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

Serum magnesium estimation was done in 19 children who had heart failure of varied etiology. Five of nine toxic patients and three of 10 nontoxic ones had magnesium deficiency (serum magnesium less than 1.5 mEq. per liter). Mean serum magnesium level was significantly lowered (P less than 0.01) in 19 children and it was further lowered in nine toxic patients (P less than 0.001) as well as in eight hypomagnesemic patients (P less than 0.001) than in healthy control subjects. Mean serum digoxin level in toxic patients was significantly higher than in nontoxic ones (P less than 0.05). In three cases magnesium sulfate was successfully used for the management of cardiac arrhythmias.
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PMID:Hypomagnesemia in relation to digoxin intoxication in children. 94 25

Serum magnesium and digoxin levels were obtained in 13 nontoxic patients with atrial fibrillation due to chronic rheumatic heart disease receiving digoxin for the control of ventricular rate and heart failure. Fairly good correlations were made between serum digoxin levels and ventricular rates. Hypomagnesemia was quite common (7 out of 13) and mean magnesium serum levels were significantly lowered in total as well in 7 hypomagnesemic patients, as compared to in healthy controls. Magnesium sulphate was successfully used in patients with magnesium deficiency to control the ventricular rates.
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PMID:Serum magnesium concentrations in atrial fibrillation. 108 31

Repeated efforts to induce beriberi heart disease by experimental thiamine deficiency (B1d) have failed in many species. To test the hypothesis that magnesium deficiency (Mgd) might be the cofactor necessary for heart failure, 10-week-old Syrian golden hamsters were divided into four groups-control (C), B1d, Mgd, and combined MgB1d-and were fed the diets ad libitum for 3 weeks. On day 21, animals were studied under intraperitoneal pentobarbital anesthesia (50 mg/kg). Electrocardiograms were taken and right and left ventricular pressures were measured by transthoracic needle puncture. Cardiac output was measured by the direct Fick method. The complete study was performed in 9 C, 13 B1d, 9 Mgd, and 14 MgB1d animals. B1d was proven by low red blood cell transketolate high B1 pyrophosphate effect, and was accompanied by tachycardia and hypercalcemia. B1 did not differ from C in any other parameter. Mgd was characterized by hypomagnesemia, hypercalcemia, prolongation of the PR interval, widening of the QRS interval, low O2 consumption, low cardiac output, and increased heart weight to body weight ratio (HW/BW) as compared to control. No differences were observed in right and left ventricular pressures or peak /dt. MgB1d was characterized by hypomagnesium, hypercalcemia, low red blood cell transkeotlase, and high B1 pyrophosphate effect. MgB1d minimized the deleterious effects of Mgd: animals were more active and the mortality was low, the PR interval remained normal, the QRS interval widened significantly less, cardiac output remained normal, and HW/BW increased significantly less. Although, once again, beriberi heart disease was not produced, B1d appeared to exert a protective effect upon the Mg-deficient myocardium.
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PMID:Protective effect of coexistent thiamine deficiency upon the experimental cardiomyopathy associated with acute magnesium deficiency in the Syrian golden hamster. 120 11

It is well established that clinically significant changes in a number of electrolytes occur in patients with congestive heart failure (CHF). Magnesium ions are an essential requirement for many enzyme systems, and evidence is rapidly emerging that magnesium deficiency is a major risk factor for survival of CHF patients. In animal experiments, magnesium has been shown to be involved in several steps of the atherosclerotic process and, although in humans the situation is somewhat more complex, magnesium ions play an extremely important role in CHF and various cardiac arrhythmias. A number of drugs commonly used to treat CHF can significantly affect not only cellular magnesium ion homeostasis, but potassium as well. These include mercurial, thiazide, and loop diuretics. It has also been reported that hypomagnesemia is common in digitalis intoxication. In contrast, a number of agents have been shown to have either a magnesium-conserving effect (potassium-sparing diuretics) or not to affect magnesium ion balance (angiotensin-converting enzyme inhibitors). The clinical consequences of magnesium deficiency include the development of various cardiac arrhythmias, all of which respond well to magnesium treatment. Thus, it is more than apparent that magnesium ion homeostasis is of major importance in CHF. Future studies should address the complex role of magnesium ions in electrolyte imbalance, particularly in relation to heart failure.
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PMID:Electrolyte balance in heart failure and the role for magnesium ions. 141 94

Electrolyte abnormalities are a frequent and potentially hazardous complication in patients with heart failure. This may be due to the pathophysiological alterations seen in the heart failure state leading to neurohumoral activation (stimulation of the renin-angiotensin-aldosterone system, sympathoadrenergic stimulation), and due to the complications of therapy with diuretics, cardiac glycosides or ACE inhibitors. Patients with heart failure may exhibit hyponatremia due to a decrease in water excretion, which may be related to the enhanced release of both angiotensin and vasopressin and can be exaggerated by diuretic therapy. Along with potassium and calcium, magnesium influences cardiovascular function. Magnesium and potassium deficiencies play an important role in the development of cardiac arrhythmias. Magnesium is essential for the maintenance of intracellular potassium concentration. Although there are conflicting data regarding the prevalence of hypomagnesemia in patients with chronic heart failure (the values range from 7-37%), multiple studies have documented lower magnesium concentrations in patients with heart failure than in normal controls. As magnesium and potassium are mainly intracellular ions, measurements in serum or plasma are of limited value to assess magnesium status. There was no correlation between the intracellular electrolyte content and the electrolyte levels in plasma, either for mononuclear cells or erythrocytes or for myocardial and skeletal muscle. Loop diuretics (e.g. furosemide) are supposed to cause a substantial loss of both magnesium and potassium in the plasma and intracellular space. The potassium-sparing diuretics amiloride and triamterene are reported to also exert magnesium-sparing effects. Recently, ACE inhibitors have been documented to have important magnesium-conserving actions, possibly via their effect on glomerular filtration. Hyperkalemia, secondary to the use of ACE inhibitors in patients with heart failure, is well documented. Digoxin directly limits the renal tubular reabsorption of magnesium, therefore increasing magnesium excretion. Low magnesium and potassium concentrations increase cardiac glycoside toxicity. In contrast, elevated levels of magnesium decrease the sensitivity of human myocardium to antiarrhythmogenic actions of cardiac glycosides, without affecting maximally developed tension. Moreover, magnesium increases binding affinity of cardiac glycosides to the receptor. The antiarrhythmic action of magnesium is suspected to be mediated by a reduced sensitivity to electrophysiological changes induced by Ca2+, thus indicating Ca2+ antagonistic properties of magnesium. Magnesium deficiency has also been implicated in sudden death, notably in patients with congestive heart failure. Therefore, when treating congestive heart failure, one must consider how to prevent depletion of electrolytes or how to replete potassium and magnesium in deficiency states.
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PMID:Heart failure and electrolyte disturbances. 150 35

Zinc, copper, and magnesium concentrations in hair were measured in groups of children varying in one condition--protein-energy malnutrition, ricketts, thalassemia, malignancy, cardiac failure, or after prolonged infection and in healthy controls. As compared with controls, copper and magnesium concentrations were low in all groups, whereas higher values were obtained for hair zinc. These results showed that a generalized copper and magnesium deficiency were observed in the southeastern part of Turkey. However, zinc deficiency couldn't be detected as far as the hair zinc values were concerned, although all of the subjects fell within the 50 percentile limits for their age-appropriate weights and heights.
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PMID:Zinc, copper, and magnesium concentrations in hair of children from southeastern Turkey. 170 58

There are many reasons to expect magnesium deficiency in patients with chronic congestive heart failure. Medical therapy, neurohormonal activation and decreased dietary intake could all contribute to low concentrations of serum and muscle magnesium. Although the ideal serum level of this electrolyte is not known, multiple studies have documented lower magnesium concentrations in patients with heart failure than in normal persons. Magnesium deficiency could theoretically produce hemodynamic deterioration and ventricular arrhythmias. These complications have been observed in animals and in patients without heart failure, and magnesium repletion has reversed the adverse effects of hypomagnesemia in some patients. However, the consequences of chronic depletion of the electrolyte have not been adequately evaluated. Because of the high incidence of sudden death in patients with severe congestive heart failure, well designed investigations to determine the importance of magnesium are needed.
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PMID:Importance of magnesium in congestive heart failure. 265 May 14

Elderly patients have a higher incidence of symptomatic cardiac arrhythmias and greater management problems than younger patients. This is due to the frequency of occult and overt cardiovascular disease, reduction in cardiac reserve as a consequence of the aging process, and coexistence of other disorders which provide a substrate for iatrogenic disease. The last problem is largely due to electrolyte disturbances induced by diuretic therapy for hypertension and heart failure. The major electrolyte disturbance implicated in arrhythmogenesis is diuretic-induced hypokalemia. There is no doubt that arrhythmias are caused by severe hypokalemia (less than 2.5 mEq/l), or by a milder degree of hypokalemia in digitalis-treated patients or those with left ventricular hypertrophy, but the literature contains conflicting data regarding the importance of milder hypokalemia. The most compelling study in support of its importance used a crossover study design in hypertensive patients with coronary disease and showed that mild degrees of hypokalemia induced by thiazide diuretics increased the tendency to arrhythmia when compared with normokalemia on a potassium-sparing diuretic. Diuretic-induced magnesium deficiency is also regarded by some to be as important as hypokalemia, but the evidence is less extensive. Thus, it appears reasonable to avoid hypokalemia and hypomagnesemia. The optimum therapeutic approach in using diuretics is to keep the dose as low as possible, restrict dietary sodium, and add potassium supplements. Since, in many cases of hypertension, hypokalemia is due to secondary hyperaldosteronism, the use of angiotensin-converting enzyme inhibitors is another therapeutic approach that is effective in hypertension and heart failure.
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PMID:Arrhythmias, electrolytes, and ACE inhibitor therapy in the elderly. 344 May 24

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

Magnesium in coronary artery disease is reviewed with regard to its role in the pathogenesis of arteriosclerosis, coronary spasm, myocardial function, acute myocardial infarction and ventricular arrhythmias. Experimentally, magnesium depletion potentiates and supplementation retards the effect of atherogenic diets. Evidence from human studies is circumstantial. Reactivity of arterial smooth muscle is enhanced by low and suppressed by high magnesium media. Evidence that magnesium depletion may initiate coronary spasm is provided by dog and retrospective human studies. Although experimental magnesium deficiency disrupts myocardial mitochondria, there are no studies which show that magnesium deficiency will lead to cardiac failure or that replacement will improve cardiac function. It is known that an infarcted or ischaemic myocardium loses magnesium and this may be the basis for ventricular arrhythmias. Coronary occlusion in a previously magnesium-depleted heart will result in a larger area of necrosis and ischaemia. The fall in serum magnesium in acute myocardial infarction is probably due to the formation of soap in fat cells undergoing catecholamine lipolysis. Ventricular fibrillation in coronary artery disease will respond to parenteral magnesium, even in the presence of normal serum concentrations.
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PMID:Magnesium in coronary artery disease. 649 97


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