UMLS:C0018801 - FACTA Search

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Query: UMLS:C0018801 (heart failure)
72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Enalapril, a novel angiotensin converting enzyme inhibitor, was given orally to 12 patients with chronic heart failure (NYHA functional class III and VI) and cardiomegaly. Heart rate, systemic arterial blood pressure, pulmonary arterial pressure, right and left ventricular filling pressures and cardiac index were monitored during dose efficacy titration. The optimal dose averaged 17 mg given once-daily. All patients were recatheterized three months later. After stabilization of cardiac filling pressures, all patients had left ventricular filling pressures in excess of 18 mmHg. Enalapril increased cardiac index acutely by 34% but at 12 weeks follow-up, cardiac index was not different from control levels. Left ventricular filling pressure was reduced acutely by 36% and by 41% at three months. Heart rate, systemic arterial and right atrial pressures and plasma concentrations of aldosterone were reduced during the observation period. Renin was markedly elevated. These changes were accompanied by marked and sustained clinical improvement and subjective well-being.
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PMID:Sustained haemodynamic effects of enalapril in left ventricular failure. 610 Jun 3

To define the short-term haemodynamic, hormonal and electrolyte effects of enalapril in chronic heart failure, we administered it to nine patients. The first dose (5 mg) induced a gradual reduction in plasma angiotensin II, systemic vascular resistance, arterial pressure, heart rate and right heart pressures, the maximum effects occurring within 4-8 h. Angiotensin II levels were still suppressed 24 h after the initial dose, but haemodynamic indices had returned almost to control values by this time. Dose-related increases in cardiac index and plasma renin, and decreases in angiotensin II, systemic vascular resistance and urine aldosterone excretion were seen with 5, 10 and 20 mg enalapril. Cumulative balances for sodium and potassium were positive, plasma potassium increased and plasma antidiuretic hormone fell. After 4-8 weeks of enalapril therapy, clinical status and exercise tolerance improved in the patients who were most severely restricted initially. Enalapril may be useful in the treatment of chronic heart failure.
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PMID:Acute haemodynamic, hormonal and electrolyte effects and short-term clinical response to enalapril in heart failure. 610 Jun 4

Enalapril (MK-421) is a new angiotensin converting enzyme inhibitor which effectively lowers elevated blood pressure and might also be useful in heart failure. Enalapril was infused into six awake dogs 2 hours after left circumflex coronary artery embolization (acute failure group) and into six other awake dogs two to six months after coronary embolization (chronic failure group). In the acute failure group 2 hours after embolization, increased left ventricular end-diastolic pressure and reduced cardiac output remained unchanged during enalapril infusion. In the chronic failure group, increased left ventricular end-diastolic pressure also remained unchanged during enalapril infusion, but cardiac output, which had fallen to 131.8 +/- 11.9 (S.D.) from 165.8 +/- 17.9 ml/min/kg (P less than 0.01) by two to six months in this group rose during enalapril infusion to 154.5 +/- 27.7 ml/min/kg (P less than 0.05). Heart rate and blood pressure were not changed during enalapril in either group, but stroke volume rose (26.0 +/- 5.9 to 29.2 +/- 6.9 ml, P less than 0.01) and systemic vascular resistance fell (58.5 +/- 10.3 to 39.3 +/- 4.3 units, P less than 0.01) during enalapril only in the chronic failure group. Plasma renin activity after embolization was slightly but not significantly higher in the acute failure group. Thus, enalapril appears to be an arterial vasodilator in dogs with chronic but not acute left ventricular failure.
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PMID:Effects of a new angiotensin converting enzyme inhibitor, enalapril, in acute and chronic left ventricular failure in dogs. 630 67

Enalapril, the new converting enzyme inhibitor, was administered to eight patients with heart failure (NYHA Functional Class II to IV) during standardised and intensive haemodynamic, hormone, and electrolyte monitoring. The first dose (5 mg) of enalapril induced a fall in plasma angiotensin II and noradrenaline levels, and prolonged decrements in systemic vascular resistance, arterial pressure, heart rate, and right heart pressures. Maximum haemodynamic effects were evident four to eight hours after the first dose, with return to baseline by 24 hours. Plasma angiotensin II levels, however, were still suppressed at 24 hours. The magnitude of haemodynamic response was related closely to baseline (pre-enalapril) activity of the renin-angiotensin system and the sympathetic system. Enalapril treatment over three days induced a positive cumulative balance of sodium and potassium, and a small increase in plasma potassium. Urine aldosterone excretion decreased in a stepwise fashion. Continued enalapril administration for four to eight weeks resulted in improved clinical status (NYHA Functional Class) and exercise tolerance in patients who initially were most severely incapacitated, but little change was observed in healthier subjects. We conclude that in heart failure, enalapril is a long acting converting enzyme inhibitor with clear cut beneficial haemodynamic effects in the short term. Long term controlled studies of enalapril in heart failure are warranted.
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PMID:Haemodynamic, hormonal, and electrolyte effects of enalapril in heart failure. 630 3

The effects of a 3-month treatment period with the angiotensin-converting enzyme (ACE) inhibitors trandolapril (0.3 mg/kg/day, p.o.) and enalapril (10 mg/kg/day, p.o.) on hemodynamics, cardiac hypertrophy, and vascular structures were examined in old spontaneously hypertensive rats (SHRs) (24 months at the end of treatment) presenting with congestive heart failure. During the course of treatment, the mortality rate was lower in the two treated groups than in the control group. At the end of treatment, serum ACE activity was inhibited by 63 and 33% by trandolapril and enalapril, respectively, but the decrease in blood pressure they induced was not significant. The atrial natriuretic factor(ANF) plasma levels and cyclic GMP urine excretion were about 10-fold and 3-fold higher, respectively, in old SHRs than in old Wistar rats. These values were markedly decreased by both ACE inhibitors. The ventricular hypertrophy was greatly decreased by both compounds (-24% by trandolapril and -26% by enalapril). In the aorta, the media hypertrophy was significantly decreased and nuclear density increased to a similar extent by both ACE inhibitors. In the mesenteric artery, trandolapril treatment induced a complete regression of the media hypertrophy and a marked decrease in extracellular matrix surface. In addition, the collagen network appeared less dissociated in the treated animals. Similarly the nuclear density was increased and the surface of cell nuclei was decreased by trandolapril. Enalapril appeared much less potent on these parameters. These data demonstrate that treatment with trandolapril of aged SHRs presenting with heart failure results in an increase in survival of the animals and a marked regression of cardiac and vascular hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of subchronic treatment with trandolapril and enalapril on cardiovascular morphologic alterations in the aged spontaneously hypertensive rat with heart failure. 752 99

A repeated-measures study was conducted on 5 dogs to clinically, radiographically, and echocardiographically characterize the actions of the angiotensin-converting enzyme inhibitor, enalapril, before and after development of experimentally induced heart failure. Heart failure was artificially induced, using a surgically implanted programmable ventricular pacemaker, which stimulated the heart at a rate of 245 beats/min until a low-output cardiomyopathic state developed. This condition was then stabilized by decreasing the pacing rate to 190 beats/min. Pacing-induced heart failure was successfully induced in a mean +/- SD 4.2 +/- 1.95 weeks. The condition closely resembled the clinical, radiographic, and echocardiographic features of naturally acquired idiopathic dilated cardiomyopathy in dogs. Enalapril was well tolerated by dogs, and clinical adverse reactions did not develop. Results of echocardiographic studies indicated that enalapril treatment during the control period resulted in a significant (P < 0.05) increase in velocity of circumferential fiber shortening and a significant (P < 0.05) decrease in left ventricular ejection time. Therapeutic responses to enalapril were evident after development of heart failure. These included reduced severity of clinical signs of disease, evidence of decreased radiographically determined cardiac size (2 of 5 dogs), radiographic evidence of a reduction in pulmonary edema and congestion (4 of 5 dogs), significant (P < 0.05) reductions in left atrial and ventricular chamber dimensions (left atrial dimension, diastolic left ventricular internal dimension as determined echocardiographically), and improvement in some echocardiographic indices of left ventricular performance (velocity of circumferential fiber shortening and left ventricular ejection time).
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PMID:Effect of enalapril in dogs with pacing-induced heart failure. 769 55

The introduction of new drugs, and a re-evaluation of older drugs, have radically changed the pharmacological management of heart failure. Angiotensin converting enzyme (ACE) inhibitors, digitalis, diuretics and the combination of nitrates and hydralazine are now used. The first Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS I) and the second Vasodilator therapy in Heart Failure Trial (V-HeFT II) have demonstrated that patients with severe or advanced heart failure should be treated with ACE inhibitors, digitalis and diuretics (other vasodilators can be used if ACE inhibitors are contraindicated) to improve symptoms and duration of life. The Studies Of Left Ventricular Dysfunction (SOLVD) and the Munich Heart Failure trial have shown that patients with mild heart failure should be treated with ACE inhibitors. However, data from several large clinical registries suggest that only 40% of patients with heart failure are being given ACE inhibitors perhaps through fear of serious renal damage or hypotension; these fears are unfounded. Patients with anterior myocardial infarcts and reduced left ventricular function also benefit from ACE inhibitors. The fourth International Study of Infarct Survival (ISIS 4) and results from the Gruppo Italiano per Io Studio della Sopravvivenza nell'Infarto miocardico 3 (GISSI 3) have indicated that patients with acute myocardial infarction benefit from early ACE inhibitor therapy and that survival is increased. Heart failure treatment can be optimized by establishing a disease etiology and stressing the need to restrict dietary sodium. ACE inhibitors should be used for depressed left systolic ventricular function, including patients in New York Heart Association class I heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Optimizing the treatment of heart failure. 782 70

Left ventricular (LV) function and plasma levels of cardiovascular hormones were examined in patients with severe chronic congestive heart failure (CHF), randomized to placebo or enalapril, in addition to conventional therapy. M-mode echocardiography and plasma hormone concentrations were available at baseline and after 6 weeks of treatment. There was a significant relationship between LV systolic function and levels of angiotensin-II and norepinephrine. Enalapril increased LV fractional shortening (FS%) (13.3 +/- 5.6 to 15.4 +/- 5.8, p < 0.05) and decreased the systolic time interval index (0.58 +/- 0.14 to 0.48 +/- 0.15, p < 0.05) concurrent with a significant decrease in angiotensin-converting enzyme activity and in aldosterone, angiotensin-II, and norepinephrine concentrations after 6 weeks. No changes were found in the placebo group. However, there was no direct relationship between the amount of change in neurohormones and improvement in LV function after 6 weeks. These findings indicate that in patients with severe chronic CHF, severe LV systolic dysfunction is associated with high plasma levels of angiotensin-II and norepinephrine, which can be favorably modified by enalapril. This may be of importance for prolonging life in severe heart failure. The lack of relationship between changes in individual hormones and systolic function suggests complex dynamic interaction. It is, therefore, not sufficient to predict changes in LV function by measuring changes in only one hormone.
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PMID:Neuroendocrine activation in relation to left ventricular function in chronic severe congestive heart failure: a subgroup analysis from the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS). 783 34

Heart failure is today one of the most serious health problems of modern industrialized societies. The increase in the mean age of the population is an additional factor which favours a high incidence of episodes of heart failure. Age is also a relevant factor in mortality linked with heart failure. On this basis more emphasis has been given by researchers and physicians to improve a preventive and therapeutic approach to heart failure. For many years the pharmacological treatment of heart failure patients was based on the increase in inotropism through the digitalis and on the reduction in sodium-water retention through diuretics, while less importance was given to the improvement of the afterload. We have had knowledge of vasodilatory drugs in chronic heart failure for at least 20 years but only 10 years ago with the Vasodilator-Heart Failure Trial (V-HeFTI), it was proved that the combination of hydralazine and nitrates in addition to the conventional treatment, improved the survival of patients affected by moderate-severe heart failure. With the advent of the ACE-inhibitors, in the '80s, the first studies concerning the role of such drugs in heart failure were carried out. In the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS I) it was proved for the first time that an ACE-inhibitor (enalapril), added to the conventional heart failure therapy, improved the survival of patients with severe congestive heart failure (NYHA class IV). The result was so extraordinary that the study was interrupted for ethical reasons. However, it has raised a considerable interest in the study of the ACE-inhibitors in heart failure and now it has been proved that such drugs are a milestone in a correct pharmacological approach to heart failure.
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PMID:[The role of ACE inhibitors in heart failure. Lessons of CONSENSUS, SOLVD and V-HeFTII]. 785 51

Clinical evidence accumulated over the past decade suggests that neurohormonal mechanisms significantly influence the pathogenesis and eventual outcome of congestive heart failure (CHF). Pharmacologic modulation of this neuroendocrine activity can, consequently, be expected to improve patient prognosis. Results of several recent clinical trials--the Studies of Left Ventricular Dysfunction (SOLVD), the second Veterans Administration Cooperative Vasodilator Heart Failure Trial (VH eFT-II), and the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS)--provide substantial evidence that addition of the angiotensin-converting enzyme (ACE) inhibitor enalapril to conventional therapeutic regimens can significantly reduce mortality and improve prognosis in patients with all grades of heart failure. Moreover, data from all three trials confirm the involvement of neurohormonal systems in the development and progression of CHF and suggest that the beneficial effects of enalapril in heart failure may in part be due to the suppression of this neurohormonal activity. It is now apparent that some form of neurohormonal activation is present early in the course of the disease before the emergence of overt heart failure symptoms. On the basis of such findings, it would seem that early introduction of therapy targeted at neurohormonal influences may well become a central component of any future CHF treatment program.
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PMID:Neurohormonal mechanisms and the role of angiotensin-converting enzyme (ACE) inhibitors in heart failure. 787 65

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