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

Studies were performed in anesthetized control dogs (n = 6) and in dogs (n = 6) with acute low-output heart failure produced by inflation of a balloon in the thoracic inferior vena cava. Studies were designed to determine the effects of synthetic atrial natriuretic peptide on renal function and renin release in this acute high-renin, sodium-retaining preparation. Intrarenal infusion of synthetic atrial natriuretic peptide (0.3 micrograms X kg-1 X min-1) resulted in decreases in arterial pressure and renal blood flow in both groups. Glomerular filtration rate increased in both low-output (delta + 10.7 +/- 3.1 ml/min) and control (delta + 8.7 +/- 2.9 ml/min) groups. Fractional lithium excretion, a marker of proximal tubule reabsorption, also increased in both low-output (delta + 12.0 +/- 4.6%) and control (delta + 14.3 +/- 5.0%) groups. Renin secretory rate decreased in the low-output group from 852.8 +/- 183.0 to 149.5 +/- 73.7 ng/min and in the control group from 308.5 +/- 84.5 to 44.5 +/- 27.5 ng/ml. Intrarenal infusion of atrial natriuretic peptide resulted in an attenuated increase in both urinary sodium excretion (delta + 42.3 +/- 10.7 vs delta + 201.2 +/- 37.9 mueq/min) and fractional excretion of sodium (delta + 0.48 +/- 0.13% vs delta + 2.85 +/- 0.45%) in the low-output as compared with the control group. Our studies demonstrate that administration of synthetic atrial natriuretic peptide results in an increase in glomerular filtration rate and a decrease in proximal tubule reabsorption, as estimated by lithium excretion, in both control dogs and those with acute low-output heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of synthetic atrial natriuretic peptide on renal function and renin release in acute experimental heart failure. 316 63

The prognosis in patients with heart failure secondary to left ventricular dysfunction is poor. Although survival can be related to the extent of cardiac functional impairment, many patients die suddenly rather than in refractory heart failure. Ambulatory electrocardiography has revealed a high prevalence of simple and complex ventricular arrhythmias in these patients, which was the most important predictor of subsequent mortality in our patients. Factors predisposing to arrhythmias are many, but increased catecholamines and electrolyte abnormalities are among the more obvious. In patients who have undergone treatment for congestive heart failure, serum and total body potassium are reduced, and this is closely and inversely related to the state of activation of the renin-angiotensin system. Renin and noradrenaline are also closely and directly correlated, while both are inversely related to the arterial pressure. Treatment with angiotensin-converting enzyme inhibitors tends to reverse these neuroendocrine and electrolyte abnormalities and reduces the frequency of ventricular arrhythmias. Whether this will have a favorable impact on mortality, and, in particular, on sudden death, remains to be seen.
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PMID:Arrhythmias, catecholamines and electrolytes. 329 95

As the characteristics of sodium and water balance in heart failure remain undefined, we evaluated the hemodynamic, metabolic, and hormonal effects of balanced sodium intake in 10 patients with chronic congestive heart failure. We discontinued diuretics to avoid their confounding influence, and all patients received 1 wk of 10 meq and 100 meq balanced sodium intake and controlled free water. Comparing sodium intake of 10 with 100 meq, the following observations were made. There was weight gain (2.0 kg) and increased sodium excretion (11 +/- 3 to 63 +/- 15 meq/24 h), unaccompanied by increase of blood volume. Both renin-angiotensin system and sympathetic nervous system activity were greater during the 10 meq diet, and suppressed with the 100 meq sodium diet. For both diets, plasma renin and urinary aldosterone excretion were correlated with urinary sodium excretion (r = -0.768, r = -0.726, respectively; P less than 0.005). Systemic hemodynamics were minimally changed with increased sodium intake. However, reversal of vasoconstriction by captopril during the 10 meq diet, and its ineffectiveness during the 100 meq diet, indicated a renin-dependent mechanism in the former, and a renin-independent mechanism in the latter diet. There were two subgroups of response to the 100 meq diet: one group (n = 5) achieved neutral balance, while the second (n = 5) avidly retained sodium and water. Renin-angiotensin system activity was significantly higher in the latter group, and the mechanism for differences in sodium excretion for the subgroups could not be identified by blood volume or hemodynamic parameters. Orthostatic hypotension during tilt was greater during the 10 meq sodium diet, and in all cases, related to ineffective hemodynamic and hormonal compensatory responses.
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PMID:Sodium and water balance in chronic congestive heart failure. 351 66

Amongst 40 patients undergoing cardiac transplantation between 1981 and 1984 and treated with cyclosporin A, 23 had hypertension. Fifteen of these patients, aged 39 years (16-57 years), without cardiac failure, treated with 8 +/- 3 mg kg-1 d-1 of cyclosporin A and 0.27 +/- 0.1 mg kg-1 d-1 of prednisolone were studied on average 288 days after transplantation (63-788 days). Blood pressure in the out-patients department of these 15 patients was 164 +/- 14/112 +/- 13 mmHg, in the absence of any antihypertensive treatment for more than 15 days, with a urinary sodium of 104 +/- 48 mEq/d and a urinary potassium of 55 +/- 13 mEq/d (mean +/- standard deviation). Two abnormalities accompany the raised blood pressure: a reduced creatinine clearance of 63 +/- 30 ml min-1 and an increased plasma volume of 445 +/- 686 ml (p less than 0.05) with reference to Hurley's norms (1975). By contrast, urinary excretion of VMA and metanephrines were invariably normal. Plasma renin activity (PRA) was normal in a lying position (1.02 +/- 0.42 ng ml-1 h-1) and after orthostatic stimulation (2.55 +/- 1.31 ng ml-1 h-1). Renin release was not stimulated by acute inhibition of converting enzyme (1.11 +/- 0.70 ng ml-1 h-1). Plasma aldosterone (110 +/- 52 pg ml-1), plasma angiotensinogen (924 +/- 213 ng/ml) and converting enzyme activity (30 +/- 6 mU ml-1) were normal. In these patients with a denervated heart, the orthostatic position increased heart rate from 85 +/- 11 to 93 +/- 12 beats/min.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Arterial hypertension in heart transplant patients treated with cyclosporin]. 393 36

Enalapril, a novel long acting angiotensin converting enzyme (ACE) inhibitor, was given orally to 12 patients with chronic heart failure (NYHA functional class III and IV) and cardiomegaly. The optimal dose averaged 17 mg given once-daily. Heart rate, systemic arterial blood pressure, pulmonary arterial pressure, right and left ventricular filling pressures and cardiac index were monitored during dose efficacy titration. Eleven patients were recatheterised 3 months later. After stabilisation of cardiac filling pressures, all patients had left ventricular filling pressures in excess of 20 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 3 months. Heart rate, systemic arterial and right atrial pressures and plasma concentrations of aldosterone were reduced during the observation period. ACE activity was inhibited at the time of peak haemodynamic effect from 25.3 +/- 9.8 to 4.9 +/- 3.4 U/ml (P less than 0.01). Renin was markedly elevated. These changes were accompanied by marked and sustained clinical improvement and subjective well-being.
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PMID:Acute and long-term response to enalapril in congestive failure. 609 34

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

Renin Activity (PRA), Aldosterone (PA), Sodium (PNa) and Potassium (PK) in plasma and Aldosterone (UA), Sodium (UNa) and Potassium (UK) in 24 hrs urine were measured in 11 cases of heart failure compensated with treatment (HFCT) consisting in digoxin 0.25 mg daily, furosemide 40 to 80 mg daily, potassium chloride 1.5 g daily and low salt diet and in 12 cases of refractory heart failure (RHF). Mean and standard deviation of PRA, PA, PNa, PK, UA, UNa and UK were 9.7 +/- 8.2 mg/cc/hr. 24.2 +/- 14.0 mg/100 cc, 142.2 +/- 4.7 mEq/1, 4.9 +/- 0.3 mEq/1, 8.7 +/- 9.1 ug/24 hrs, 89.3 +/- 50.0 mEq/24 hrs and 50.0 +/- 26.7 mEq/24 hrs, respectively for cases with HFCT and 61.7 +/- 37.5, 120.3 +/- 125.8, 133.1 +/- 4.3, 4.9 +/- 0.4, 21.3 +/- 19.2, 9.9 +/- 19 and 33.3 +/- 12.0 respectively for subjects with RHF. The statistical analysis of PRA, PA, PNa and UNa, revealed differences between the two groups with p values of less than or equal to 0.05, less than or equal to 0.001, less than or equal to 0.001, less than or equal to 0.001, respectively. The other values were statistically non significant. These data suggest the existence of an stimulatory state of the renin-angiotensin-aldosterone system (RAAS) in the RHF and a normal state in HFCT. The lack of electrolytic changes suggestive of aldosteronism in RHF may be due to an alteration of aldosterone receptors or to hemodynamic renal factors. In heart failure hemodynamic changes rather than humoral factor seems to control RAAS.
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PMID:[The renin-angiotensin-aldosterone system in compensated and uncompensated cardiac insufficiency]. 701 36

The successful introduction of angiotensin converting enzyme (ACE) inhibitors in the treatment of patients with essential hypertension or heart failure has increased interest in the (patho)physiological role of the renin-angiotensin system (RAS). ACE is not only involved in the formation of angiotensin II from angiotensin I, but also inactivates vasoactive substances such as bradykinin and substance P. Accumulation of these substances during treatment with ACE inhibitors may contribute to both their therapeutic action and certain adverse effects associated with their use, such as cough and angioneurotic oedema. Renin inhibitors offer an alternative approach to inhibit the RAS. The major advantage of these, still experimental, drugs is their high specificity for the RAS since angiotensinogen is the only known substrate of renin. The currently available renin inhibitors are pseudopeptides that are rapidly taken up by the liver and excreted in the bile. Consequently, these drugs are subjected to a considerable first pass effect which limits their oral bioavailability. Additionally, plasma elimination half-life times are short and the duration of action is limited. Despite these shortcomings, single oral or intravenous administration results in a 80 to 90% inhibition of plasma renin activity and a slight reduction in blood pressure in patients with hypertension. The extent of blood pressure reduction is dependent on the patient's salt balance. After 1 week of oral treatment with the renin inhibitor remikiren, the antihypertensive effect was reduced in salt-repleted hypertensive patients. Subsequent intravenous administration of the drug did not further affect blood pressure, indicating that it was not the first pass effect that was limiting the efficacy of remikiren.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical pharmacokinetics and efficacy of renin inhibitors. 758 99

The analysis of currently used therapeutic targets provides considerable input in the choice of current and future therapies for dilated cardiomyopathy and congestive heart failure. Of the ion flux agents, a definitive answer concerning digoxin will soon be available. Currently, digoxin is likely of benefit to patients with persistent heart failure and significantly enlarged hearts despite therapy with preload and afterload reducing agents. Most currently available calcium channel blocking agents do not appear to be effective, although newer agents such as amlodipine and felodipine have yet to be adequately tested. Vesnarinone, which operates through the sodium and potassium rectifying channels and has limited phosphodiesterase inhibition, appears to provide a significant improvement in mortality and in symptoms. Part of the latter effect may be due to its anticytokine properties, which are currently being investigated. Analysis of vascular endothelial agents indicate that not all of the vasoactive agents improve survival, as demonstrated with prazosin and flosequinan. The dose of agents may be important, again demonstrating that less is better. Finally, those with additional effects, such as inositol triphosphate stimulation, may offer additional unique properties that may, in the future, provide benefit. Phosphodiesterase inhibitors are potentially beneficial in the short term but clearly should be avoided for long-term use. Lower doses of these agents are now being investigated, but the weight of evidence is against agents that operate primarily through phosphodiesterase inhibition. Renin angiotensin agents are the most efficacious of therapies available at this time. New angiotensin converting enzyme inhibitors are likely to add little to what is already known.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:New medical therapies for advanced left ventricular dysfunction. 779 29

Renin-angiotensin-aldosterone system (RAAS) in patients with rheumatic valve defects clearly tends to activation which in its turn aggravate chronic heart failure (CHF). Plasma renin activity in CHF depends on the cause of the latter, humoral changes in rheumatic heart disease being the most considerable. At the same time activated RAAS was characteristic of patients with rhythm disorders. All this evidence an important role of morphological changes and affected intracardiac haemodynamics in development of humoral vicious circle.
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PMID:[The renin-angiotensin-aldosterone system in chronic heart failure]. 803 Mar 1


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