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

1. To determine the response of plasma atrial natriuretic peptide (ANP) to treatment with an angiotensin converting enzyme (ACE) inhibitor in heart failure, seven patients (NYHA Functional Class III-IV) were studied before and after the addition of ramipril to maintenance digoxin and diuretic treatment. 2. Baseline arterial ANP levels were raised, but fell during ramipril treatment in parallel with changes in both haemodynamic recordings (arterial pressure, pulmonary artery diastolic pressure, and right atrial pressure) and hormone levels (angiotensin II and aldosterone). 3. Coronary sinus ANP, measured in three patients, was greater than concomitant arterial levels, and the coronary sinus ANP secretion rate was calculated to be between 15 and 119 pmol/min. 4. These results demonstrate that improvement in haemodynamic function during ACE inhibitor treatment is associated with a decline in elevated ANP levels, and support the concept that atrial stretch or pressure regulates the secretion of atrial peptides in man.
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PMID:Atrial natriuretic peptide levels in congestive heart failure in man before and during converting enzyme inhibition. 252 56

The renal response to atrial natriuretic factor (ANF) has been shown to be blunted in several experimental models of acute and chronic congestive heart failure. The mechanism responsible for this blunted response has been postulated to be activation of the renin-angiotensin system with associated potent antinatriuretic effects and/or the reduction in renal perfusion pressure (RPP) characteristic of heart failure. The present study was designed to examine the relative role of these two factors in mediating the blunted response to ANF in a model of acute low output heart failure produced by thoracic inferior vena cava constriction (TIVCC) in the anesthetized dog. TIVCC was produced in five groups of dogs. In group 1, ANF was infused after TIVCC to document the blunted natriuretic response. In group 2, ANF was infused after TIVCC in the presence of blockade of intrarenal angiotensin II (ANG II) by the intrarenal infusion of saralasin (Sar) at a dose without systemic effects. In group 3, ANF was infused after TIVCC in the presence of restoration of RPP by infusion of ANG II at a dose titrated to restore RPP to the level present before TIVCC. In group 4, ANF was infused in the presence of restoration of RPP with ANG II and blockade of intrarenal ANG II with Sar. Group 5 served as an additional control group where the effect of ANG II and Sar in TIVCC was examined in the absence of ANF. Restoration of RPP but not blockade of intrarenal ANG II resulted in a restoration of the response of sodium excretion and glomerular filtration rate to ANF. ANG II plus Sar in the absence of ANF did not produce a natriuresis. We conclude that RPP, more than intrarenal ANG II, modulates the blunted renal response to ANF observed in this model of acute low-output heart failure.
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PMID:Restoration of renal response to atrial natriuretic factor in experimental low-output heart failure. 252 85

Congestive cardiac failure is a syndrome in which a decrease of cardiac output triggers a series of neuro-humoral compensatory mechanisms in part involving the kidney. In this response, dysfunction of atrial volume receptors as well as disturbances of the autonomic nervous system have recently been demonstrated and are held responsible for excessive stimulation of angiotensin II, followed by adverse regulatory effects. Renal hemodynamic compensation for heart failure primarily involves constriction of efferent arterioles thereby defending glomerular filtration. In this setting, the occurrence of prerenal insufficiency is indicative of a far advanced reduction in renal blood flow. Apparent diuretic resistance in the treatment of heart failure is usually caused by iatrogenic vascular compromise or by the use of a single diuretic rather than an appropriate combination. Hyponatremia, vasopressin stimulation and elevation of plasma N-epinephrine concentration have been found to be the most reliable indicators of a poor prognosis of heart failure. Atrial natriuretic peptide is stimulated in proportion to the degree of atrial distension in heart failure, however its intrarenal effects are markedly blunted or may even be absent in this particular disease.
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PMID:[Kidney function in heart failure]. 253 Mar 91

Alterations in the vasopressor system found in cardiac failure are part of compensatory measures that may modify pharmacologic-therapeutic response. Therefore, in 64 patients with dilated cardiomyopathy, we investigated its enhanced activity in different clinical stages of the disease as compared to normal controls. Patients in NYHA class II (n = 20) demonstrated increased activity of the sympathico-adrenal, renin-angiotensin-aldosterone, vasopressin, and atrial natriuretic factor systems, while maximum values were found in patients of NYHA class IV (n = 24). In these patients, noradrenaline was enhanced by a factor of 7, adrenaline by a factor of 2, plasma-renin-activity by a factor of 7, angiotensin II by a factor of 2.5, aldosterone by a factor of 5, vasopressin by a factor of 1.5, and ANF by a factor of 4 as compared to normal controls. Clinical NYHA classes correlated to a certain degree with the various plasma hormones. Patients treated with an aldosterone inhibitor in addition to digitalis and diuretics revealed significantly higher values for aldosterone, vasopressin, and angiotensin II as compared to those who received digitalis and diuretics alone. The addition of ACE-inhibitor therapy resulted in a decrease of angiotensin II, aldosterone, and vasopressin. Plasma catecholamines and ANF, however, did not change under the influence of cardiac medication. Diuretic treatment in NYHA class II patients reduced plasma volumes (p less than 0.01). Plasma volume in NYHA class IV patients only was found to be higher than in normal controls. Thus, analysis of the neurohumoral system can aid both in the identification of the clinical degree of dilated cardiomyopathy and in its optimal therapy.
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PMID:The vasopressor system in patients with heart failure due to idiopathic dilated cardiomyopathy--influence of the clinical stage of disease and of chronic drug treatment. 253 2

Angiotensin-converting enzyme (ACE) inhibitors are of benefit in the management of heart failure. In some studies in patients with heart failure, a decline in renal function occurred more frequently in patients treated with enalapril maleate, a longer-acting agent, than in those treated with captopril, a shorter-acting drug. Patients experiencing a decline in renal function had a number of predisposing hormonal and hemodynamic factors. In one report, these factors included an initial fall in blood pressure that was sustained, lower cardiac output, and a relatively high fixed dose of enalapril that contributed to renal impairment. In a second study, the decline in renal function was most severe in patients with a lower systemic arterial pressure in whom glomerular filtration may have been dependent on angiotensin II. In a third study, intravascular volume depletion and an activated renin-angiotensin system led to reduced renal function. Reduction of angiotensin II level in plasma and tissues by ACE inhibitors decreases systemic vascular resistance and efferent arteriolar tone, which tends to decrease glomerular filtration rate. If compensatory increases in cardiac output are inadequate or preexisting renal impairment or volume depletion is present, renal function will deteriorate. Long-acting ACE inhibitors prolong the decreased efferent arteriolar tone and may compromise cardiac muscle response to catecholamines. The use of shorter-acting agents in patients who exhibit deterioration in renal function may be preferable.
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PMID:Renal hemodynamic consequences of angiotensin-converting enzyme inhibition in congestive heart failure. 253 12

The two major causes of death in congestive heart failure (CHF) are progressive heart failure (approximately 60% of cases) and sudden death (30%). Sudden death in CHF is caused primarily by malignant ventricular arrhythmias. The underlying mechanism has yet to be established, but myocardial metabolic factors are probably involved. Although there is a clear association between complex ventricular arrhythmias and left ventricular function, it has not been shown convincingly that antiarrhythmic agents can reduce sudden death in CHF. Progressive deterioration of myocardial function is associated with altered myocardial energy production. Notably, the physiological effects of neuroendocrine activation in chronic CHF may be deleterious to myocardial function. The CONSENSUS study was carried out to evaluate the association between neuroendocrine activation and deterioration of myocardial function using ACE inhibitors. A marked reduction in mortality rate occurred in the enalapril-treated group, where the one-year mortality was reduced by 31%. The reduction in mortality was solely among patients with progressive CHF (a reduction of 50%); there was no difference in the incidence of sudden death. Analysis of blood samples drawn at baseline in the placebo group showed a significant positive correlation between mortality and plasma angiotensin II (P less than 0.05), aldosterone (P = 0.003), noradrenaline (P less than 0.001), adrenal levels (P less than 0.001), and atrial natriuretic peptide (P = 0.003). This was not observed in enalapril-treated patients. The significant reduction in mortality in the enalapril group was found consistently among patients with baseline hormone levels above the median value. In CHF, the underlying disease may induce serious arrhythmias and/or progressive failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms for improved survival in heart failure. 255 Jun 46

Congestive heart failure is a complex clinical syndrome characterized by circulatory and metabolic abnormalities. It has been apparent for more than 25 years that the sympathetic nervous system and the renin-angiotensin-aldosterone system are markedly activated in the late stages of heart failure. These two systems interact to facilitate sympathetic drive and promote salt and water retention. Circumstantial evidence is now accumulating to indicate that excessive sympathetic drive and angiotensin II activity may contribute to the pathophysiology of heart failure. These observations suggest that a dual strategy of modulating sympathetic nervous system activity to the heart while blocking angiotensin II activity may provide a rational therapeutic approach to the treatment of heart failure. Xamoterol, a beta 1 partial agonist, may enhance myocardial contractile force in the steady state, while acting to inhibit excessive sympathetic drive during exercise or severe heart failure. The concomitant use of a converting-enzyme inhibitor would be expected to blunt the detrimental effects of excessive angiotensin II activity. Modulation of adrenergic drive coupled with inhibition of marked angiotensin II activity may be potentially more effective in the treatment of congestive heart failure than either strategy used alone.
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PMID:The relationship of the sympathetic nervous system and the renin-angiotensin system in congestive heart failure. 257 May 21

Angiotensin II can stimulate the sympathetic system and inhibit vagal (parasympathetic) outflow under experimental circumstances in animals. Blockade of angiotensin II formation by angiotensin-converting enzyme (ACE) inhibitors might therefore be expected to result in a reduction of sympathetic activity and enhanced parasympathetic activity. Whether this is so in normotensive or hypertensive humans and in human cardiac failure is unclear, since available techniques for recording activity of the sympathetic and parasympathetic systems are imperfect. Nevertheless, most evidence that comes from measurements of venous norepinephrine suggests that the ACE inhibitors have little or no effect on sympathetic activity in normotension and hypertension, although the activated sympathetic system in severe cardiac failure is probably suppressed. It appears that the ACE inhibitors have a parasympathomimetic action that may contribute to the hemodynamic effects of these drugs. Additional information using direct recordings of sympathetic traffic or measurements of norepinephrine "spillover" is needed to clarify the effects of ACE inhibitors on the sympathetic system.
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PMID:Sympathetic nervous system during converting enzyme inhibition. 257 49

Vasoactive humoral factors were measured in 27 patients before and during the first week of conventional treatment of acute heart failure. On admission, all patients were given frusemide intravenously, followed by oral digoxin and diuretic therapy. Before drug treatment, plasma renin activity and plasma angiotensin II concentrations were within normal ranges in the group of patients without previous diuretic treatment, but were significantly higher in those 16 patients already on diuretic drugs when admitted to hospital. After diuretic treatment, however, even the former group revealed activation of the renin-angiotensin system. Plasma concentrations of catecholamines were increased initially but normalized within 1 day. A majority of the patients initially had very high plasma concentrations of atrial natriuretic peptide (mean 276.9 +/- 39.0 pg ml-1) which decreased but did not normalize during the study period. High plasma levels of arginine vasopressin (mean 56.8 +/- 14.6 pg ml-1) were found, but tended to be reduced during treatment. Thus, patients with acute heart failure displayed increased plasma concentrations of atrial natriuretic peptide, arginine vasopressin and catecholamines, but these vasoactive hormones decreased in parallel to clinical improvement during diuretic therapy. In contrast, the renin-angiotensin system became clearly activated.
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PMID:Neuroendocrine response in acute heart failure and the influence of treatment. 257 29

The renin-angiotensin-aldosterone system plays an important role in the development of congestive heart failure (CHF). In patients with chronic heart failure, angiotensin-converting enzyme (ACE) inhibitors, such as captopril, enalapril, and quinapril, have been shown to improve hemodynamics, reduce symptoms of fatigue and dyspnea, increase exercise capacity, correct hyponatremia, reduce diuretic requirements and ventricular arrhythmias, and conserve potassium and magnesium. ACE inhibitors reduce circulating levels of angiotensin II and aldosterone and may reduce plasma norepinephrine and vasopressin levels. They are equally effective in patients with mild to moderate heart failure and in patients with severe cardiac impairment. ACE inhibitors are at least as beneficial as digitalis in patients with mild heart failure, and they may even be considered as first-line therapy. Promising results have also been obtained in patients with myocardial infarction, in whom long-term therapy with ACE inhibitors has prevented an increase in heart size. ACE inhibitors improve prognosis in patients with severe heart failure and in patients with hyponatremia; the question of effect on survival in mild to moderate heart failure has yet to be answered.
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PMID:ACE inhibitors in congestive heart failure. 267 Feb 20


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