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)

Angiotensin converting enzyme inhibitors are known to improve cardiac performance in patients with severe heart failure, and are probably safer and more effective than other vasodilators. Less is known about their effects in mild and moderate heart failure. Results at one year are presented about an ongoing double-blind, placebo-controlled parallel-group study on 94 outpatients in New York Heart Association functional class II and III. After a three-week period during which appropriate doses of digoxin were administered and a stable response to exercise was obtained, diuretic therapy was withdrawn if in use and captopril or placebo treatment was assigned randomly. The assessment of patients was performed by symptom history, clinical examination, New York Heart Association functional class, chest radiograph, 12-lead electrocardiogram, 24-hour Holter monitoring, M-mode echocardiography, and bicycle exercise at the time of random selection and at specified times during a two-year follow-up. Preliminary data after one year suggest that patients receiving placebo may have a greater tendency to need diuretics and may improve New York Heart Association functional class less often than those receiving captopril. No statistically significant treatment differences were found for the noninvasive test results. Detailed analysis suggests that treatment with an angiotensin converting enzyme inhibitor may be more advantageous than that with placebo for some groups of patients. Investigations are under way to determine which patients might benefit most from angiotensin converting enzyme inhibitors.
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PMID:Converting enzyme inhibition and heart failure. 306 4

Angiotensin II (AII), aldosterone (Aldo) and arginine vasopressin (AVP) in plasma were determined during basal conditions in seventeen patients with congestive heart failure and in seventeen control subjects. The same parameters were measured before and 1, 2 and 3 h after an oral water load of 20 ml (kg body weight)-1 together with urine volume (V) and free water clearance (CH2O) in seven patients with congestive heart failure and in seven control subjects. AII, Aldo and AVP were significantly higher in heart failure than in control subjects (AII:81 and 12 pmol l(-1) (medians), P less than 0.01; Aldo: 411 and 103 pmol l(-1), P less than 0.01; AVP: 5.3 and 2.0 pmol l)-1), P less than 0.01). AVP was positively correlated to Aldo in both heart failure (p = 0.593, n = 17, P less than 0.02) and control subjects (p = 0.511, n = 17, P less than 0.05), but in neither of the groups to AII. V and CH2O were significantly lower in heart failure when compared to control subjects (maximum increase in CH2O 3.55 and 5.86 ml min-1, P less than 0.02), but did not correlate directly with either A II, Aldo or AVP. Creatinine clearance was reduced in heart failure. It is concluded that the activity of both the renin-angiotensin-aldosterone system and the osmoregulatory system is enhanced in congestive heart failure, presumably as a compensatory phenomenon in order to maintain arterial blood pressure. It is suggested that the decrease in free water clearance may be attributed to both an elevated level of vasopressin and a reduced glomerular filtration rate.
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PMID:Angiotensin II, aldosterone and arginine vasopressin in plasma in congestive heart failure. 308 74

We examined existing evidence concerning the relative efficacy of various vasodilator agents in chronic congestive heart failure. Only randomized placebo-controlled trials with clinical end points and treatment durations of four weeks or more were selected from an exhaustive search of the English-language medical literature. Twenty-eight trials involving 1976 patients were found. Treatment durations of the trials varied from one month to two years. Patients with symptomatic heart failure despite digitalis and diuretic therapy were studied; most were middle-aged men and approximately half had coronary artery disease. Results of the trials were appraised by three independent observers, and mortality and functional status outcomes were pooled in a meta-analysis. All vasodilator agents except hydralazine hydrochloride were associated with improvements in functional status. Angiotensin converting-enzyme inhibitors were the only agents associated with both decreased mortality (odds ratio, 0.51; 95% confidence interval, 0.34 to 0.75) and improved functional status (odds ratio, 4.53; 95% confidence interval, 3.46 to 5.92). The optimal timing for initiation of these agents was not established.
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PMID:Relative efficacy of vasodilator therapy in chronic congestive heart failure. Implications of randomized trials. 328 14

To diagnose latent dilated cardiomyopathy (latent DCM), we performed loading echocardiography with Angiotensin II and ergometer exercise in 41 patients. Twenty-one patients were suspected of having latent DCM because of histories, of heart failure of myocarditis; 10 patients had DCM; and 10 normal persons served as controls. On angiotensin II loading, cardiac function deteriorated in the DCM group, but it was maintained in the normal controls. Nine patients in the latent DCM group showed the same pattern as normals (L1-group), and 12 did as the DCM group (L2-group). Although % fractional shortening, end-diastolic and end-systolic dimensions of the left ventricle did not differ between the L1 and L2-groups, the A/R, the ratio of the pulsed Doppler echocardiogram at the left ventricular inflow tract, was larger and the exercise change of the % fractional shortening and exercise tolerance were less in the L2-group than in the L1-group. Furthermore, the biopsy findings of the L2-group were similar to those of the DCM group in terms of myocardial degeneration, myocardial hypertrophy and interstitial fibrosis. Thus, patients in the L2-group were thought to have a risk for DCM, and were cases of latent DCM. Angiotensin II loading is thought to be useful for diagnosing such cases.
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PMID:[A trial diagnosis of latent dilated cardiomyopathy]. 350 4

Angiotensin converting enzyme inhibitors are effective therapy in hypertension. They are particularly useful in severe drug resistant or accelerated hypertension, in renal hypertension and in hypertensive heart failure. Although their exact mode of action has not been determined it is a consequence of the inhibition of angiotensin converting enzyme. They offer distinct advantages over conventional drugs in the treatment of high blood pressure particularly as they have no central or autonomic side effects and as a consequence the patients feel well. There is no postural effect on blood pressure and patients retain their normal cardiovascular reflex mechanisms and sexual function. They are particularly useful when combined with diuretics or salt restriction as not only do they have additive hypotensive effects but angiotensin converting enzyme inhibitors prevent the secondary hyperaldosteronism and hypokalemia associated with diuretic administration. Lastly, unlike many other forms of treatment for hypertension, renal blood flow and renal function tend to be maintained with converting enzyme inhibitors. Their overall role in the management of hypertension has yet to be determined, and the ultimate incidence of adverse effects after prolonged therapy is not yet known. They are however, an exciting new development in the treatment of hypertension.
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PMID:Treatment of hypertension with angiotensin converting enzyme inhibitors. 609 8

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

The available evidence suggests that angiotensin plays an important role in sodium homeostasis not only via aldosterone release but also through control of the renal circulation, and thereby renal sodium handling. Perhaps this intrarenal action is the renin-angiotensin system's original, primitive function. Through its vascular action, angiotensin has an important influence on glomerular filtration and tubular reabsorption. Angiotensin almost certainly also has an additional intraglomerular action. More circumstantial, but compelling, evidence suggests that angiotensin contributes to the renal response in a host of conditions characterized by renal vasoconstriction, a reduction in filtration rate, and sodium retention, including heart failure, cirrhosis of the liver, complications of pregnancy, the renal response to trauma and shock, and in selected patients with essential and secondary hypertension. Pharmacologic interruption of the renin-angiotensin system is proving useful not only for blood pressure control in patients with hypertension but also because of its influence on the kidney in some or all of these conditions--at least in part attributable to restoration of more normal renal sodium handling.
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PMID:The renin-angiotensin system and sodium homeostasis. 620 38

The relationships between hemodynamic state and plasma components of the renin-angiotensin and adrenergic nervous systems were studied in 42 patients admitted to an intensive care unit with acute heart failure. Patients were allocated to four subsets according to cardiac output and pulmonary wedge pressure. Plasma renin activity and angiotensin II were abnormally high in most patients with cardiac output less than or equal to 3.81 X min-1 and pulmonary wedge pressure greater than or equal to 18 mm Hg in contrast with values of patients of the 3 other subsets, which overlapped the normal range. On the other hand, plasma catecholamines were abnormally high in most patients. Angiotensin II was positively correlated with pulmonary wedge pressure, urea and catecholamines and negatively correlated with cardiac output and natremia. Norepinephrine was uncorrelated with hemodynamic parameters but epinephrine was negatively correlated with cardiac output. A discriminant linear function was calculated for prognosis of survival: cardiac output was the most important factor. The rise of angiotensin II and epinephrine were not unfavorable factors if their correlations with other factors (e.g. cardiac output and urea) were taken into account.
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PMID:Relationships between plasma epinephrine, norepinephrine, dopamine and angiotensin II concentrations, renin activity, hemodynamic state and prognosis in acute heart failure. 637 23

New agents for treating chronic heart failure include angiotensin converting enzyme (ACE) inhibitors, betablockers and phosphodiesterase inhibitors. The ACE inhibitors represent the major therapeutic advance of the 1980-1990 decade. This is the most effective class of drugs on survival, whatever the stage of heart failure and it shows the evolution towards symptoms in asymptomatic patients. Studies currently under way are evaluating the dose-effect relationship of ACE inhibitors. Betablockers improve the quality of life and physical performance but a benefit on mortality has not been shown in two recent trials. Phosphodiesterase inhibitors improve quality of life and physical performance at the price of an increase in mortality. Therefore, they are not indicated in the treatment of heart failure. However, new molecules such as vesnarininone or pimobendan are under trial. Finally, in the next few years, the introduction of antagonists to Angiotensin II receptors is eagerly awaited.
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PMID:[Treatment of chronic heart failure: current views]. 748 9

Neurohormonal activation may provide a pathophysiological link between acute myocardial infarction and chronic congestive heart failure, and modulation of neurohormonal activity may be an important therapeutic target in these conditions. Plasma neurohormones were studied in 55 patients with acute myocardial infarction. Angiotensin II, noradrenaline and ANP were elevated in the early phase but tended to normalize during the first week in patients without signs of heart failure. In patients with heart failure angiotensin II and noradrenaline remained elevated for 1 month and ANP for 4-6 months. During head-up tilt, angiotensin II and noradrenaline increased most in patients with heart failure. In patients with a first myocardial infarction there was a positive correlation between sustained neurohormonal activity and infarct size. Almost complete suppression of plasma ACE activity was achieved within 30 min in 48 patients treated with intravenous enalaprilat, initiated within 24 h from the onset of infarction. The drug was tolerated in dosages of 1.0-1.2 mg given over 1-2h. Patients with systolic blood pressure between 100 and 110 mmHg incurred a greater risk of hypotension than those with higher blood pressure at baseline. Tolerance was not worse among patients treated with intravenous diuretics, metoprolol or nitroglycerin. A total of 98 patients were randomized to treatment with enalapril or placebo, initiated within 24 h from onset of infarction and continued for 4-6 months. During treatment there were no significant differences in plasma levels of angiotensin II, aldosterone, ANP or catecholamines between groups. Echocardiographic recordings were performed in 28 patients. Among patients on placebo there was a positive correlation between plasma levels of noradrenaline at days 5-7 and the increase in left ventricular volumes during the study period, and an inverse correlation between plasma aldosterone at days 5-7 and the increase in left ventricular ejection fraction during the study. No such correlation was found among patients on enalapril. ANP levels at 1 month correlated inversely with the left ventricular ejection fraction at the same time. Plasma neurohormones were measured in 223 patients with mild or moderately severe chronic heart failure, randomized to treatment with ramipril or placebo for 3 months. There was wide variation in hormone levels. Noradrenaline and aldosterone correlated inversely with exercise duration at baseline. Noradrenaline correlated positively with the degree of symptoms. Aldosterone and ANP were reduced with ramipril compared with placebo. Noradrenaline was reduced among patients with baseline levels in the highest tertile. Plasma hormones were also measured at peak exercise in 54 patients. Hormonal levels at rest correlated strongly with those at peak exercise.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neurohormonal activation in patients with acute myocardial infarction or chronic congestive heart failure. With special reference to treatment with angiotensin converting enzyme inhibitors. 759 49


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