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

Magnesium (Mg2+) plays a significant role in the electrical stability of the heart and hypomagnesemia may predispose patients to arrhythmias and digitalis toxicity. We measured the serum and skeletal muscle Mg2+ content of patients with chronic Chagasic cardiomyopathy (CCC) during treatment for congestive heart failure and compared it to 15 normal patients who were used to establish the normal values of our population. There is a high frequency of muscle Mg2+ deficiency (66%) in patients with CCC during treatment for heart failure. However, serum Mg2+ is not a sensitive index of deficiency, since hypomagnesemia occurred in only 50% of the patients whose muscle Mg2+ was low. Digitalis toxicity was observed in all muscle Mg2+-deficient patients (100%) and in 25% of patients with normal Mg2+ levels (P less than or equal to 0.05). Ventricular tachycardia (VT) occurred in 75% of muscle Mg2+-deficient patients and in none of the patients with normal magnesium levels (P less than or equal to 0.05). The frequency and severity of premature ventricular contractions (PVC) were higher in muscle Mg2+-deficient patients. We conclude that muscle Mg2+ deficiency is very common in patients with CCC being treated for congestive heart failure and that muscle Mg2+ deficiency defines a higher risk CCC group in terms of digitalis toxicity and severe ventricular arrhythmias such as ventricular tachycardia.
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PMID:Muscle magnesium content and cardiac arrhythmias during treatment of congestive heart failure due to chronic chagasic cardiomyopathy. 380 26

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

The action of nystatin, a polyene antibiotic, was studied in rat myocardial cells, isolated rat hearts, and intact rats. Myocardial cells responded to 10 and 25 micrograms nystatin/ml with arrhythmias that could be minimized by elevated concentrations of K+ and Mg2+ or reversed by washing the cells. Similarly, the isolated heart responded to 100 micrograms nystatin/ml with arrhythmias that could be tempered by addition of elevated concentrations of K+ and Mg2+. The i.v. injection of the drug caused heart failure in intact animals at the 4-mg/kg dose level. At the subcellular level, nystatin made the myocardial cell membranes more rigid, as measured by electron spin resonance spectrometry. These findings indicate a parallel between physiocochemical changes caused by nystatin in the myocardial cell membrane and the biological changes caused by this drug in myocardial cells, isolated heart, and heart of the intact animal.
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PMID:Studies on the action of nystatin on cultured rat myocardial cells and cell membranes, isolated rat hearts, and intact rats. 609 60

Various methods have been proposed and tried to limit the extent of myocardial damage at the time of infarction. We chose to assess the usefulness of intravenous magnesium in this regard because of its important role in myocardial metabolism and function and the suggestion of its deficiency in ischemic hearts. A double-blind randomized trial was carried out and results analyzed in 76 patients. At the end of the infusion period the mean serum Mg++ level for the treated group was 3.6 versus 1.9 mg/dl for the control group. The estimated size of infarction (as measured by MB-CK release) was not significantly smaller overall in the treated group (37.4 +/- 4.3 vs. 45.6 +/- 4.6 MB-CK g/Eq), but was significantly smaller in the treated subgroup without heart failure (31.6 +/- 5.8 vs. 44.7 +/- 4.8 MB-CK g/Eq). A trend toward less ventricular ectopy was seen in the group treated with magnesium. There was significantly less lidocaine used for the treatment of ventricular dysrhythmias in this group. Magnesium supplementation in patients undergoing acute coronary events is promising and deserves further study.
Magnesium 1984
PMID:Magnesium therapy in acute myocardial infarction--a double-blind study. 639 46

The role of daily dietary intake of potassium and magnesium in the maintenance of potassium balance was studied in 104 digitalized outpatients with chronic cardiac insufficiency receiving 50 mg hydrochlorothiazide twice daily for 6 weeks. The food consumption data were collected once a week by the 24-hour recall method during the 1st, 2nd and 3rd weeks of the investigation. Serum potassium and magnesium values were followed throughout the study, and total body potassium was measured at the end. During the hydrochlorothiazide treatment, potassium and magnesium levels decreased significantly (p less than 0.001). 46% of the patients became hypokalemic (serum potassium less than or equal to 3.5 mmol/l), hypokalemia being more common (64%) in the patients with a concomitant decrease (-0.063 +/- 0.08 mmol/l) in serum magnesium values. Mean intake of potassium and magnesium was 3.4 g and 299 mg in females and 4.2 g and 380 mg in males, respectively. There was no significant difference in the daily intake of potassium and magnesium between the patients becoming hypokalemic and those remaining normokalemic.
Magnesium 1984
PMID:Role of dietary potassium and magnesium in diuretic-treated patients with cardiac insufficiency. 648 9

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

The importance of metals in normal and pathologic cardiovascular function has been recognized. Significant derangements in myocardial Ca2+, Mg2+, and Cu2+ have been reported in ischemic heart injury. We studied 3 groups of hearts: 1) fifteen specimens obtained from patients who had no heart disease, 2) nine specimens from patients who had expired from cyanotic congenital heart disease, and 3) ten specimens from patients who had expired from acute rheumatic heart disease with carditis and severe heart failure. None of the patients had undergone cardiac surgery. Left ventricular lateral wall Mg2+, Ca2+, Cu2+, and Zn2+ contents were measured by atomic absorption spectrometry. The results showed a significant decrease in myocardial Mg2- (Group I 177.06 +/- 32.71; Group II 155.66 +/- 14.79; Group III 149.00 +/- 13.29, p less than 0.05 and p less than 0.01, respectively), and Cu2+ contents (Group I 3.22 +/- 0.37; Group II 2.94 +/- 0.22; Group III 2.56 +/- 0.32, p less than 0.02 and p less than 0.001, respectively), and a rise in myocardial Ca2+ content (Group I 36.06 +/- 10.72; Group II 43.22 +/- 7.01; Group III 46.30 +/- 4.85, p = not significant, and p less than 0.01, respectively). The myocardial Zn2+ content did not change significantly (Group I 26.53 +/- 3.99; Group II 26.00 +/- 4.15; Group III 26.40 +/- 3.53). The myocardial Mg2+/Ca2+ ratio was reduced markedly in both groups (Group I 5.328 +/- 1.879; Group II 3.685 +/- 0.735; Group III 3.135 +/- 0.291, p less than 0.001 for both Groups II and III vs Group I). The latter results correlated closely with the myocardial Mg2+/Ca2+ ratios reported in experimental models in peri-infarction zones. Thus, the myocardium of patients who had expired from cyanotic congenital heart disease and acute rheumatic carditis is jeopardized by ischemia, with metal contents similar to the border areas in myocardial infarction.
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PMID:Myocardial metal content in patients who expired from cyanotic congenital heart disease and acute rheumatic heart disease. 717 80

Whether sarcolemmal (SL) calcium handling is altered in endstage heart failure produced by chronic rapid pacing is not known. To investigate this we paced 7 rabbits at a rate of 400 beats/min for 35 +/- 11 days. 6 animals served as non-paced controls. Purified left ventricular SL membranes were then prepared and tested for [3H]-nitrendipine binding and (Ca(2+) + Mg2+)-dependent ATPase (Ca(2+)-pump) activity. Results show a 50% reduction in calcium channel antagonist binding sites with Bmax values reduced from 450 +/- 40 to 230 +/- 8 fmoles/mg protein in response to chronic rapid pacing (P < 0.01). This change was accompanied by a modest decrease in Kd from 0.29 +/- 0.09 to 0.22 +/- 0.03 nM (not significant). Vmax values for the SL Ca(2+)-pump ATPase were decreased from 387 to 164 nmoles/mg protein/min (P < 0.01) with KCa2+ values reduced from 0.91 to 0.28 microM Ca2+ (P < 0.05) in response to tachycardia induced failure as compared to controls. ATPase activity in both groups was very sensitive to 25 microM calmidazolium and 5 microM vanadate. Results from this study indicate that both a reduction in SL calcium channel density and decrease in SL Ca(2+)-pump ATPase activity are evident in tachycardia heart failure. We conclude that sarcolemmal calcium handling is altered in heart failure induced by chronic rapid pacing and that such changes may contribute to systolic dysfunction associated with this model to heart failure.
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PMID:Altered sarcolemmal calcium channel density and Ca(2+)-pump ATPase activity in tachycardia heart failure. 785 49

Sixty eight patients operated on for valvular abnormalities were examined. In Group 1 (n = 34) myocardial protection was made by potassium solutions containing different potassium concentrations: 30 mM and 5 mM for induction and reinfusion, respectively. In Group 2 (n = 34) a hyperosmolar oxygenized cardioplegic solution containing K+, 15 mM, and Mg2+, 16 mM was administered under the same conditions. In the early postoperative period, no differences were found in the frequency and size of inotropic support, as evidenced by central hemodynamic parameters. ECG showed that in Group 2 there was a reduction in the frequency of changes of S-T segment, indicating the presence of myocardial ischemic changes. A 24-hour Holter monitoring demonstrated that life-threatening ventricular arrhythmias occurred significantly more infrequently in Group 2. The ultrastructural study of intraoperative biopsy specimens of the myocardium, including their treatment with colloid lanthanum showed that the tracer had penetrated virtually into all cardiomyocytes at the peak of ischemia and reperfusion in Group 1. In Group 2, ultrastructural changes were less profound and the particles of the tracer lanthanum had penetrated into the sarcoplasm of 15% of cells. Inadequate myocardial protection cannot be regarded as a cause of one of three deaths from acute heart failure. The studies demonstrated that crystalloid potassium cardioplegia was highly effective. However, the possibility of additionally affecting the permeability of a cell membrane by changing the solution composition (elevating magnesium concentrations) and the reduction of frequency of cardiac arrhythmias suggest that each components of the cardioplegic solution should be studied.
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PMID:[Comparative assessment of variants of potassium crystalloid cardioplegia]. 814 72

The oxidation states of intracellular myoglobin and cytochrome oxidase aa3 were monitored by reflectance spectrophotometry in isolated perfused rat hearts subjected to an acutely magnesium deficient environment. After exposure to low extracellular [Mg2+]o (i.e., 0.3 mM) for 30 min, more than 80% of the oxymyoglobin converted to its deoxygenated form. The level of reduced cytochrome oxidase aa3 also increased about 80% in low [Mg2+]o. The deoxymyoglobin was converted further to a species identified as ferrylmyoglobin by its reaction with Na2S to form ferrous sulfmyoglobin which was optically visible. This process, set into motion by acute Mg deficiency, resulted from a direct accessibility of the exogenous peroxide to the cytosolic protein. The results suggest that a pathway leading to cardiac tissue damage, induced by magnesium deficiency, is probably involved in the generation of a ferrylmyoglobin radical which could be prevented by addition of ascorbate, which is known to be a one-electron reductant of this hypervalent form of myoglobin. In further studies, we also investigated whether addition of different concentrations of ascorbic acid (AA) to the perfusate could enhance myocardial function after exposure to low [Mg2+]o perfusion. Four concentrations of AA (0.5, 1, 5, 10 mM) were tested, and the results indicate that they exert their effects in a concentration-dependent manner; 1 mM AA was the most effective dose in improving aortic output in a Mg-deficient heart. Ferrylmyoglobin formation was found to be formed considerably before intracellular release of either creatine phosphokinase or lactic dehydrogenase. These studies may have wide implications as a new mechanism by which low extracellular Mg2+ can induce myocardial injury and subsequent cardiac failure.
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PMID:Ferrylmyoglobin formation induced by acute magnesium deficiency in perfused rat heart causes cardiac failure. 828 Jul 83


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