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

The therapeutic efficacy of magnesium has been studied during recent years in a number of cardiovascular diseases: supraventricular and ventricular arrhythmias (multifocal atrial tachycardia, Torsade de pointes-tachycardia, glycoside-associated arrhythmias, sustained ventricular tachycardia), acute myocardial infarction, heart failure and arterial hypertension. Although only a few of these arrhythmias were studied under controlled conditions, the therapeutic efficacy of intravenous magnesium given in a high dose in these arrhythmias seems to be established. By contrary, the efficacy of magnesium in acute myocardial infarction, congestive heart failure and arterial hypertension remains controversial up to now. Magnesium cannot be regarded as standard therapy for example for patients with acute myocardial infarction.
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PMID:[Magnesium: current studies--critical evaluation--consequences]. 906 59

The intracellular Ca(2+)-homeostasis may be affected by changes of the extracellular K(+)- and/or Mg(2+)-concentrations. Mg2+ reduces the Ca(2+)-influx via L-type Ca(2+)-channels, facilitates Ca(2+)-uptake into the sarcoplasmic reticulum, modulates the Ca(2+)-induced Ca(2+)-release and the Ca(2+)-binding to troponin C. The extracellular K+ activates the Na+/K(+)-ATPase and changes the membrane potential thereby affecting the mode of action of the Na+/Ca(2+)-exchanger. Especially when intracellular Ca2+ regulation is altered, for example in heart failure, Mg2+ and K+ exert beneficial effects on the frequency-dependent force-generation in human myocardium. Thus, extracellular Mg2+ and K+ influence contraction coupling in the human myocardium.
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PMID:[Effect of changed extracellular K(+) and Mg(2+)-concentration on intracellular Ca(2+) homeostasis, contraction coupling and force-frequency relations in the human myocardium]. 933 87

Skeletal muscle fatigue develops gradually during all forms of exercise, and develops more rapidly in heart failure patients. The fatigue mechanism is still not known, but is most likely localized to the muscle cells themselves. During high intensity exercise the perturbations of the Na+ and K+ balance in the exercising muscle favour depolarization, smaller action potentials and inexcitability. The Na+, K+ pump becomes strongly activated and limits, but does not prevent the rise in extracellular Na+, K+ pump concentration and intracellular Na+ concentration. However, by virtue of its electrogenic property the pump may contribute in maintaining excitability and contractility by keeping the cells more polarized than the ion gradients predict. With prolonged exercise perturbations of Na+ and K+ are smaller and fatigue may be associated with altered cellular handling of Ca2+ and Mg2+. Release of Ca2+ from the sarcoplasmic reticulum (SR) is reduced in the absence of changes of the cellular content of Ca2+ and Mg2+. In heart failure several clinical reports indicate severe electrolyte perturbations in skeletal muscle. However, in well controlled studies small or insignificant changes are found. We conclude that with high intensity exercise perturbations of Na+ and K+ in muscle cells may contribute to fatigue, whereas with endurance type of exercise and in heart failure patients the skeletal muscle fatigue is more likely to reside in the intracellular control of Ca2+ release and reuptake.
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PMID:Skeletal muscle fatigue in normal subjects and heart failure patients. Is there a common mechanism? 957 67

There is a high incidence of mitral valve prolapse (MVP), an abnormal displacement of one or both mitral valve leaflets during systole, in Cavalier King Charles Spaniels (CKCS). In humans, MVP is known to be associated with a low magnesium status. In this study, the plasma magnesium concentration was measured in 30 CKCS without heart failure. It was also investigated whether MVP-severity and degree of regurgitation correlated with plasma magnesium and a number of parameters of the renin-angiotensin system, and whether 4 weeks magnesium supplementation affected plasma magnesium or the high renin/low aldosterone profile associated with MVP. A high prevalence of hypomagnesemia was observed: plasma concentrations < 0.70 mmol/l were found in 15 dogs (50%) before and in 12 dogs (40%) after 4 weeks magnesium supplementation. The mean plasma level was 0.69 +/- 0.07 mmol/l before and 0.71 +/- 0.07 mmol/l after magnesium (P = 0.22). Plasma magnesium concentrations did not correlate with MVP-severity and degree of regurgitation. Plasma aldosterone levels correlated negatively with MVP-severity and positively with the degree of regurgitation, and serum angiotensin-converting enzyme activities correlated negatively with the degree of regurgitation. Magnesium supplementation had no effects on renin and aldosterone nor on the ratio between the two. In conclusion, many CKCS without heart failure have hypomagnesemia whether they are fed supplementary magnesium or not--a finding which may be associated with the high prevalence of MVP in this breed. Further studies, however, are needed to clarify the role of a low magnesium status in canine MVP.
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PMID:Hypomagnesemia and mitral valve prolapse in Cavalier King Charles spaniels. 992 43

Alcoholic heart muscle disease is characterized by structural changes which include chamber dilation, ventricular hypertrophy, and myocyte damage. These effects often lead to contractile dysfunction and ultimately to heart failure if alcohol consumption is not terminated. In rat models for heart failure in which heart failure is induced by pressure or volume overload, there is a shift in the myosin heavy chain (MHC) isoforms, from alpha to beta. As a result of this MHC transition, there is typically a decrease in myosin ATPase activity. We utilized a rat model of chronic alcohol consumption in order to determine if alcohol causes a similar shift in MHC isoforms and changes in myosin ATPase activity. A liquid diet containing 9% ethanol (46% of daily calories; 11.8 g/kg/day) was administered to adult rats for a period of 60 or 90 days. This heavy consumption of ethanol resulted in an average blood ethanol content of 150 mg %. The relative abundance of beta-MHC isoform protein increased from a control level of 9.7% to 35.1% in hearts of ethanol-fed rats, following 90 days of ethanol consumption. In a separate set of experiments, the levels of alpha-MHC and beta-MHC mRNA were demonstrated to increase by 150% and 230%, respectively. Following a 60 day treatment, there was a significant reduction in the actomyosin Mg2+ -ATPase activity in the myofibrillar preparations from hearts of ethanol-fed rats compared to hearts from control-fed rats. In addition, the myosin Ca2+ -ATPase activity was decreased 17% and 30% after 60 and 90 days of ethanol consumption, respectively. The present study demonstrates that chronic ethanol consumption induces an increase in the proportion of the total MHC content composed of the beta-isoform. This isoform transition is accompanied by an accumulation of beta-MHC mRNA, suggesting that the switch is organized pretranslationally. A functional consequence of this transition in MHC phenotype is demonstrated by significant decreases in the myofibrillar and myosin ATPase activities.
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PMID:Heavy long-term ethanol consumption induces an alpha- to beta-myosin heavy chain isoform transition in rat. 1065 Nov 60

The distributions of Mg2+ and Ca2+ in serum and lymphocyte from 51 arrhythmic patients (15 cases of atrial premature beat, 12 cases of atrial fibrillation, 24 cases of ventricular premature beat) and 30 healthy subjects were detected by flame atomic absorption spectrophotometry. The results showed that the distribution of Mg2+ of the arrhythmia cases was significantly lower than that of the control group (P < 0.01) and the concentration of Ca2+ in lymphocytes of arrhythmia case group was significantly higher than that of the control group (P < 0.01). The above distribution of Mg2+ and Ca2+ was somewhat related to the degree of heart failure. It is suggested that the lower distribution of Mg2+ in lymphocytes may cause arrhythmias.
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PMID:[Distribution of Mg2+ and Ca2+ in serum and lymphocyte of the patients with arrhythmia]. 1068 6

Sphingomyelin and its metabolic products are now known to have second messenger functions in a variety of cellular signaling pathways. At the epicenter of the sphingomyelin--cell signaling pathway is a family of phospholipases called sphingomyelinases. These enzymes cleave sphingomyelin to produce ceramide and phosphocholine. Ceramide in turn serves as a lipid second messenger that induces a variety of cell regulatory phenomenon such as programmed cell death (apoptosis), cell differentiation, cell proliferation, and sterol homeostasis. Neutral sphingomyelinase (N-SMase) is a Mg2+ sensitive enzyme that can be activated by a host of physiologically relevant and structurally diverse molecules like tumor necrosis factor-alpha (TNF-alpha), oxidized human low density lipoproteins (Ox-LDL), and several growth factors. Large amounts of ceramide accumulate in human fatty streaks and plaques along with Ox-LDL, growth factors, and proinflammatory cytokines in human atherosclerosis. A further role of ceramide and N-SMase in atherosclerosis was uncovered by the finding that Ox-LDL and TNF-alpha stimulated N-SMase activity. In turn, ceramide and/or a homolog serves as an important stress signaling molecule in signal transduction, which leads to apoptosis. Interestingly, an antibody against N-SMase can abrogate Ox-LDL and TNF-alpha induced apoptosis, and therefore may be useful for additional studies of apoptosis in experimental animals. Overexpression of recombinant human N-SMase in human aortic smooth muscle cells markedly stimulate apoptosis, presumably via the multioligomerization of the 'death domain'. Since plaque stability is an integral aspect of atherosclerosis management, activation of N-SMase and subsequent apoptosis may be vital events in the onset of plaque rupture, stroke and heart failure. In contrast to these observations in human hepatocytes, TNF-alpha mediated N-SMase activation did not induce apoptosis. Rather it stimulated the maturation of sterol regulatory element (SRE) binding protein (SREBP-1). Moreover, a cell permeable ceramide was found to reconstitute the phenomenon above in a sterol-independent fashion. These findings provide alternate avenues for therapy of patients with hypercholesterolemia and atherosclerosis. The findings reported here suggests that N-SMase plays important cell regulatory roles and provide an exciting opportunity to further these findings to understand the pathophysiology of human disease states.
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PMID:Neutral sphingomyelinase: past, present and future. 1100 63

Meta-analysis of previous relatively small clinical trials, comparing intravenous magnesium with placebo in acute myocardial infarction (AMI) patients, mainly without thrombolytic therapy, demonstrated that magnesium reduced in-hospital mortality by 19%, mainly by reducing the incidence of serious arrhythmias and left ventricular heart failure by one quarter. These findings have led us to hypothesize that magnesium treatment inhibits platelet-dependent thrombosis in patients with coronary artery disease (CAD). In a prospective, double blind, and crossover study, we have recently demonstrated that oral magnesium treatment inhibits thrombus formation measured by platelet-dependent thrombosis in stable CAD patients by 35%. This effect appears to be independent of platelet aggregation and activation, and is additive to that of aspirin. High dose of intravenous magnesium can inhibit thrombus formation and is associated with suppression of platelet aggregation. Magnesium treatment can dose-dependently inhibit a wide variety of agonists of platelet aggregation, such as thromboxane A2 and stimulate prostacyclin synthesis. The molecular basis for these effects is likely modulated via reduction of intracellular calcium mobilization. Hypomagnesemia also selectively impaired the release of nitric oxide from the coronary endothelium. We have recently demonstrated that oral magnesium treatment can improve endothelium-dependent vasodilation in CAD patients with optimal lipid values. Because nitric oxide is a potent endogenous vasodilator and inhibitor of platelet aggregation and adhesion, hypomagnesemia could promote vasoconstriction and coronary thrombosis in hypomagnesemic states. These findings suggest a potential mechanism whereby magnesium may beneficially alter outcomes in CAD patients.
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PMID:The role of magnesium as antithrombotic therapy. 1110 30

Experimental heart failure is associated with cardiac magnesium loss, causing increased beat-to-beat variability in the action potential. Unstable repolarization contributes to sudden death, but no therapy has been shown to reduce repolarization variability safely. We sought to test whether a prolonged infusion of magnesium sulfate (MgSO(4); 40 mmol/24 hours) would normalize QT interval variability in patients with compensated heart failure. Fifteen patients (New York Heart Association class II to III; mean age 63 years) were enrolled in a placebo-controlled, double-blind study. Surface electrocardiograms were recorded and digitized at entry and at 48 and 168 hours (drug washout). Repolarization stability was assessed using an automated method measuring each QT interval in a 5-minute epoch. The QT variability index was derived as the ratio of normalized QT-to-normalized heart rate variability. Seven of 15 patients received MgSO(4). Mean heart rate and QT did not change in either group. The QT variability index was stable in the placebo group (-0.69 +/- 0.15 at entry, -0.71 +/- 0.22 at 48 hours, -0.70 +/- 0.18 at 168 hours), but decreased significantly in the treated group at 48 hours (-0.95 +/- 0.19 to -1.36 +/- 0.13, p <0.05 repeated-measures analysis of variance), returning to baseline at 168 hours (-0.84 +/- 0.18). Regression analyses showed that administration of MgSO(4) resulted in a stronger correlation between the QT and RR interval (p <0.01). Thus, MgSO(4) stabilizes cardiac repolarization in patients with compensated heart failure due to ischemic heart disease. Magnesium therapy may be useful in altering the proarrhythmic substrate in heart failure.
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PMID:Usefulness of magnesium sulfate in stabilizing cardiac repolarization in heart failure secondary to ischemic cardiomyopathy. 1147 98

A considerable number of experimental, epidemiological and clinical studies are now available which point to an important role of Mg2+ in the etiology of cardiovascular pathology. In human subjects, hypomagnesemia is often associated with an imbalance of electrolytes such as Na+, K+ and Ca2+. Abnormal dietary deficiency of Mg2+ as well as abnormalities in Mg2+ metabolism play important roles in different types of heart diseases such as ischemic heart disease, congestive heart failure, sudden cardiac death, atheroscelerosis, a number of cardiac arrhythmias and ventricular complications in diabetes mellitus. Mg2+ deficiency results in progressive vasoconstriction of the coronary vessels leading to a marked reduction in oxygen and nutrient delivery to the cardiac myocytes. Numerous experimental and clinical data have suggested that Mg2+ deficiency can induce elevation of intracellular Ca2+ concentrations, formation of oxygen radicals, proinflammatory agents and growth factors and changes in membrane perrmeability and transport processes in cardiac cells. The opposing effects of Mg2+ and Ca2+ on myocardial contractility may be due to the competition between Mg2+ and Ca2+ for the same binding sites on key myocardial contractile proteins such as troponin C, myosin and actin. Stimulants, for example, catecholamines can evoke marked Mg2+ efflux which appears to be associated with a concomitant increase in the force of contraction of the heart. It has been suggested that Mg2+ efflux may be linked to the Ca2+ signalling pathway. Depletion of Mg2+ by alcohol in cardiac cells causes an increase in intracellular Ca2+, leading to coronary artery vasospasm, arrhythmias, ischemic damage and cardiac failure. Hypomagnesemia is commonly associated with hypokalemia and occurs in patients with hypertension or myocardial infarction as well as in chronic alcoholism. The inability of the senescent myocardium to respond to ischemic stress could be due to several reasons. Mg2+ supplemented K+ cardioplegia modulates Ca2+ accumulation and is directly involved in the mechanisms leading to enhanced post ischemic functional recovery in the aged myocardium following ischemia. While many of these mechanisms remain controversial and in some cases speculative, the beneficial effects related to consequences of Mg2+ supplementation are apparent. Further research are needed for the incorporation of these findings toward the development of novel myocardial protective role of Mg2+ to reduce morbidity and mortality of patients suffering from a variety of cardiac diseases.
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PMID:Protective role of magnesium in cardiovascular diseases: a review. 1234 4


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