Urinary and plasma magnesium and risk of ischemic heart disease

Joosten, Michel M.; Gansevoort, Ron T.; Mukamal, Kenneth J.; Harst, Pim van der; Geleijnse, Johanna M.; Feskens, Edith J. M.; Navis, Gerjan; Bakker, Stephan J. L.

doi:10.3945/ajcn.112.054114

Cited by 91 publications

(61 citation statements)

References 46 publications

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“…Low urinary magnesium excretion has been previously associated with an increased risk of ischemic heart disease [46]. In addition, urinary magnesium excretion can estimate the amount of absorbed magnesium, considering that renal elimination is highly relevant for an adequate magnesium homeostasis.…”

Section: Discussionmentioning

confidence: 99%

Oral magnesium supplementation improves endothelial function and attenuates subclinical atherosclerosis in thiazide-treated hypertensive women

Cunha

d'El-Rei

Medeiros

et al. 2017

Journal of Hypertension

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Oral magnesium supplementation improves endothelial function and attenuates subclinical atherosclerosis in thiazide-treated hypertensive women. Journal of Hypertension, 35(1), pp. 89-97.There may be differences between this version and the published version. You are advised to consult the publisher's version if you wish to cite from it.http://eprints.gla.ac.uk/130809/ Condensed AbstractThis study evaluated the effects of magnesium supplementation on blood pressure (BP) and vascular function in thiazide-treated hypertensive women, mean 24-h BP≥130/80 mmHg, in a randomized, double-blind, clinical trial comparing placebo and magnesium chelate 600 mg/day supplementation. Brachial flow-mediated dilatation (FMD) and central hemodynamic parameters were measured at inclusion and after 6 months. The magnesium group demonstrated a significant reduction in systolic and diastolic BP, and a significant increase in variation of FMD versus the placebo group (+3.7±2.1 vs 2.4±1.2 %, p=0.015). In conclusion, magnesium supplementation was associated with better BP control and improved endothelial function in thiazide-treated hypertensive. AbstractEpidemiological studies demonstrate an inverse association between serum magnesium and incidence of cardiovascular disease. Diuretics commonly cause hypomagneseamia.We evaluated effects of magnesium supplementation on blood pressure (

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Section: Discussionmentioning

confidence: 99%

Oral magnesium supplementation improves endothelial function and attenuates subclinical atherosclerosis in thiazide-treated hypertensive women

Cunha

d'El-Rei

Medeiros

et al. 2017

Journal of Hypertension

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“…Magnesium depletion is associated with cardiovascular disease, probably through several mechanisms, includ ing abnormal cardiac conduction, and might increase the risk of sudden cardiac death. 6,7 An association between magnesium depletion and type 2 diabetes mellitus has also been reported. 8 On the other hand, magnesium sulphate has an established place in the treatment and prevention of eclampsia.…”

Section: Introductionmentioning

confidence: 96%

Magnesium and cardiovascular complications of chronic kidney disease

Massy

Drüeke

2015

Nat Rev Nephrol

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Cardiovascular complications are the leading cause of death in patients with chronic kidney disease (CKD). Abundant experimental evidence suggests a physiological role of magnesium in cardiovascular function, and clinical evidence suggests a role of the cation in cardiovascular disease in the general population. The role of magnesium in CKD-mineral and bone disorder, and in particular its impact on cardiovascular morbidity and mortality in patients with CKD, is however not well understood. Experimental studies have shown that magnesium inhibits vascular calcification, both by direct effects on the vessel wall and by indirect, systemic effects. Moreover, an increasing number of epidemiologic studies in patients with CKD have shown associations of serum magnesium levels with intermediate and hard outcomes, including vascular calcification, cardiovascular events and mortality. Intervention trials in these patients conducted to date have had small sample sizes and have been limited to the study of surrogate parameters, such as arterial stiffness, vascular calcification and atherosclerosis. Randomized controlled trials are clearly needed to determine the effects of magnesium supplementation on hard outcomes in patients with CKD.

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“…Details of this study have been described elsewhere. 20 In brief, from 1997 to 1998, all inhabitants of Groningen, the Netherlands aged 28 to 75 years, were sent a questionnaire and a vial to collect a first morning void urine sample. Pregnant women and subjects with type 1 diabetes mellitus were excluded.…”

Section: Study Design and Populationmentioning

confidence: 99%

Sodium Excretion and Risk of Developing Coronary Heart Disease

et al. 2014

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Background— Despite compelling evidence for sodium’s adverse effects on blood pressure, it remains uncertain whether excess sodium intake is a risk factor for coronary heart disease (CHD) in the overall population and in potentially more susceptible subgroups. Methods and Results— We prospectively followed 7543 adults aged 28 to 75 years and free of cardiovascular and kidney disease in 1997/1998 of the Prevention of Renal and Vascular End-stage Disease (PREVEND) study. Sodium excretion was measured in two 24-hour urine collections at baseline. Potential susceptibility factors were blood pressure and plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP). Median 24-hour sodium excretion was 137 mmol (Q1–Q3, 106–171 mmol). During a median follow-up of 10.5 (Q1–Q3: 9.9–10.8) years, 452 CHD events occurred. In the entire cohort, there was no association between each 1-g/d (43 mmol/24 h) increment in sodium excretion and CHD risk (adjusted hazard ratio, 1.07; 95% confidence interval, 0.98–1.18; P =0.15). However, the association of sodium excretion with CHD risk tended to be modified by mean arterial pressure ( P interaction =0.08) and was modified by NT-proBNP ( P interaction =0.002). When stratified, each 1-g/d increment in sodium excretion was associated with an increased risk for CHD in subjects with hypertension (adjusted hazard ratio, 1.14; 95% confidence interval, 1.01–1.28; n=2363) and in subjects with NT-proBNP concentrations above the sex-specific median (adjusted hazard ratio, 1.16; 95% confidence interval, 1.03–1.30; n=3771). Conclusions— Overall, there was no association between sodium excretion and risk of CHD. The association between sodium excretion and CHD risk was modified by NT-proBNP. Higher sodium excretion was associated with an increased CHD risk among subjects with increased NT-proBNP concentrations or with hypertension.

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Urinary and plasma magnesium and risk of ischemic heart disease

Cited by 91 publications

References 46 publications

Oral magnesium supplementation improves endothelial function and attenuates subclinical atherosclerosis in thiazide-treated hypertensive women

Oral magnesium supplementation improves endothelial function and attenuates subclinical atherosclerosis in thiazide-treated hypertensive women

Magnesium and cardiovascular complications of chronic kidney disease

Sodium Excretion and Risk of Developing Coronary Heart Disease

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