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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the hemodynamic, echocardiographic, phonomechanographic and hormonal changes during acute (25 mg) and chronic (6 months--75 to 225 mg/day) treatment of 10 patients with congestive cardiac failure due to cardiomyopathy with dilatation with SQ 14 225 (Captopril). The following changes were observed after the single dose: an increase in cardiac output (p less than 0,001), in stroke volume (p less than 0,01), a reduction in heart rate (p less than 0,01), in peripheral resistance (p less than 0,001) and pulmonary capillary pressure (p less than 0,001). There were no significant changes in end systolic or end diastolic left ventricular internal diameter. Plasma renin activity increased (p less than 0,001); there was a concurrent fall in serum aldosterone (NS): the plasma concentration of converting enzyme decreased (p less than 0,001). There was a correlation between the increase in peripheral resistance under basal conditions and the basal plasma renin activity (R = 0,72, p less than 0,02). The decrease in peripheral resistance after captopril also correlated with basal plasma renin activity (R = 0,89, p less than 0,01). After six months continuous therapy, the hemodynamic effect was sustained and was accompanied by a significant symptomatic improvement. Left ventricular internal end systolic and end diastolic diameters decreased (p less than 0,01 and p less than 0,01 respectively). The pre-ejectional period decreased (p less than 0,05). Serum aldosterone fell significantly (p less than 0,001) as did plasma renin activity (p less than 0,01); the serum level of converting enzyme remained low with respect to its initial value. These results show that captopril may be useful in severe cardiac failure without tolerance during long-term administration. No renal or hematological toxicity was observed in this group of patients.
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PMID:[Long-term treatment of chronic heart failure by an inhibitor of angiotensin converting enzyme]. 630 39

Seven women with primary pulmonary hypertension underwent hemodynamic evaluation, at rest and during exercise, before and after the oral administration of captopril. Dose-response curves were generated for the 25-, 50- and 100-mg doses. Captopril significantly reduced systemic blood pressure and systemic vascular resistance; these effects persisted at submaximal levels of exercise. Captopril did not alter pulmonary artery pressure or resistance, cardiac output or stroke volume at rest or during exercise. Exercise tolerance did not improve. Four of the patients also received captopril chronically for 12 weeks at doses of 75 and 100 mg every 8 hours. Resting and exercise hemodynamic evaluation was repeated at the end of the 12-week period. Except for a persistent reduction in mean systemic blood pressure at rest, chronic captopril administration did not elicit hemodynamic changes. Measured exercise duration did not change during continuous captopril treatment, although one patient reported mild subjective improvement in activity tolerance. In primary pulmonary hypertension, captopril exerts its major effect on systemic vasculature, with little or no effect on the pulmonary circuit. While an occasional patient may experience some clinical improvement with captopril therapy, the majority of adult patients with severe primary pulmonary hypertension will not benefit from its chronic administration.
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PMID:Captopril in primary pulmonary hypertension. 633 5

The angiotensin-converting enzyme inhibitor, captopril, was given to 19 patients with severe heart failure. Seven patients had acute myocardial infarction and the remainder had chronic myocardial damage caused by ischaemia or valvular disease. Cardiac filling pressures were raised in all, the pulmonary capillary "wedge" pressure being 17 mmHg or more. Captopril, 50 mg orally, raised stroke volume and cardiac output, and reduced heart rate, cardiac filling pressures, systemic arterial pressure, and the plasma concentrations of aldosterone and noradrenaline. These changes were attended by clinical improvement. Decrements in cardiac filling pressures, systemic arterial pressure, and total peripheral resistance were positively correlated with pretreatment plasma renin. Long-term treatment with captopril was offered to 14 patients. Four patients with severe coronary disease died suddenly after initial clinical improvement. In nine patients haemodynamic measurements were repeated after three months. The results showed sustained effects on cardiac output and filling pressures but there was no loss of body weight. The haemodynamic effects were at least as good as with previous vasodilators. The fall in systemic arterial pressure, however, was greater with captopril. Captopril may become a valuable adjunct to the treatment of acute and chronic heart failure, but more information about its effect on coronary blood flow is required.
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PMID:Effects of captopril in acute and chronic heart failure. Correlations with plasma levels of noradrenaline, renin, and aldosterone. 633 40

There are few data to support the potential efficacy of combined vasodilator therapy for severe congestive heart failure. For documentation of the feasibility of such an approach, a short-term hemodynamic study utilizing captopril, an oral converting enzyme inhibitor, followed by the addition of nitroprusside infusion, was made of 11 patients with severe chronic congestive heart failure. Captopril alone resulted in reduction of mean arterial pressure (84 +/- 7 to 70 +/- 3 mm Hg), associated with increase of cardiac index and stroke index. There was also a significant reduction of systemic resistance and pulmonary wedge pressure. The initial hemodynamic response to captopril was correlated with initial plasma renin activity (all values at least p less than 0.05). The addition of nitroprusside to captopril resulted in further hemodynamic improvement. Reduction of mean arterial pressure, systemic vascular resistance, and pulmonary wedge pressure were all significant, as were increases of cardiac index and stroke index. The degree of hemodynamic improvement with this sequence of vasodilator therapy was linearly related to the reduction of mean arterial pressure. Therefore vasodilators with dissimilar mechanisms of action may have an additive effect. These data support the potential feasibility of combined, long-term oral vasodilator therapy in selected subgroups of patients with congestive heart failure.
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PMID:Combined vasodilator therapy for chronic congestive heart failure. 634 Apr 48

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

Captopril is an orally active converting enzyme inhibitor lowering blood pressure (BP) in different types of hypertension. A combination of captopril and a diuretic is often used in the treatment of severe hypertension. We have examined the chronic haemodynamic effect of combined captopril and hydrochlorothiazide treatment at rest and during 50 and 100 W dynamic exercise in 12 patients with severe therapy resistant essential hypertension. Blood pressure was measured intra-arterially before and after a mean treatment period of 8.7 months. Cardiac index (CI) was measured by dye dilution (Cardiogreen) and body fluid volumes by radioisotope dilution techniques. During rest sitting BP was reduced by 31/17 mmHg (15%) from a pretreatment value of 205/119 mmHg. Total peripheral resistance index (TPRI) fell 17% whereas CI, heart rate (HR) and stroke index (SI) did not show any significant changes. The fall in mean arterial pressure (MAP) was slightly less during exercise (12%) and the BP reduction was associated with a fall in CI and SI of 15 and 17%, respectively and no fall in TPRI. No significant changes were observed in body fluid volumes.
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PMID:Combined captopril and hydrochlorothiazide therapy in severe hypertension: long-term haemodynamic changes at rest and during exercise. 639 25

From a hemodynamic point of view, an adequate response to antihypertensive therapy would be restoration of a normal circulatory system. In most patients with mild to moderate essential hypertension considered to need drug therapy, the cardinal hemodynamic disturbance is an increased total peripheral resistance (TPR) and a normal or reduced cardiac output (CO). During a 10- to 17-year follow-up of untreated hypertensives, a gradual increase in TPR, increase in MAP, and a decrease in CO and stroke volume (SV) were seen. Hemodynamic responses to chronic drug therapy were studied at rest and during exercise in 250 men with mild to moderate essential hypertension in WHO Stage I. A significant reduction in TPR was seen on thiazide diuretics, nifedipine and verapamil, but there was no increase of subnormal CO or SV. A greater normalization of central hemodynamics was achieved by prazosin, which induced a reduction in TPR and an increase in CO and SV, particularly during exercise. In contrast, beta-blocker therapy was associated with a chronic reduction in CO and heart rate (HR) and usually no reduction in TPRI below pretreatment values. The chronic CO reduction was associated with an increase in arteriovenous oxygen difference. In 14 patients with therapy-resistant hypertension, a marked increase in TPR was found. Captopril induced a reduction in TPR with rest and exercise, and also a reduction in cardiac output. Prolonged therapy for 5 years with beta-blockers did maintain blood pressure control, but with no further decrease in TPR.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic response: decrease in cardiac output vs reduction in vascular resistance. 662 61

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

Antihypertensive effects of captopril, an orally active converting enzyme inhibitor were examined in the young and adult stroke-prone SHR (SHRSP) rats. The treatment was initiated at 6-7 and 14-18 weeks of age, and was continued for 12 and 17 weeks, respectively. The dosage of captopril was changed stepwise 3-30 and 3-100 mg/kg, orally per day in the young and adult rats, respectively. The effects of hydralazine were also determined for comparison. Captopril had a chronic antihypertensive effect when given in doses of 30 mg/kg in the young and 100 mg/kg in the adult rats. Captopril had no significant effect on heart rate throughout the experiments, while hydralazine increased the heart rate. Treatment with captopril decreased the incidence of vascular disease in the young and the severity in the adult rats, respectively. A decrease in incidence of cerebral stroke in the adult SHRSP was also apparent. More than a ten fold increase in plasma renin activity and about a two fold increase in kidney renin activity were observed in both the young and adult SHRSP at the end of the treatments. The results demonstrate the efficacy of long-term treatment with captopril in the management of hypertensive disease in SHRSP rats.
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PMID:Effects of long-term treatments with captopril on blood pressure and renin activity in the stroke-prone spontaneously hypertensive rats. 701 11

Hypertension frequently is associated with a number of changes in heart structure and function, such as left ventricular hypertrophy, disturbed diastolic function, and subnormal stroke volume during exercise. Most of these changes probably are related to myocardial fibrosis. Antihypertensive agents reverse the structural and functional changes to different degrees. The hemodynamic changes in central hemodynamics at rest and during exercise were studied before and after angiotensin-converting enzyme (ACE) inhibition in 68 patients with essential hypertension (ranging from severe to moderately severe). In patients with moderately severe hypertension who were administered perindoprilat intravenously, mean arterial pressure was reduced by approximately 17% due to reduction in total peripheral resistance and no changes in heart pump function. Chronic treatment with captopril, enalapril, or lisinopril for 6-12 months induced reduction in blood pressure associated with decreased peripheral resistance. In general, there were only minor changes in cardiac output, stroke volume, and heart rate. Studies from other laboratories have shown that ACE inhibitors reverse left ventricular hypertrophy and improve left ventricular diastolic function. Captopril also appears to improve coronary circulation. The effect of ACE inhibitors on heart structure and function appears promising with regard to cardioprotection during chronic use, but long-term studies are needed to prove that this will occur in clinical practice.
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PMID:Cardiac effects of ACE inhibition. 750 38


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