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

he influence of the neurohumoral system, as adrenergic system or renin-angiotensin system, on cardiac performance in heart failure is not yet know. In order to evaluate the influence of neurohumoral activation in chronic heart failure we followed 51 patients, 47 males and 4 females of mean age 58 +/- 10 years. They suffered from chronic heart failure of different origin and were classified according to NYHA classification: 42 patients were in class III and 9 were in class II. They were treated with digoxin and diuretics since long time. Ejection fraction (EF) was obtained by RVG at baseline and 8 months later. In order to test the influence of adrenergic system on EF we checked plasmatic norepinephrine levels and we divided the patients in two groups: Group A with high levels of plasmatic norepinephrine (1114 +/- 594 pg/ml) and Group B with normal level (426 +/- 139 pg/ml). Group A showed a reduction of EF (-3.73 +/- 1.27%) while, Group B showed a small increase of EF (+ 2.57 +/- 4.32%). To test the influence of renin-angiotensin system we also evaluated the patients according to the value of plasmatic renin activity: normal or high level. We did not observe a significant difference between the 2 groups. Patients with high plasmatic norepinephrine value presented a significant reduction of EF compared to those with low plasmatic norepinephrine. The adrenergic system seems to be more important than renin-angiotensin system or cardiac performance.
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PMID:[Influence of the neurohumoral system on left ventricular performance in chronic congestive heart failure]. 160 May 30

Symptoms of chronic cardiac failure depend on four determinants: The initial event concerns a decrease in contractility. The resulting complex neurohumoral regulatory mechanisms are essentially sympathicomimetic and stimulate the renin-angiotensin system. Accordingly, pre- and afterload will increase and symptoms may become aggravated by dys- or arrhythmias. Symptomatic pharmacotherapy of cardiac failure is directed to these four determinants. The actual rationale for its use is presented, putting emphasis on the renewed controversy on digitalis and on the importance of vasodilators, in particular ACE inhibitors. The relevance of diagnostic evaluation before and during treatment is indicated. The adaptation of treatment according to different causative disorders leading to cardiac failure is outlined. Finally, open questions and unsolved problems are brought up.
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PMID:[Therapy of chronic heart failure]. 160 80

The objective of the present study was to determine whether pretreatment neurohormonal and renal hemodynamic parameters predict the change in renal function with the administration of quinapril, a new angiotensin-converting enzyme (ACE) inhibitor. Twenty patients with New York Heart Association (NYHA) class III and IV heart failure were evaluated. Following pretreatment determination of renal function and plasma neurohormones, patients were treated daily with 10 mg of quinapril. Measurements of glomerular filtration rate (GFR) and renal plasma flow (RPF) were repeated after 7 weeks to assess changes in function (delta GFR and delta RPF). Mean GFR increased from 49 +/- 6 to 56 +/- 7 ml/min/1.73 m2 (p = 0.10), but decreased in five patients. Mean RPF increased from 235 +/- 23 to 252 +/- 23 ml/min/1.73 m2 (p = 0.08), but decreased in five patients. There was no relation between delta GFR and baseline determinations of GFR, RPF, plasma renin activity, plasma angiotensin II, or serum Na. Only a high filtration fraction (GFR/RPF) predicted a decreased GFR (r = 0.61, p less than 0.005). In contrast, no baseline renal hemodynamic parameter correlated with delta RPF. We conclude that poor renal function does not increase the risk of renal deterioration with quinapril. However, dependence of renal function upon the renin-angiotensin system may be predicted by a high filtration fraction.
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PMID:Determinants of the renal response to ACE inhibition in patients with congestive heart failure. 161 96

The diuretic and natriuretic response to an intravenous dose of frusemide 40 mg was assessed in the erect and supine positions in 10 patients with cardiac failure who were being treated with enalapril 10 mg twice daily in addition to diuretics (Enalapril group) and in 10 patients with cardiac failure taking diuretics alone (Control group). Total 4 h diuresis in the erect position was 728 ml and in the supine position was 824 ml in the patients taking enalapril compared to 655 ml in the erect position and 1166 ml in the supine position in those patients taking diuretics alone. Total 4 h natriuresis in the erect positions was 78 mmol and in the supine position was 85 mmol in patients taking enalapril 10 mg twice daily but in those patients taking diuretics alone total 4 h natriuresis in the erect position was 67 mmol increasing to 120 mmol in the supine position. Measurements of plasma renin activity and plasma angiotensin II concentration confirmed effective converting enzyme inhibition, in the group of patients taking enalapril, but in those patients taking diuretics alone the erect position was associated with an increase in plasma renin activity, and plasma concentrations of angiotensin II and aldosterone. We conclude that the renin angiotensin system is a major factor in mediating the effect of posture on loop diuretic drugs.
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PMID:The influence of posture on the response to loop diuretics in patients with chronic cardiac failure is reduced by angiotensin converting enzyme inhibition. 162 97

Therapeutic approaches to the management of heart failure have traditionally focused on shortterm hemodynamic and symptomatic goals, but present evidence suggests that most therapeutic decisions have long-term consequences. Treatment may change the rate of disease progression, modify the need for additional therapy, influence the number of hospitalizations, and alter the risk of death. However, there may be little relation between a drug's short-term effect on cardiac function or cardiovascular symptoms and its long-term effect on survival. Some therapeutic interventions favorably influence the outcome of patients with heart failure, even though they exert negative inotropic effects; others adversely affect the outcome of patients, even though they markedly improve cardiac performance. This discordance might be explained if the most important predictor of response to a therapeutic intervention in heart failure were the effect of the pharmacologic agent on neurohormonal systems rather than on hemodynamic variables. In general, drugs that decrease the effects of the sympathetic nervous system (digitalis glycosides) and the renin-angiotensin system (angiotensin-converting enzyme [ACE] inhibitors) reduce the risk of worsening heart failure. Conversely, drugs that potentiate the effects, or increase the activity, of the sympathetic nervous system (phosphodiesterase inhibitors) or the renin-angiotensin system (calcium antagonists) increase cardiovascular morbidity and mortality. These observations suggest that physicians should no longer focus on short-term hemodynamic or symptomatic goals in the treatment of heart failure but, instead, should manage patients to improve both the quality and quantity of life.
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PMID:Long-term strategies in the management of heart failure: looking beyond ventricular function and symptoms. 162 88

The hemodynamic, hormonal, and renal effects of angiotensin II-type 1 receptor antagonism (AT1A) have not been documented previously in heart failure (HF) or compared with angiotensin-converting-enzyme inhibition (ACEI). Accordingly, we investigated the acute (2-h) response to losartan (1 and 10 mg/kg iv) or vehicle (N saline) followed by captopril (12.5 mg) on separate days in an ovine model of HF induced by 7 days of rapid ventricular pacing. Losartan induced a significant rise in plasma renin activity (PRA) and plasma angiotensin II levels (P less than 0.01 and P less than 0.001, respectively), in association with a fall in the plasma aldosterone-to-PRA ratio (P less than 0.001) and plasma atrial natriuretic peptide (P less than 0.05). Mean arterial and left atrial pressure both fell significantly after losartan (P less than 0.001), whereas the rise in cardiac output was not sustained. The response to captopril was similar except for plasma angiotensin II, which declined (P less than 0.001). Glomerular filtration and urine sodium excretion were maintained despite a fall in renal perfusion pressure. In conclusion, the vasodilatation and renal effects of AT1A were similar to ACEI. Thus AT1A may be a useful therapeutic alternative to ACEI in HF.
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PMID:Angiotensin II receptor antagonism in ovine heart failure: acute hemodynamic, hormonal, and renal effects. 163 62

Chagas disease is a leading cause of heart failure in Latin America. Sudden death occurs in approximately 40% of patients with heart failure due to Chagas disease. We report a single blind, cross-over trial of prolonged treatment with captopril and placebo in 18 Chagas disease patients with class IV NYHA heart failure. Ventricular dimensions, neurohormones, electrolytes and ventricular arrhythmias were analysed in 11 men and seven women receiving stable doses of digoxin and frusemide who were randomly divided into two intervention groups. Group I patients were given increasing doses of captopril up to 150 mg.day-1 maintained for 6 weeks, group II received the placebo. A 24 h Holter, 2-D echocardiogram, urinary catecholamines, plasma renin and electrolyte determinations were performed at the end of each phase. After a 2-week washout period, the two groups crossed over and another period of 6 weeks was observed. Ventricular arrhythmias were analysed by either Mann-Whitney or the Wilcoxon test. Remaining data were assessed by the Student t-test. A significant reduction in heart rate and urinary catecholamine levels, and enhanced plasma levels of renin, together with a reduction in ventricular couplets was found in the captopril-treated group. We conclude that captopril has a beneficial effect on neurohormones with a subsequently reduced heart rate and diminished incidence of ventricular arrhythmias in patients with Chagas disease. This effect might result in a reduction of mortality caused by the disease, suggesting the need for further investigations.
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PMID:Chagas cardiomyopathy and captopril. 164 89

The effect of diuretic dose on the haemodynamic response to captopril was assessed in nine patients with chronic cardiac failure. Each patient was given an intravenous dose of captopril while maintained on (a) a low dose diuretic regime, and (b) a high dose diuretic regime. Activity of the renin angiotensin aldosterone system, as assessed by plasma concentrations of these hormones, was greater when patients were receiving the higher dose diuretic regime. The magnitude of haemodynamic response produced by intravenous captopril was greater when the patients were maintained on the high dose diuretic regime, although no significant correlation was found between resting plasma renin activity and resting plasma angiotensin II concentration and the change produced by captopril in any haemodynamic response on either diuretic regime. An increased dosage of loop diuretic potentiates the haemodynamic effects of captopril in patients with cardiac failure. Reduction of diuretic dose prior to introduction of captopril may protect against severe first dose hypotension.
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PMID:The relationship between diuretic dose, and the haemodynamic response to captopril in patients with cardiac failure. 164 90

Renal plasma flow (RPF), glomerular filtration rate (GFR), renal proximal tubular delivery of sodium and water evaluated by lithium clearance, and hormonal parameters were measured in 12 patients with congestive heart failure NYHA class II-IV before and after captopril treatment for 4 wk and in 13 healthy control subjects. RPF and GFR were significantly decreased in heart failure, whereas the filtration fraction (FF) was increased. Treatment with captopril increased RPF and decreased FF, whereas GFR was unchanged. Total and fractional urinary excretion of sodium were reduced in the patients compared with the controls, but increased after captopril. Fractional excretion of lithium was normal in heart failure and was increased by captopril. Atrial natriuretic peptide, guanosine 3',5'-cyclic monophosphate, and aldosterone in plasma were significantly elevated in heart failure and were reduced by treatment with captopril. Plasma renin activity was increased in patients, correlated inversely with RPF, and increased further after captopril treatment. It is concluded that the reduced sodium excretion in heart failure was caused by a combination of diminished glomerular filtration and enhanced tubular reabsorption beyond the proximal tubule and that treatment with captopril increased urinary sodium excretion partly due to an attenuated sodium reabsorption in the proximal tubule. The present data in patients with congestive heart failure are consistent with an increased intrarenal angiotensin II generation and an elevated plasma level of aldosterone being involved in the pathogenesis of the glomerular hemodynamic changes and the enhanced distal tubular reabsorption, respectively.
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PMID:Mechanisms of sodium retention in heart failure: relation to the renin-angiotensin-aldosterone system. 164 90

In addition to the circulating renin-angiotensin system, recent data demonstrate the existence of tissue renin-angiotensin systems that may be important in cardiovascular homeostasis. However, the relative activities of the circulating and tissue renin-angiotensin systems have not been examined previously in pathophysiological states, such as congestive heart failure. The present study was performed to examine the status of plasma and tissue angiotensin converting enzyme (ACE) activities in compensated experimental heart failure induced by coronary artery ligation in the rat. Three groups of male Sprague-Dawley rats were examined: 1) nonoperated rats (NO, n = 5), 2) sham-operated rats (SO, n = 5), and 3) heart failure rats (HF, n = 11). Rats were studied an averaged of 85 days postoperatively. In HF animals, plasma renin concentration and serum ACE activities were not different compared with NO and SO control animals. Cardiac ACE activity was 50% greater in the right ventricle than the interventricular septum in NO and SO rats. Both right ventricular and interventricular septal ACE activity increased approximately twofold in HF animals as compared with NO and SO groups (p less than 0.05). In contrast, pulmonary, aortic, and renal ACE activities were not altered in HF rats compared with control animals. A positive correlation existed between the histopathological size of myocardial infarction and the level of right ventricular ACE activity (r = 0.75, p less than or equal to 0.05). Such a relation between infarct size and either serum or noncardiac tissue ACE activities was not observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tissue-specific activation of cardiac angiotensin converting enzyme in experimental heart failure. 165 Feb 97


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