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

Magnesium levels in serum, erythrocytes, skeletal muscle, and bone were measured in 10 patients with valvular heart disease who had received diuretic therapy for heart failure for an average of 3.3 years. Five patients were found to have diminished values for skeletal muscle, indicating significant magnesium deficit. Values for erythrocytes were low in only two of the five patients, and none had low values for serum ultrafiltrate and bone: Magnesium replacement therapy restored skeletal muscle values to normal. Clinical features consistent with the presence of magnesium deficiency were found in all five magnesium-deficient patients. These features were, with few exceptions, corrected by magnesium replacement. The latter also corrected low skeletal muscle potassium values present in all five patients with low skeletal muscle magnesium, four of whom showed clinical features of digoxin poisoning before magnesium therapy was given. Concomitant secondary aldosteronism, inadequate dietary intake, and digoxin therapy had probably augmented the magnesium loss due to diuretic therapy.
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PMID:Magnesium deficiency in patients on long-term diuretic therapy for heart failure. 507

Ten years of experience with three different converting enzyme inhibitors (CEI; teprotide, captopril and enalapril) in over 300 hypertensive patients reveals that CEI act largely to block renin-angiotensin mediated vasoconstriction. Thus, their effectiveness or lack of it is predicted by the baseline plasma renin measurement. Accordingly, responses to these pharmacological agents can be used to identify and quantify renin-mediated vasoconstriction in the spectrum of hypertensive diseases. The converse is also generally true. Patients failing to respond to CEI exhibit low renin values and their increased peripheral resistance appears related to other mechanisms, possibly involving a subtle increase in total body sodium. Thus, low renin states such as low-renin essential hypertension, primary aldosteronism, and anephric man exhibit little or no response to CEI. The relationship between the renin system activity and effectiveness of CEI reflects a specific interference with a particular pathogenic mechanism which is further supported by the fact that two other types of renin system inhibitors (beta-blockers and saralasin) are similarly effective or ineffective according to the operant renin profile also by studies in patients with congestive heart failure without hypertension in whom the same relationships can be demonstrated. Like hypertensives, heart failure patients exhibit a broad spectrum of renin activity values, and their pretreatment renin levels predict the responses to CEI. We have also found that plasma renin values in heart failure are dependent on sodium intake. When salt is administered, renin falls and patients then become unresponsive to CEI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Converting enzyme inhibition to identify and treat renin-mediated or sodium-volume related forms of increased peripheral resistance in hypertension and in congestive heart failure. 608 35

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

Many metabolic and hormonal changes are observed during the acute phase of myocardial infarction (glucose metabolism, lipoproteins...). Mineralocorticoid function may also be disturbed but there have been few studies of this problem. The aim of this study was to confirm the elevation of serum aldosterone during the acute phase of myocardial infarction and to determine the effects of antialdosterone treatment in these patients. Hyperaldosteronism was confirmed in 74% of 72 consecutive patients admitted for acute myocardial infarction, in 85% if patients previously treated by an antialdosterone drug or admitted after the acute phase are excluded, and in 96% if patients with cardiac failure are included. One thousand consecutive patients admitted for myocardial infarction were given an antialdosterone agent systematically (intravenous potassium canrenoate , 600 mg daily for 5 days). The serum and red blood cell potassium concentrations rose, the number of ventricular extrasystoles and the administration of anti-arrhythmic drugs fell, and, above all, the prevalence of ventricular fibrillation decreased significantly: 0,8% (p less than 0,001), compared with comparable previously reported series.
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PMID:[Hyperaldosteronism in the acute phase of myocardial infarction. Effects of its treatment on the prevention of ventricular fibrillation]. 642 61

Serum aldosterone and plasma renin were measured in 20 normal infants and 15 infants with congestive cardiac failure. Serum aldosterone was significantly increased (151 +/- 38 ng/dl mean +/- standard error of the mean) in patients before treatment when compared with aldosterone in normal infants (29 +/- 7 ng/dl). Increasing serum aldosterone was related to increasing plasma renin. The response to furosemide appeared to be inversely related to serum aldosterone concentrations. In four infants, administration of an aldosterone antagonist (spironolactone) resulted in improved diuresis and decreased serum aldosterone. Hyperaldosteronism is an important factor contributing to fluid and sodium retention in infants with heart failure.
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PMID:The occurrence of hyperaldosteronism in infants with congestive heart failure. 698 45

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

In 14 elderly male residents of a veterans' care complex who were receiving diuretic therapy for cardiac failure, oral potassium (K) supplements were withdrawn. Plasma and erythrocyte K levels were measured immediately before and six weeks after withdrawal of the supplements (38 mEq K daily). The controls comprised 19 elderly residents without disease and not taking drugs likely to influence K status. Study subjects and controls were receiving the same diet (average daily K content 100 mEq). After withdrawal of K supplements, the mean plasma K level fell significantly but the mean erythrocyte K level remained unchanged and did not differ from the control values. For a further six weeks after the withdrawal period, 7 subjects were treated with Aldactazide (diuretic hydrochlorothiazide plus K-sparing spironolactone). The plasma K level increased significantly but the erythrocyte K level remained unchanged. It was concluded that, in this setting, diuretic-induced hypokalemia is not necessarily accompanied by intracellular K depletion and that routine prophylaxis with K supplements or K-sparing agents is unnecessary and not without risk. Such therapy should be reserved for patients considered at special risk of K depletion because of known poor dietary intake, advanced liver disease, secondary hyperaldosteronism with renovascular hypertension, gastrointestinal losses, or nondiuretic medication known to affect K status adversely.
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PMID:Diuretics and the institutional elderly: a case against routine potassium prescribing. 720 9

The results of clinical and instrumental examination of 67 patients and experimental findings provide evidence of myocardial resistance to cardiac glycosides in acute myocardial infarction complicated by the initial stage of cardiac insufficiency. It is suggested that symptoms of secondary hyperaldosteronism may develop in acute myocardial infarction and that medication with cardiac glycosides in combination with spironolactones is expedient.
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PMID:[Debatable questions of strophanthin and spironolactone treatment in certain forms of acute myocardial infarct]. 720 22

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

The pathophysiologic cycle that links myocardial failure with the appearance of congestive heart failure is not fully understood. It is clear, however, that an activation of several neurohormonal systems and the interplay between kidneys, adrenal glands, and heart contribute to abnormal sodium and water homeostasis. Aldosterone, the body's most potent mineralocorticoid hormone, contributes to intravascular and extravascular volume expansion, and thus to the appearance of symptomatic failure. Antialdosterone therapy in patients with secondary hyperaldosteronism due to heart failure must achieve one or more of the following goals: reduce or, preferably, normalize plasma aldosterone levels by limiting synthesis; antagonize the renal and systemic effects of aldosterone at its receptor sites; and eliminate or minimize the multiple stimuli to aldosterone secretion.
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PMID:Aldosterone and antialdosterone therapy in congestive heart failure. 842 2


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