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

In 16 patients with critical condition due to severe heart failure associated with digitalis toxicity, the effects of potassium canrenoate (AldactoneR) administered intravenously were studied. Rhythm and conduction disturbances disappeared or improved in all instances. This effect was well correlated with an increase of serum potassium concentration. In 13 patients, after 1-2 days of Aldactone therapy, heart failure improved, which could be explained by a diuretic effect and by a possible inotropic action of aldactone. It is concluded that intravenous Aldactone is useful in patients with severe heart failure and digitalis toxicity in whom diuretics are often ineffective and even dangerous.
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PMID:The effect of intravenous potassium canrenoate in patients with severe heart failure and digitalis toxicity. 84 Dec 50

In order to examine the question, whether improved digitalis tolerance by Spirolactone may be partially a result of antagonism on myocardial potassium balance, 6 patients without clinical signs of heart failure were given 400 mg, 3 were given 200 or 300 mg Spirolactone orally daily and 6 patients received placebo during a 5 to 7 days period. During cardiac catheterization hemodynamics and serum potassium concentrations were determined repeatedly prior to and following intravenous administration of 0,375 to 0,625 mg Strophanthin. Injection of Strophanthin resulted in a significant drop in left ventricular enddiastolic pressure and a rise in dp/dt max. In the control group a significant increase in arterial and coronary sinus potassium concentration was observed. Myocardial potassium balance was definitely negative from the third to the eighth minute. Values in the group receiving Spirolactone did not differ significantly from the placebo group. It is suggested that therapeutic doses of Strophanthin resllt in a loss of potassium from the myocardium by inhibition of the Na+, K+ membrane ATPase not influenced by pretreatment with Spirolactone.
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PMID:[Influence of spirolactone on the myocardial potassium balance following strophanthin in man (author's transl)]. 97 68

Aldactone-saltucine was used in 52 patients with Stage IIB-III cardiac failure. The efficiency of the drug was evaluated by the dynamics of the clinical course, diuresis, body weight, blood and urine levels of electrolytes, and in some patients by the urine excretion of aldosterone. Aldactone-saltucine is a sufficiently effective diuretic agent that, without producing excessively fast diuresis, exerts after a course of therapy a beneficial effect, increasing mainly natriuresis, without concomitant hypokalemia. The diuretic effect of the drug ensued irrespectful of the initial level of urine aldosterone excretion. After a course of treatment urine aldosterone excretion tended to increase. Hyperaldosteronuria was noted in only 1/3 of the patients.
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PMID:[Use of aldactone-saltucine in patients with heart failure]. 115 18

The aims of treatment of chronic heart failure are to improve the symptoms and the quality of life, reduce mortality and prevent left ventricular dysfunction. Before the first symptom occurs, neurohormonal activation takes place (increased catecholamines and atrial natriuretic peptide levels). Diuretics improve symptoms and are irreplaceable for the elimination of salt and water overload. Loop diuretics are used more often than the thiazides. Their deleterious effects on electrolyte balance are well known. The fact that they activate the renin angiotensin system is a more recent acquisition; the increase in plasma renin activity is a poor prognostic factor. Diuretics potentialize the vasodilator effect of angiotensin converting enzyme inhibitors which inhibit the neurohumoral activation induced by the diuretics. This therapeutic association is very logical, effective and allows reduction in the dosage of the diuretic. To date, there are no large scale controlled studies of the effects of diuretics on mortality. Spironolactone corrects hypokalaemia and hypomagnesaemia induced by loop diuretics. Moreover, it has been shown experimentally in renovascular hypertension and in hyperaldosteronism, that this molecule can prevent myocardial fibrosis, a factor which leads to ventricular dysfunction. The RALES study will analyse the effect of associating spironolactone to diuretic and ACE inhibitor therapy on the mortality of patients in NYHA classes III-IV. The value of digitalis in heart failure patients with sinus rhythm is a classical controversy. Digitalis has a positive inotropic effect (inhibition of NaK-dependent ATPase). More recently, a favourable neurohormonal effect has been reported; digitalis decreases the activation of the sympathetic and renin-angiotensin systems.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Classic treatment of chronic heart insufficiency. What if new?]. 748 8

In chronic heart failure, a diuretic plus an angiotensin-converting enzyme (ACE) inhibitor only partially suppresses aldosterone despite the fact that aldosterone has many harmful effects independent of angiotensin II. These possible harmful effects of aldosterone are magnesium loss, increased cardiac sympathetic activity, and increased ventricular arrhythmias. We have therefore assessed whether adding the aldosterone antagonist, spironolactone, to a loop diuretic and ACE inhibitor reverses any of these potentially harmful effects of residual aldosterone. In a preliminary animal study, we found that exogenous aldosterone reduced myocardial norepinephrine uptake by 24% in anesthetized rats in vivo. In our main study, 42 patients with New York Heart Association II to III congestive heart failure were randomized to spironolactone (50 to 100 mg/day, titrated to blood pressure and plasma potassium) or placebo in a double-blind fashion. Our principal finding is that cardiac norepinephrine uptake as assessed by 123I-metaiodobenzylguanidine scintigraphy increased with spironolactone (p < 0.01). Spironolactone also elevated plasma magnesium (p < 0.05), reduced urinary magnesium excretion (p < 0.05), and caused a reduction in ventricular arrhythmias on 24-hour ambulatory electrocardiography (p < 0.05). Spironolactone increased plasma renin activity, plasma aldosterone (p < 0.01), 24-hour urinary sodium excretion (p < 0.05), and urinary sodium/potassium ratio (p < 0.01). Echocardiographic-determined measurements of left ventricular systolic and diastolic function were unaltered by spironolactone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of adding spironolactone to an angiotensin-converting enzyme inhibitor in chronic congestive heart failure secondary to coronary artery disease. 750 7

Despite the findings in randomized trials of a significant effect of angiotensin-converting enzyme (ACE) inhibitors in reducing morbidity and mortality of patients with symptomatic left ventricular dysfunction, the morbidity and mortality of these patients remains relatively high. One potential strategy to further improve morbidity and mortality in these patients is blockade of a aldosterone. Many clinicians have assumed that ACE inhibitors would block both angiotensin II and aldosterone. However, there are data to suggest that aldosterone production may "escape" despite the use of an ACE inhibitor. An escape of aldosterone production has several important consequences, including: sodium retention, potassium and magnesium loss, myocardial collagen production, ventricular hypertrophy, myocardial norepinephrine release, endothelial dysfunction, and a decrease in serum high density lipoprotein cholesterol. Due to the potential importance of these mechanisms, the finding that there is a significant correlation between aldosterone production and mortality in patients with heart failure, as well as evidence that an aldosterone antagonist, spironolactone, when administered to patients with heart failure treated with conventional therapy including an ACE inhibitor results in increased diuresis and symptomatic improvement, an international prospective multicenter study has been organized, the Randomized Aldactone Evaluation Study (RALES Pilot Study), to evaluate the safety of blocking the effects of aldosterone in patients with heart failure treated with an ACE inhibitor.
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PMID:"Escape" of aldosterone production in patients with left ventricular dysfunction treated with an angiotensin converting enzyme inhibitor: implications for therapy. 778 35

Heart failure has emerged as a major cardiovascular public health syndrome with increasing incidence, reduced quality life, risk of progression, and high mortality. It's therapy still continues to pose a major clinical problem. The main goals of therapy are: improving the quality life and prolonging the survival. For many years digitalis and diuretics have been the cornerstones of pharmacologic treatment recently completed with vasodilators. Regarding the results of experimental and clinical investigations efforts to refine therapy have focused on choosing a combination of drugs particularly those that effectively inhibit the renin-angiotensin-aldosterone (RAA) system. The ACE inhibitors proved to be effective in managing heart failure of all degrees of severity including left ventricular dysfunction and end-stage of syndrome and in prolonging survival in patients. Spironolactone which inhibits the activity of aldosterone may exert an independent and additive effect to that of ACE inhibitors. The standard therapy of heart failure became: digitalis, diuretics--including spironolactone--and ACE inhibitors. In end-stage of heart failure refractory to therapy the only choice is heart transplantation.
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PMID:[Current management of heart failure]. 806 47

Antialdosterone therapy in patients with secondary hyperaldosteronism due to myocardial failure must accomplish the following: (1) reduce or preferably normalize plasma aldosterone levels by blockade of excessive synthesis, (2) antagonize the renal and systemic effects of aldosterone at its receptor sites, and (3) minimize the presence of multiple stimuli to aldosterone secretion. Fulfillment of these goals likely requires the blockade of angiotensin II-induced aldosterone secretion (ie, angiotensin-converting enzyme inhibition) with an antagonist of aldosterone receptors (ie, spironolactone [Aldactone]). Despite the potential for hyperkalemia with this combined use of medications, particularly in patients with impaired renal function, such therapy is likely to attenuate the salt-acquisitive state that is characteristic of myocardial failure.
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PMID:Role of aldosterone in congestive heart failure. 846 78

In the setting of chronic heart failure (CHF), therapy with angiotensin converting enzyme (ACE) inhibitors generally reduces serum aldosterone levels acutely. However, long-term ACE inhibition is associated with aldosterone suppression that is weak, variable, and unsustained, i.e. aldosterone 'escape'. Magnesium loss caused by aldosterone and by diuretics can contribute to coronary artery spasm and arrhythmias. Aldosterone can block noradrenaline uptake by the myocardium; extracellular catecholamines may lead to arrhythmias and ischaemia. Aldosterone has been shown to have an acute arrhythmogenic effect as well as a potential detrimental effect on baroreflex function, a marker of prognosis in CHF. Both angiotensin II and aldosterone may stimulate myocardial fibrosis, which is associated with a higher incidence of malignant ventricular arrhythmias. ACE inhibition initiated early in the progression of CHF may prevent development of patchy myocardial fibrosis and its inherent arrhythmias and thus reduce the incidence of sudden death. Spironolactone therapy added to the regimen of an ACE inhibitor and diuretic can induce natriuresis and magnesium retention, increase myocardial noradrenaline uptake, and reduce the incidence of arrhythmias.
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PMID:Aldosterone escape during ACE inhibitor therapy in chronic heart failure. 868 54

Angiotensin converting enzyme (ACE) inhibitor therapy in conjunction with loop diuretics and, possibly, digoxin, is associated with a relatively high incidence of recurrent heart failure and death. Even high doses of ACE inhibitors may not completely suppress the renin-angiotensin-aldosterone system; aldosterone "escape' may occur through non-angiotensin II dependent mechanisms involving corticotropin, atrial natriuretic peptide, serum potassium, and deficient high-density lipoprotein cholesterol concentrations. Addition of spironolactone (an aldosterone receptor blocker) to an ACE inhibitor regimen causes marked diuresis and symptomatic improvement. The Randomized Aldactone Evaluation Study (RALES) was organized to explore the role of combination therapy with spironolactone in patients with heart failure. Patients with New York Heart Association Functional Class II-IV heart failure and left ventricular ejection fractions < or = 40% who were on regimens comprising an ACE inhibitor, loop diuretic, and, possibly, digoxin were randomized to receive placebo or spironolactone in doses of 12.5, 25, 50, or 75 mg per day. Eve at the lowest dose of spironolactone, a significant decrease in plasma N-terminal pro-atrial natriuretic peptide occurred, with concomitant increase in concentrations of plasma renin and urinary aldosterone. As prophylaxis for heart failure, a daily dose of 25 mg of spironolactone and monitoring of serum potassium concentrations are recommended; symptomatic therapy in refractory or severe heart failure may require doses as high as 100 mg b.i.d. The RALES Mortality Trial will follow up 1400 similar patients for 3 years to determine the effect of the addition of spironolactone on combined mortality and hospitalization for heart failure.
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PMID:ACE inhibitor co-therapy in patients with heart failure: rationale for the Randomized Aldactone Evaluation Study (RALES). 868 55


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