Role of Magnesium in Cardiac Disease

Ebel, H.; Günther, Theodor

doi:10.1515/cclm.1983.21.5.249

Cited by 53 publications

(33 citation statements)

References 70 publications

(96 reference statements)

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“…2,3 Early diagnosis is decisive to avoid neurological problems that can lead to permanent neurological injury or even sudden death as a consequence of arrhythmias in extreme cases. 4,5 In HSH patients, serum magnesium (Mg 2 þ ) levels dramatically fall below the normal range (0.2-0.4 vs 0.70-0.95 mmol/l). 6,7 The body's Mg 2 þ balance is tightly regulated by a concerted action of intestinal absorption and excretion/reabsorption of Mg 2 þ via the kidney.…”

Section: Introductionmentioning

confidence: 99%

New TRPM6 missense mutations linked to hypomagnesemia with secondary hypocalcemia

et al. 2013

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Despite recent progress in our understanding of renal magnesium (Mg 2 þ ) handling, the molecular mechanisms accounting for transepithelial Mg 2 þ transport are still poorly understood. Mutations in the TRPM6 gene, encoding the epithelial Mg 2 þ channel TRPM6 (transient receptor potential melastatin 6), have been proven to be the molecular cause of hypomagnesemia with secondary hypocalcemia (HSH; OMIM 602014). HSH manifests in the newborn period being characterized by very low serum Mg 2 þ levels (o0.4 mmol/l) accompanied by low serum calcium (Ca 2 þ ) concentrations. A proportion of previously described TRPM6 mutations lead to a truncated TRPM6 protein resulting in a complete loss-of-function of the ion channel. In addition, five-point mutations have been previously described. The aim of this study was to complement the current clinical picture by adding the molecular data from five new missense mutations found in five patients with HSH. To this end, patch-clamp analysis and cell surface measurements were performed to assess the effect of the various mutations on TRPM6 channel function. All mutant channels, expressed in HEK293 cells, showed loss-of-function, whereas no severe trafficking impairment to the plasma membrane surface was observed. We conclude that the new TRPM6 missense mutations lead to dysregulated intestinal/renal Mg 2 þ (re)absorption as a consequence of loss of TRPM6 channel function.

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Section: Introductionmentioning

confidence: 99%

New TRPM6 missense mutations linked to hypomagnesemia with secondary hypocalcemia

et al. 2013

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“…In vitro experiments with adipocytes support this view. Intact adipocytes showed an increased magnesium uptake after treatment with adrenalin [16].…”

Section: Whole Blood and Serum Magnesium Measurementsmentioning

confidence: 96%

Determination of Magnesium in whole Blood and Serum of Ischemic Heart Disease(IHD) Patients by Flame Atomic Absorption Spectrometry

Abdulsahib¹

2011

AJAC

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Flame atomic absorption spectrometric determination of magnesium in whole blood and serum of ischemic heart disease patients and control with different ages and sex was proposed. The limiting interfering phosphate/magnesium ratio have been estimates. 2% w/v AlCl 3 ·6H 2 O was found to be very influential in removing phosphate interference effects. The detection limit was 0.065 μg/ml. Magnesium added to blood and serum sample, and carried through this method may be recovered completely (96% -100%) recovery percentage. The suggested method is simple, fast and selective. The statistical analysis of magnesium levels in blood and serum showed that blood and serum magnesium levels in patients were lower than magnesium contents of control group. Magnesium levels in blood and serum of males were significantly higher than females and the magnesium levels were age independent. These findings indicate that there was an association between blood and serum magnesium deficiency which can induce an entire array of path physiological phenomena known to be important in ischemic heart disease.

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“…Likewise, intravenous magnesium therapy has proven efficient in the treatment of toxemia of pregnancy,*-10 preterm labor,'1*12 certain tachyarhythmias, ventric~lar'~-~~ as well as supraventricular," and digitalis-toxic arrhythmias. l 8 In spite of this increasing therapeutic use of intravenous magnesium, only a few noncontrolled studies have investigated the effects of intravenous magnesium infusions on cardiovascular hemodynamics in humans, and the results are conflicting.19*20 Therefore, we have camed out a double-blind, placebo-controlled, cross-over study with the specific aim of evaluating the effect of these infusions on cardiac inotropism and maximal work capacity in healthy volunteers. Myocardial inotropism was evaluated by echocardiography and maximal work capacity by an ergometer bicycle exercise test.…”

Section: Introductionmentioning

confidence: 99%

Myocardial contractility and performance capacity after magnesium infusions in young healthy persons: A double‐blind, placebo‐controlled, cross‐over study

Rasmussen

Videbæk

Melchior

et al. 1988

Clinical Cardiology

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Summary: To evaluate the effect of intravenous magnesium (Mg) treatment on the inotropic state of the heart and maximal work capacity, 9 healthy volunteers were entered in a double-blind, placebo-controlled, cross-over study. Separated by an interval of three weeks, the volunteers were tested twice, each time randomly allocated to receive either an intravenous injection of 10 mmol magnesium chloride dissolved in 100 ml isotonic sodium chloride or placebo of isotonic sodium chloride only. Before and after each infusion myocardial inotropism was evaluated by echocardiography . Mitral-septal distance (MSA) was used as a measure for ejection fraction. On each test day an ergometer bicycle exercise test was performed, and maximal work capacity was calculated. Magnesium treatment reduced the MSA (from 4.2 to 2.9 mm, p=0.07), while no difference was found after placebo treatment. Likewise, a tendency toward increasing fractional shortening after magnesium treatment was detected, although this difference was not statistically significant (p=O.l). No difference in maximal work capacity between the magnesium and placebo periods was found. Serum magnesium concentrations rose significantly after the infusions (from 0.82 to 1.38 mmol/l, p

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Role of Magnesium in Cardiac Disease

Cited by 53 publications

References 70 publications

New TRPM6 missense mutations linked to hypomagnesemia with secondary hypocalcemia

New TRPM6 missense mutations linked to hypomagnesemia with secondary hypocalcemia

Determination of Magnesium in whole Blood and Serum of Ischemic Heart Disease(IHD) Patients by Flame Atomic Absorption Spectrometry

Myocardial contractility and performance capacity after magnesium infusions in young healthy persons: A double‐blind, placebo‐controlled, cross‐over study

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