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)

In an attempt to study the possible mechanism(s) by which captopril controls resistant heart failure, sequential haemodynamic studies (radioisotope technique) and humoral measurements (plasma renin activity, plasma aldosterone and plasma catecholamines) were obtained in 11 such patients. The studies were made at the time patients became unresponsive to other vasodilators (hydralazine or prazosin); the vasodilator drug was then discontinued and five days later, the 'no-vasodilator' studies were obtained. Captopril therapy was then started. Optimum daily maintenance dose of captopril varied from 75 to 200 mg in different patients. Studies were again repeated after a period of time equal to the duration of the previous vasodilator therapy. Digitalis and diuretic doses were kept constant throughout. Captopril improved effort tolerance in ten patients. Haemodynamically, mean blood pressure and peripheral resistance were lower than during vasodilator therapy (85 +/- 3.1 v. 92 +/- 3.3 mmHg and 47 +/- 4.4 v. 59 +/- 4.4 U.M2, respectively; p less than 0.05 for both). Cardiac index was higher during captopril treatment (1.95 +/- 0.15 v. 1.63 +/- 0.10 l/m2, p less than 0.01) and pulmonary mean transit was normalized by captopril (14.6 +/- 1.7 v. 18.4 +/- 1.3 s, p less than 0.05). Humoral indices revealed a significant (p less than 0.05) reduction in plasma aldosterone during captopril therapy (25.9 +/- 5.6 ng/dl during captopril, v. 62 +/- 22 ng/dl with no vasodilators and 50.9 +/- 6.1 ng/dl with other vasodilators). Moreover, there was a decrease in circulating plasma catecholamines during captopril treatment, but differences between the three treatment periods were not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Captopril in congestive heart failure resistant to other vasodilators. 636 32

Hemodynamic and hormonal responses to captopril were measured in 10 patients with severe chronic heart failure poorly controlled by digitalis and diuretics. After administration of a 25-mg dose, stroke volume (SV) increased from 53 +/- 7 to 63 +/- 9 ml (p less than 0.05), while pulmonary wedge pressure (PWP) decreased from 20 +/- 2 to 14 +/- 2 mm Hg (p less than 0.01). The hemodynamic changes were associated with increases in plasma renin activity (PRA; p less than 0.05) and in plasma levels of a novel bicyclo-prostaglandin E2 metabolite (bicyclo-PGE-m; p less than 0.01), whereas norepinephrine (NE) showed a falling tendency. In general, basal hemodynamic and basal hormonal levels did not correlate. Captopril-induced changes in mean artery pressure (MAP) and mean pulmonary artery pressure (mPAP) were positively correlated to pre-captopril PRA (r = 0.74, p less than 0.01; r = 0.64, p less than 0.05) and to changes in PRA (r = 0.85, p less than 0.01; r = 0.80, p less than 0.01) with a similar trend for angiotensin II (AII); decreases of systemic vascular resistance were more pronounced in patients with higher control NE levels (r = 0.62, p less than 0.05), the reduction of NE levels being highest in patients with higher basal concentrations (p less than 0.001); the captopril-induced decreases of mPAP and PWP were inversely related to basal bicyclo-PGE-m levels (r = 0.60, p less than 0.05; r = 0.61, p less than 0.05), and changes in mPAP were closely related to basal ratios of AII/bicyclo-PGE-m (r = 0.67, p less than 0.01). Thus, captopril exerts its acute beneficial hemodynamic effect by inhibiting the generation of AII, associated with toning down of sympathetic stimulation and increased production of vasodilating prostaglandins, such as PGE2. The relation between AII and PGE2-counteracting substances-might determine the hemodynamic response to captopril in the patients.
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PMID:Endogenous prostaglandin E2 metabolite levels, renin-angiotensin system and catecholamines versus acute hemodynamic response to captopril in chronic congestive heart failure. 637 Apr 31

The angiotensin converting enzyme inhibitor captopril improves the altered hemodynamics in many patients with chronic heart failure, but the first dose may precipitate hypotension. Ten patients with chronic heart failure were studied, nine with high plasma concentrations of renin and one with a low concentration. Frequent measurements of plasma concentrations of angiotensin II, renin, and catecholamines were made over 60 minutes after a small dose (6.25 mg) of captopril and related to concurrently measured hemodynamic variables. Captopril caused a decrease in systemic and pulmonary artery pressure and an increase in cardiac index, and these changes coincided with reductions in the plasma concentrations of angiotensin II and increases in plasma concentrations of renin. The hemodynamic changes were accompanied by reductions in the plasma concentrations of norepinephrine but transient increases in plasma concentrations of epinephrine in patients in whom vasomotor syncope developed. The patient with a low plasma renin concentration showed little hemodynamic response to the drug. It is concluded that vasomotor syncope occurs quite frequently in patients with severe chronic heart failure after captopril in a small dose and is associated with a selective increase in epinephrine secretion from the adrenal medulla.
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PMID:Angiotensin II levels, hemodynamics, and sympathoadrenal function after low-dose captopril in heart failure. 638 25

The effect of the converting enzyme inhibitor captopril as long term treatment was investigated in 14 patients with severe congestive heart failure in a double blind trial. Captopril reduced plasma concentrations of angiotensin II and noradrenaline, with a converse increase in active renin concentration. Effective renal plasma flow increased and renal vascular resistance fell; glomerular filtration rate did not change. Serum urea and creatinine concentrations rose. Both serum and total body potassium contents increased; there were no long term changes in serum concentration or total body content of sodium. Exercise tolerance was appreciably improved, and dyspnoea and fatigue lessened. Left ventricular end systolic and end diastolic dimensions were reduced. There was an appreciable reduction in complex ventricular ectopic rhythms. Adverse effects were few: weight gain and fluid retention were evident in five patients when captopril was introduced and two patients initially experienced mild postural dizziness; rashes in two patients did not recur when the drug was reintroduced at a lower dose; there was a significant reduction in white cell count overall, but the lowest individual white cell count was 4000 X 10(6)/l. Captopril thus seemed to be of considerable value in the long term treatment of severe cardiac failure.
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PMID:Captopril in heart failure. A double blind controlled trial. 638 12

The oral inhibitor of the converting enzyme of angiotensin has previously been used successfully in the treatment of chronic cardiac failure. Its action as an arterial and venous vasodilator and in significantly reducing the heart rate which we have previously reported, led us to assess its effects in left ventricular failure during acute myocardial infarction. The effects of captopril were compared with those of isosorbide dinitrate in 10 patients with left ventricular failure during acute myocardial infarction. An arterial and venous vasodilatation was obtained with both drugs. Captopril induced a greater fall in left ventricular filling pressures and significantly reduced the heart rate, leading to a slight increase in left ventricular systolic work index. Pulmonary arterial resistances decreased more significantly with captopril whilst systemic arterial resistances fell equally. The left ventricular function curve was shifted to the left by both captopril and isosorbide dinitrate, but only captopril induced an upward shift and only captopril caused very significant reductions in the rate-pressure product. The plasma renin activity of these patients was high but the correlation with the vasodilator effect was poor. There was little change in medium-term survival (50% mortality). These results indicate that captopril may be a valuable drug in the treatment of left ventricular failure in acute myocardial infarction. However, its oral presentation makes it difficult to determine the optimal dose.
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PMID:[Effect of captopril in left ventricular failure during the acute stage of myocardial infarction]. 642 72

The optimal dose of Captopril was evaluated by hourly haemodynamic monitoring in 10 patients with chronic congestive cardiac failure (Stage IV of the NYHA Classification) after administration of 25 mg, 50 mg, and 100 mg of Captopril. A similar improvement was observed in all the parameters considered with all three dosages. At its peak effect (90 minutes) 25 mg of Captopril caused a fall in pulmonary capillary, and mean pulmonary artery pressures, and a fall in systemic resistance of 40%, 20% and 30% respectively; with 50 mg of Captopril, the effect was a fall of 36%, 24% and 35% respectively. The cardiac index rose by 17% with 25 mg of Captopril, 28% with 50 mg and 12% with 100 mg of Captopril. Although the fall in pulmonary capillary pressure remained significant up to the 6th hour, the improvement in cardiac index was not significant after the 3rd hour. After 8 days' treatment, plasma renin activity increased from 7.01 +/- 4.68 to 23.6 +/- 18.3 ng/ml/hour (p less than 0.02) and serum aldosterone fell from 1.175 +/- 386 p. moles/l to 497 +/- 277 p. moles/l (p less than 0.001). There was no correlation between basal plasma renin activity and pre- or post-therapeutic systemic resistances. The clinical and haemodynamic improvement was sustained after 2 months' treatment in 5 of these patients without side effects. Increasing the dosage of Captopril does not reinforce or prolong its action; moderate doses (25 mg) are as effective as high doses (100 mg). Captopril, which acts by inhibiting the renin- angiotensin-aldosterone system is the current treatment of choice in severe refractory cardiac failure.
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PMID:[Determination of the optimal dose of captopril in the treatment of severe cardiac failure by hourly hemodynamic monitoring]. 642 32

The favourable haemodynamic effects of vasodilator drugs in refractory cardiac failure sometimes alter rapidly after the initial dose. This tachyphylactic phenomenon was looked for during captopril therapy in 14 patients with chronic cardiac failure resistant to digitalo-diuretic therapy and conventional vasodilator drugs. The average age of the patients was 64,4 +/- 3,8 years. Eleven patients had signs of congestive cardiac failure while the remaining three patients had only left ventricular failure. Four patients were classified as Stage III and the other ten Stage IV of the NYHA classification. Right heart catheter studies were performed with a Swan Ganz catheter and systemic pressures were measured by femoral artery catheterisation. Right and left pressures and cardiac output were measured under basal conditions, and 1 and 5 hours after a single dose of captopril (early and late periods). Captopril was given in between meals in 3 to 6 daily doses; in 10 of the 14 cases the dose was 50 mg 6 hourly. The haemodynamic parameters were recorded again during the early and late periods after the dose of captopril 24 and 48 hours after starting therapy. Captopril is a mixed vasodilator and is effective from the first hour of administration. It preferentially lowered pulmonary capillary pressure (PCP) from 29,6 +/- 0,92 mmHg to 21,4 +/- 1,04 mmHg (delta PCP: -27,7%, p less than 0,01). Mean systemic blood pressure (MBP) fell less from 92,4 +/- 3,51 mmHg to 76,6 +/- 3,4 mmHg (delta MBP: -17%, p less than 0,01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Enhancement of the effect of captopril in the 1st 48 hours of treating refractory heart failure. A comparison with intravenous trinitrine]. 643 36

Captopril was administered to 23 patients in cardiac failure refractory to digitalo-diuretic therapy. Four patients had a large fall in systolic blood pressure (less than 70 mmHg) with a single dose of 25 mg of captopril. In the other 19 patients a significant fall in mean pulmonary capillary pressure (16,8 +/- 6,1 mmHg vs 27,2 +/- 8,5 mmHg, p less than 0,001), mean pulmonary artery pressure (26,3 +/- 11,3 mmHg vs 38,3 +/- 12,4 mmHg, p less than 0,001), mean right atrial pressure (5 +/- 5 mmHg vs 8 +/- 6 mmHg, p less than 0,01) was observed: there was a moderate fall in mean systemic arterial pressure (13%, p less than 0,001). There was a significant fall in pulmonary resistance (27%, p less than 0,001). The cardiac index increased (2,8 +/- 0,5 l/min/m2, p less than 0,001) and systemic resistance fell by 25% (p less than 0,001). The heart rate decreased by an average of 7 beats/min (p less than 0,02). The treatment was stopped in one patient because of the inefficacy of captopril at 100 mg per dose. The average daily dose in the 18 patients on long-term treatment was 212,5 +/- 106,8 mg. At the second month, the haemodynamic parameters were remeasured before the morning dose of captopril. The effects observed after the single dose were maintained apart from the systemic blood pressure, heart rate and systemic resistances which had returned to the value observed before administration of captopril. The mean pulmonary capillary pressure was significantly lower than before treatment but was higher than after the single dose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Captopril in cardiac insufficiency. Immediate and long-term effects]. 643 36

The acute effects of captopril on haemodynamics, coronary flow and myocardial metabolism were studied in 12 patients with chronic severe cardiac failure (primary cardiomyopathy: 10 cases; ischaemic: 2 cases) in functional Classes III or IV of the NYHA. All patients were male and their average age was 51.3 +/- 14.1 years (range 27 to 68 years). Measurements were carried out under basal conditions and 90 minutes after a single dose of 50 mg (5 cases) or 100 mg (7 cases) of captopril. Captopril administration leads to an increase in cardiac index from 2.05 +/- 0.32 to 2.34 +/- 0.35 l/min/m2 (p less than 0.05) and a greater increase in systolic index from 23.9 +/- 6.7 to 29.8 +/- 6.9 ml/syst/m2 (p less than 0.01), because the heart rate decreased slightly (p less than 0.05). These changes were the result of a decrease in afterload: mean aortic pressure fell from 85 +/- 11.8 to 68 +/- 19.6 mmHg (p less than 0.01) and systemic arterial resistance fell from 2 886 +/- 745 to 2 010 +/- 610 dynes/cm-5/sec/m-2 (p less than 0.01). Captopril also led to a fall in venous tone, i.e. pre-load: left ventricular end diastolic pressure fell from 26.9 +/- 6.1 to 20.8 +/- 6.6 mmHg: p less than 0.01. There was no change in contractility as shown by the absence of variation of the V.max (0.92 +/- 0.18 under basal conditions, and 0.90 +/- 0.15 after 90 minutes).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute hemodynamic and coronary effects of captopril in chronic cardiac failure]. 643 65

1 The clinical and haemodynamic effects of low doses of the oral converting-enzyme inhibitor captopril were studied in 18 patients with severe chronic heart failure. Increasing doses of 1 mg, 2.5 mg, 6.25 mg, 12.5 mg, and 25 mg captopril were given at two hour intervals with haemodynamic monitoring. Graded haemodynamic improvement (increased stroke volume index and reduced mean pulmonary capillary wedge pressure) occurred from one hour with reduction of blood pressure closely associated. 2 Maximal haemodynamic improvement for the group was seen at six and seven hours after the 6.25 mg and 12.5 mg doses, when stroke volume index was increased by 35% and mean pulmonary capillary wedge pressure reduced by 40% from control. Captopril 12.5 mg-50 mg eight hourly was continued long-term but withdrawn in two patients with symptomatic hypotension and one patient with altered taste. 3 Four patients died and one was non-compliant with therapy. At three months 10 patients showed significant improvement in symptoms, treadmill exercise duration, and echocardiographic indices of left ventricular size and function. The results of repeat haemodynamic measurements were similar to optimal measurements obtained during the initial study. 4 At two years six patients remained alive, five having maintained their symptomatic improvement. Thus small doses of captopril produce haemodynamic improvement in heart failure with a closely associated reduction of blood pressure. Symptomatic and haemodynamic benefit is maintained with long-term treatment.
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PMID:Clinical and haemodynamic effects of low dose captopril in severe chronic heart failure. 675 97


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