Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical responses to captopril, an oral converting-enzyme inhibitor, in five patients with resistant heart failure are described. Earlier treatment consisting of digoxin, diuretics and vasodilators had proven inadequate, and each patient was considered end-stage. Captopril therapy resulted in clear-cut improvements in exercise tolerance, a decrease in decubitus and effort dyspnoea, increased energy, a sense of well-being, and enabled all to become ambulatory. Captopril is a major advance in the treatment of patients with severe resistant heart failure.
 ...
PMID:Captopril in patients with terminal cardiac failure. 675 19

Captopril is a specific inhibitor of kininase II which is responsible for the conversion of angiotensin I into the active angiotensin II and also for the inactivation of bradykinin. In different types of experimental and clinical hypertension, Captopril has a pronounced blood pressure-reducing action particularly when it is given together with a diuretic. Serious side-effects have hitherto restricted the use of Captopril to patients who do not respond or do not respond satisfactorily to routine antihypertensives. Since it has been shown that a considerable improvement in disturbed hemodynamics in hypertension and in certain forms of heart failure can be achieved with quite low doses of the preparation (2 x 2 mg daily) the use of Captopril may be indicated in greater amounts in moderate and severe hypertension.
 ...
PMID:[Captopril - profile of a new antihypertensive (author's transl)]. 679 55

Depressed baroreflex sensitivity (BRS) after acute myocardial infarction (AMI) is considered an indication of decreased vagal and/or increased sympathetic tone. To determine the effect of angiotensin converting enzyme inhibitors (ACEI) on BRS after AMI we studied 27 patients with a first Q wave AMI, no signs of heart failure and no history of arterial hypertension or diabetes mellitus. An additional group of 10 patients with the same clinical characteristics served as controls. On the 5th day after the onset of AMI, three consecutive boluses of phenylephrine were given intravenously and baseline BRS was taken as the mean slope of the linear regression lines of RR intervals over systolic blood pressure. QT interval was also measured and corrected according to Bazett's formula (QTc). Consequently, a single oral dose of captopril 50 mg or placebo was given to treatment or control group patients, respectively; BRS and QTc were reassessed 1 h later. One hour after captopril administration BRS increased from 5.95 +/- 2.80 to 9.14 +/- 3.46 ms.mmHg-1 (P < 0.0001); QTc increased from 414 +/- 46 to 425 +/- 46 ms (P < 0.0001), systolic blood pressure decreased from 125 +/- 19 to 115 +/- 15 mmHg (P = 0.0002), while heart rate did not change significantly. Baseline BRS was correlated only with age (r = -0.74, P < 0.0001). In the control group, 1 h after placebo, no difference was observed in any variable compared to baseline. Captopril appears to improve BRS immediately in the early phase of AMI.
 ...
PMID:Acute effect of captopril administration on baroreflex sensitivity in patients with acute myocardial infarction. 749 6

Cyclooxygenase inhibitors may affect the hemodynamic status of patients with heart failure adversely and may also block the vasodilatory effects of angiotensin-converting enzyme (ACE) inhibitors in such patients. Relatively low doses of the cyclooxygenase inhibitor acetylsalicylic acid (ASA) are now used routinely in ischemic heart disease, the most important cause of heart failure. Therefore, we investigated the hemodynamic interaction between ASA and captopril in heart failure. In a randomized, cross-over study, 13 patients with congestive heart failure (CHF) who were already receiving maintenance treatment with an ACE inhibitor received a single dose of 25 mg captopril combined with 236 mg ASA or placebo. Peripheral blood flow was studied noninvasively by venous occlusion plethysmography of the calves. Liver blood flow was estimated from indocyanine green (ICG) clearance. Administration of captopril alone significantly decreased blood pressure (BP), and ICG clearance. Calf blood flow remained unchanged. However, after arterial occlusion, hyperemic calf blood flow persisted for longer. Captopril alone did not significantly change the plasma levels of the vasodilating prostaglandins PGI2 and PGE2 or the vasoconstricting thromboxane A2 (TXA2). In contrast, captopril combined with ASA reduced the plasma levels of these vasoactive substances, with significant decreases in PGE2 and TXA2 as compared with captopril alone, yet the hemodynamic alterations after captopril plus ASA were similar to those observed after captopril alone. A single antithrombotic dose of ASA (236 mg) in 13 patients with CHF [New York Heart Association (NYHA) class II-IV] undergoing chronic treatment with ACE inhibitors had no discernible effect on hemodynamic status.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effects of acetylsalicylic acid on peripheral hemodynamics in patients with chronic heart failure treated with angiotensin-converting enzyme inhibitors. 751 53

In congestive heart failure (CHF), sympathetic neurotransmitter release is enhanced. We investigated the possibility that this is due in part to alterations in activation of either release-inhibiting alpha 2-adrenoceptors or release-enhancing angiotensin II (AII) receptors at postganglionic sympathetic nerve endings. CHF was induced in rabbits by adriamycin [1 mg/kg intravenously (i.v.), twice weekly for 8 weeks] and was characterized by reduced cardiac output (CO) and enhanced norepinephrine (NE) release rate in pentobarbital-anesthetized rabbits. After pithing and stimulation of the spinal sympathetic outflow, there was no difference in NE release rate between the two groups, suggesting that the enhanced NE release rate observed in adriamycin-treated anesthetized rabbits was of central origin. The alpha 2-adrenoceptor-blocking drug yohimbine (1 mg/kg, i.v.) enhanced NE release rate, which is an indication of feedback inhibition of NE release through presynaptic alpha 2-adrenoceptors. In anesthetized rabbits, this effect of yohimbine was greater in adriamycin-treated than in vehicle-treated animals. However, in pithed rabbits with electrically stimulated sympathetic outflow, there was no difference in the facilitative effect of yohimbine between the two groups, suggesting that inhibitory presynaptic alpha 2-adrenoceptors are activated to a greater extent in heart failure due to the increased transmitter release. Removing inhibitory alpha 2-adrenoceptor input has a functional consequence in that yohimbine increased heart rate (HR) in adriamycin-treated but not in vehicle-treated anesthetized rabbits. Captopril (1 mg/kg, i.v.) decreased NE release rate in pithed rabbits with stimulated sympathetic outflow but had no effect on NE release rate in anesthetized rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Modulation of norepinephrine release in adriamycin-induced heart failure in rabbits: role of presynaptic alpha 2-adrenoceptors and presynaptic angiotensin II receptors. 751 88

To determine whether cardiac unloading by inhibition of angiotensin I (AI) to AII conversion by captopril or blockade of the AII receptor (AT1) by losartan was more effective in prevention of the detrimental hemodynamic consequences of myocardial infarction (MI), inhibition of metabolic production of AII by captopril was compared with blockade of AT1 with losartan in Sprague-Dawley rats with large MI. Infarcts were created by surgical occlusion of the left main coronary artery and oral drug therapy initiated immediately and continued until hemodynamic evaluation seven days later. Heart weight was unchanged in untreated infarcted animals, whereas captopril reduced heart weight in control animals and losartan increased heart weight in infarcted animals. Left ventricular (LV) peak systolic blood pressure (SBP) was lower in treated and untreated infarcted animals. Although captopril reduced end-diastolic pressure (EDP) to a greater degree than losartan, all infarcted group showed an increase in this parameter with respect to similarly treated controls. LV peak rates of pressure increase and decay in infarcted hearts were decreased significantly more by captopril than by losartan administration. Captopril also impaired right side cardiac function more than losartan when peak rate of pressure increase was evaluated. Thus, inhibition of the effects of AII during cardiac failure improved but did not normalize cardiac pump performance.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Efficacy of angiotensin-converting enzyme inhibition and AT1 receptor blockade on cardiac pump performance after myocardial infarction in rats. 751 8

Losartan, a recently developed nonpeptide angiotensin II (AII) receptor antagonist, was orally administered for 14 days to mice with viral myocarditis, beginning 7 days after encephalomyocarditis virus inoculation. The angiotensin-converting enzyme inhibitors (ACEI) captopril and enalapril were also administered in the same manner to compare the therapeutic effects of these three drugs on the degree of myocarditis, acute heart failure, and left ventricular (LV) hypertrophy. Heart weight and the heart weight/body weight ratio were reduced by losartan (60 mg/kg/day) and captopril (7.5 mg/kg/day), but not by enalapril (1 mg/kg/day). LV wall thickness and cavity dimension were decreased in the losartan and captopril groups. Captopril reduced both myocardial necrosis and inflammation, whereas enalapril reduced myocardial necrosis but not inflammation. However, none of the studied losartan doses (1.2, 12, 60 mg/kg/day) influenced myocardial necrosis and inflammation resulting from viral infection. Thus, specific blockade of AII is beneficial in congestive heart failure (CHF) and LV hypertrophy but is not effective in viral-evoked inflammation and injury.
 ...
PMID:Comparative effects of losartan, captopril, and enalapril on murine acute myocarditis due to encephalomyocarditis virus. 756 67

Captopril was the first oral inhibitor of the angiotension converting enzyme (ACE). Its introduction into clinical practice in 1981 was a great advance in the treatment of essential hypertension. In subsequent years a number of other ACE inhibitors was developed. They are nowadays, due to their favourable effects and good tolerance, basic antihypertensive drugs. They are indicated either as monotherapy or part of combined treatment, in particular in moderate to severe hypertension or when other antihypertensive drugs are ineffective, poorly tolerated or contraindicated. They are suitable also for hypertensive patients with left ventricular hypertrophy, cardiac failure, in diabetics and in dyslipoproteinaemia. Recent reports indicate that ACE inhibitors preserve the quality of life of hypertonic patients better than other hypotensive drugs. It seems that some can it, even improve.
 ...
PMID:[Captopril and other angiotensin converting enzyme inhibitors in the treatment of hypertension]. 765 65

58,050 patients entering 1086 hospitals up to 24 h (median 8 h) after the onset of suspected acute myocardial infarction (MI) with no clear contraindications to the study treatments (in particular, no cardiogenic shock or persistent severe hypotension) were randomised in a "2 x 2 x 2 factorial" study. The treatment comparisons were: (i) 1 month of oral captopril (6.25 mg initial dose titrated up to 50 mg twice daily) versus matching placebo; (ii) 1 month of oral controlled-release mononitrate (30 mg initial dose titrated up to 60 mg once daily) versus matching placebo; and (iii) 24 h of intravenous magnesium sulphate (8 mmol initial bolus followed by 72 mmol) versus open control. There were no significant "interactions" between the effects of these three treatments, and the results for each are based on the randomised comparison of about 29,000 active versus 29,000 control allocated patients. Captopril There was a significant 7% (SD 3) proportional reduction in 5-week mortality (2088 [7.19%] captopril-allocated deaths vs 2231 [7.69%] placebo; 2p = 0.02), which corresponds to an absolute difference of 4.9 SD 2.2 fewer deaths per 1000 patients treated for 1 month. The absolute benefits appeared to be larger (perhaps about 10 fewer deaths per 1000) in certain higher-risk groups, such as those presenting with a history of previous MI or with heart failure. The survival advantage appeared to be maintained in the longer term (5.4 [SD 2.8] fewer deaths per 1000 at 12 months). Captopril was associated with an increase of 52 (SD 2) patients per 1000 in hypotension considered severe enough to require termination of study treatment, of 5 (SD 2) per 1000 in reported cardiogenic shock, and of 5 (SD 1) per 1000 in some degree of renal dysfunction. It produced no excess of deaths on days 0-1, even among patients with low blood pressure at entry. Mononitrate There was no significant reduction in 5-week mortality, either overall (2129 [7.34%] mononitrate-allocated deaths vs 2190 [7.54%] placebo) or in any subgroup examined (including those receiving short-term non-study intravenous or oral nitrates at entry). Further follow-up did not indicate any later survival advantage. The only significant side-effect of the mononitrate regimen studied was an increase of 15 (SD 2) per 1000 in hypotension. Those allocated active treatment had somewhat fewer deaths on days 0-1, which is reassuring a bout the safety of using nitrates early in acute MI.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:ISIS-4: a randomised factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulphate in 58,050 patients with suspected acute myocardial infarction. ISIS-4 (Fourth International Study of Infarct Survival) Collaborative Group. 775 87

To study the effects of captopril pretreatment on vascular capacitance in acute heart failure, anesthetized splenectomized dogs were subjected to rapid right ventricular pacing (RRVP) at 250 beats/min for 60 min combined with an intravenous (i.v.) 20-ml/kg volume load of dextran 70 over 10 min. Captopril pretreatment [50 mg every 8 h for 3 days plus 0.5 mg/kg intravenously (i.v.) at induction of anesthesia] attenuated development of acute heart failure associated with RRVP, maintaining normal cardiac output (CO) and pulmonary capillary wedge pressures (PCWP). Total vascular capacitance after a volume load plus RRVP was higher in captopril-pretreated animals (129.8 +/- 3.2 vs. 100.4 +/- 4.8 ml/kg) owing to an increase in unstressed volume (118.6 +/- 3.1 vs. 88.4 +/- 5.6 ml/kg). Arterial capacity and pulmonary (central) vascular capacitance were also increased.
 ...
PMID:Captopril attenuates pacing-induced acute heart failure by increasing total vascular capacitance. 769 88


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>