures were unaltered. Although plasma aldosterone levels increased three-fold, neither sodium retention nor potassium depletion occurred. Cortisol levels rose in parallel with angiotensin II levels. These results indicate that in the short term cardiac performance is not impaired and electrolyte balance is not adversely affected by the abrupt withdrawal of captopril.
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PMID:Haemodynamic, hormonal, and electrolyte responses to withdrawal of long-term captopril treatment for heart failure. 611 29

Limb blood flow and respiratory function were compared in ten patients with severe heart failure inadequately controlled by diuretics and normal control subjects matched for age and sex. Both forearm and calf blood flow, at rest and after exercise, were lower in the patients than in the control subjects. Oxygen consumption during submaximal exercise was also lower in the patients and minute ventilation was higher. Captopril, administered in a single-blind controlled study to the patients, resulted in an improvement in these abnormalities, with the exception of oxygen consumption. It also improved exercise tolerance and reduced perceived exertion during exercise. Captopril is effective treatment for severe heart failure and improves some of the peripheral haemodynamic and respiratory abnormalities.
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PMID:Effects of captopril on abnormalities of the peripheral circulation and respiratory function in patients with severe heart failure. 615 Jan 83

Treatment of angina pectoris should follow the clinical course: Stable angina is most often responding to nitropreparations, betablockers or calciumantagonists; differentialtherapy should consider the basic state of the patient: age, heart-rate, hypo- or hypertension, cardiac failure or asthma bronchiale etc. Unstable angina needs more attention and should be transferred to a coronary care unit. Analgetics, sedatives, oxygen and nitrates should be applied under hemodynamic monitoring. Only in rare cases with cardiac failure or with rapid atrial fibrillation glycosides will be necessary. In extreme bradiacardias a pacemaker can be helpful. Captopril might be a new substance in nonresponders.
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PMID:[Therapy of angina pectoris]. 615 89


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