Blood pressure response during long-term treatment with magnesium is dependent on magnesium status. A double-blind, placebo-controlled study in essential hypertension and in subjects with high-normal blood pressure. Nutritional dose of magnesium in hypertensive patients on beta blockers lowers systolic blood pressure: a double-blind, cross-over study. Reduction of blood pressure with oral magnesium supplementation in women with mild to moderate hypertension. Magnesium administration and dysrhythmias after cardiac surgery. A placebo-controlled, double-blind, randomized trial. Metabolic and hemodynamic effects of magnesium supplementation in patients with essential hypertension. Efficacy of potassium and magnesium in essential hypertension: a double-blind, placebo controlled, crossover study. Nutritional magnesium supplementation does not change blood pressure nor serum or muscle potassium and magnesium in untreated hypertension. A double-blind crossover study. Effects of magnesium supplementation in hypertensive patients: assessment by office, home, and ambulatory blood pressures. Effect of single dose magnesium on arrhythmias in patients undergoing coronary artery bypass surgery. A randomized, double-blind, placebo-controlled pilot trial of intravenous magnesium sulfate in acute stroke.
Both experimental and epidemiological studies support the idea of magnesium supplementation in essential hypertension. We added 15 mmol Mg to a free diet in 71 subjects with mild essential hypertension or a high-normal blood pressure in a double-blind, placebo-controlled study over 6 months. The treatment, which raised urinary magnesium excretion 30%, induced no general effects on the blood pressure. However, when the changes in blood pressure in the actively treated group were related to the pretreatment magnesium status, a correlation was found between pretreatment urinary magnesium excretion and the induced change in supine blood pressure (P less than .05) with a blood pressure reduction in subjects with a low pretreatment urinary excretion of magnesium, and a pressor effect in the subjects with the highest pretreatment levels of urinary magnesium. The induced change in blood pressure was furthermore found to be inversely correlated to the changes in serum magnesium and urinary excretion of sodium (P less than .03) induced by treatment indicating that both a direct calcium antagonist action of magnesium at the cellular level as well as a diuretic effect of the increased magnesium load might be involved in the blood pressure effects of magnesium. Pretreatment serum potassium concentration also appeared to be a predictor of the induced change in standing blood pressure (P less than .03). In conclusion, magnesium supplementation does not seem to be effective in unselected mild hypertensive subjects or in subjects with a high-normal blood pressure and can therefore not be generally recommended.(ABSTRACT TRUNCATED AT 250 WORDS) To evaluate if magnesium alters blood pressure in hypertensive patients treated with beta blockers and if such effect can be coupled to a change in potassium and magnesium levels in muscle, serum and urine.
                A randomized double-blind, cross-over study with magnesium and placebo taken orally, each for 8 weeks.
                Outpatient clinic, University Hospital, Umeå, Sweden.
                Thirty-nine patients aged 26-69 years with moderate essential hypertension, treated before entry and during the study with continuous, unchanged beta blockers completed the study.
                Random allocation to receive magnesium aspartate or placebo. Daily magnesium dose was 15 mmol (365 mg) distributed three times a day over 8 weeks.
                Blood pressure, serum, urine and muscle magnesium and potassium. Measurements performed at the start, after 8 and 16 weeks.
                Systolic supine and standing blood pressure significantly decreased when magnesium was supplemented following placebo but not when magnesium was given at start. When magnesium and placebo groups were independently compared there was no significant change in supine and standing systolic and diastolic pressure. Serum and urine magnesium and serum potassium were significantly higher after magnesium treatment, whilst no change was present in urine potassium or in muscle magnesium and potassium.
                This study showed that 15 mmol magnesium day-1 given to mild to moderate hypertensive patients treated with beta blockers could be the cause of a significant decrease in supine and standing systolic blood pressure. In a double-blind controlled trial, 91 middle-aged and elderly women with mild to moderate hypertension who were not on antihypertensive medication were randomly assigned to treatment with magnesium aspartate-HCl (20 mmol Mg/d) or placebo for 6 mo. Magnesium aspartate-HCl in the given dose was well-tolerated and was not associated with an increased frequency of diarrhea compared with placebo. At the end of the study, systolic blood pressure had fallen by 2.7 mm Hg (95% CI -1.2, 6.7; P = 0.18) and diastolic blood pressure by 3.4 mm Hg (1.3, 5.6; P = 0.003) more in the magnesium group than in the placebo group. Blood pressure response was not associated with baseline magnesium status, as measured by dietary magnesium intake and urinary magnesium excretion. Urinary magnesium excretion in the magnesium group increased by 50% during the intervention period. No changes were seen in other biochemical indexes, including serum concentrations of total and high-density-lipoprotein cholesterol. The findings suggest that oral supplementation with magnesium aspartate-HCl may lower blood pressure in subjects with mild to moderate hypertension. To determine whether magnesium administration is effective in reducing postoperative morbidity and mortality after cardiac surgery.
                Randomized, double-blind, placebo-controlled trial.
                A tertiary acute-care 500-bed university teaching hospital.
                Over a 6-month period, 100 patients electively scheduled for cardiac surgery involving cardiopulmonary bypass were studied.
                Fifty patients were randomized to receive an intravenous infusion of magnesium chloride, 2 g, and 50 patients received placebo intraoperatively after the termination of cardiopulmonary bypass.
                Magnesium-treated patients had a significantly decreased frequency (P < .04) of postoperative ventricular dysrhythmias (eight [16%] of 50) compared with placebo-treated patients (17 [34%] of 50). Patients who were normomagnesemic postoperatively had new supraventricular dysrhythmias less frequently (P < .03) than patients who were hypomagnesemic postoperatively (eight [17%] of 48 vs 19 [37%] of 52). Compared with placebo-treated patients, magnesium-treated patients had significantly higher (P < .02) postoperative cardiac indices in the intensive care unit (2.8 +/- 0.1 vs 2.5 +/- 0.1 L/min per m2). Patients with postoperative total and ultrafilterable hypomagnesemia had postoperative ventricular dysrhythmias (P < .04) and required prolonged mechanical ventilatory support (P < .01) more frequently than patients without postoperative hypomagnesemia.
                Total and ultrafilterable hypomagnesemia are prevalent findings in cardiac surgery patients, and postoperative hypomagnesemia is strongly associated with clinically important morbidity. Magnesium administration decreased the frequency of postoperative ventricular dysrhythmias and increased the stroke volume and thereby cardiac index in the early postoperative period. The effect of magnesium supplementation on blood pressure, erythrocyte cation metabolism, and serum lipids was evaluated in 13 patients with mild hypertension. After randomization and a 3-wk placebo run-in period, seven patients received 40 mmol Mg aspartate (20 mmol elemental Mg twice daily) and six received placebo for 3 mo. In comparison with placebo treatment, magnesium aspartate therapy had no effect on blood pressure, lipid concentrations, or erythrocyte cation metabolism. These results demonstrate that in magnesium-repleted hypertensive subjects, magnesium supplementation does not affect blood pressure or lipids probably because magnesium has no effect on cellular cation metabolism in magnesium-replete individuals. To evaluate the antihypertensive activity of potassium given alone or in combination with magnesium in patients with mild hypertension.
                A double blind, randomised, placebo controlled, crossover trial of 32 weeks' duration.
                Cardiology outpatient department, Sassoon General Hospitals, Pune, India.
                37 Adults with mild hypertension (diastolic blood pressure less than 110 mm Hg).
                Patients received either placebo or potassium 60 mmol/day alone or in combination with magnesium 20 mmol/day in a crossover design. No other drug treatment was allowed.
                Blood pressure and heart rate assessed at weekly intervals and biochemical parameters at monthly intervals.
                Potassium alone or in combination with magnesium produced a significant reduction in systolic and diastolic blood pressures (p less than 0.001) and a significant reduction in serum cholesterol concentration (p less than 0.05); other biochemical variables did not change. Magnesium did not have an additional effect. Urinary potassium excretion increased significantly in the groups who received potassium alone or in combination with magnesium. The drug was well tolerated and compliance was satisfactory.
                Potassium 60 mmol/day lowers arterial blood pressure in patients with mild hypertension. Giving magnesium as well has no added advantage. The aim of this study was to evaluate if a nutritional dose of magnesium given orally changes the blood pressure in untreated hypertensive patients and if orally-given magnesium had any influence on serum and muscle magnesium and potassium. A randomized, double-blind crossover study design was followed with magnesium 15 mmol/day or placebo treatment for two months. Thirty-nine patients aged 20-59 years, were treated. Samples for magnesium and potassium in blood, muscle and urine were taken at entry time, after two months (crossover time) and after four months (end of study). Systolic and diastolic supine and standing blood pressures were measured at the same times. No significant change in blood pressure, serum or muscle concentrations of electrolytes were observed on magnesium treatment. Urine magnesium rose significantly on magnesium, and it decreased significantly on placebo. Therefore results suggest that 15 mmol magnesium/day, given to untreated mild-to-moderate hypertensives does not alter blood pressure nor the concentrations of magnesium and potassium in serum and muscle, in patients with normal magnesium turnover. An increase in magnesium intake has been suggested to lower blood pressure (BP). However, the results of clinical studies are inconsistent. We studied the effects of magnesium supplementation on office, home, and ambulatory BPs in patients with essential hypertension. Sixty untreated or treated patients (34 men and 26 women, aged 33 to 74 years) with office BP >140/90 mm Hg were assigned to an 8-week magnesium supplementation period or an 8-week control period in a randomized crossover design. The subjects were given 20 mmol/d magnesium in the form of magnesium oxide during the intervention period. In the control period, office, home, and average 24-hour BPs (mean+/-SE) were 148.6+/-1.6/90.0+/-0.9, 136.4+/-1.3/86.8+/-0.9, and 133.7+/-1.3/81.0+/-0.8 mmHg, respectively. All of these BPs were significantly lower in the magnesium supplementation period than in the control period, although the differences were small (office, 3.7+/-1.3/1.7+/-0.7 mmHg; home, 2.0+/-0.8/1.4+/-0.6 mmHg; 24-hour, 2.5+/-1.0/1.4+/-0.6 mm Hg). Serum concentration and urinary excretion of magnesium increased significantly with magnesium supplementation. Changes in 24-hour systolic and diastolic BPs were correlated negatively with baseline BP or changes in serum magnesium concentration. These results indicate that magnesium supplementation lowers BP in hypertensive subjects and this effect is greater in subjects with higher BP. Our study supports the usefulness of increasing magnesium intake as a lifestyle modification in the management of hypertension, although its antihypertensive effect may be small. To evaluate the safety and role of prophylactic administration of magnesium in preventing arrhythmias.
                This double blind randomized placebo controlled clinical trial was conducted at Aga Khan University Hospital on coronary artery bypass surgery patients. All patients were connected to holter monitor before induction of anaesthesia and this monitoring continued for 24 hours. Study drug containing either 2-grams of magnesium or normal saline was given after intubation. Levels of serum magnesium was checked preoperatively and then in ICU at 0, 6, 12, and 24 hours. Independent t-test and chi square test were used for analysis. Statistical significance was defined as p-value < 0.05.
                A total of 104 patients consented to participate in the study, 53 patients were randomly allocated in magnesium (Mg) group and 51 in placebo group. Two (3.77%) patients in magnesium group and five patients (9.8%) in placebo group developed atrial fibrillation. Incidence of ventricular and supraventricular tachycardia was also slightly higher in placebo. Mg level after arrival in CICU (Cardiac Intensive Care Unit) showed mean of 2.1 in magnesium group and 1.6 in placebo group (p = 0.6).
                Low magnesium levels were noticed in the placebo group after cardiopulmonary bypass and although prophylactic administration of magnesium sulphate was relatively safe but significant benefit on prevention of arrhythmias could not be attained. Magnesium ions act as endogenous vasodilators of the cerebral circulation and act pharmacologically as noncompetitive antagonists of the N-methyl-D-aspartate receptor by virtue of their role as endogenous voltage-sensitive blockers of the ion channel. The preclinical efficacy of magnesium has been demonstrated in standard models of stroke.
                Sixty patients were randomized to magnesium sulfate (8 mmol IV over 15 minutes and 65 mmol over 24 hours) or placebo within 12 hours of clinically diagnosed middle cerebral artery stroke. Pulse, blood pressure, and serum magnesium levels were monitored. Primary outcome was death or significant functional impairment (Barthel Index score < 60) at 3 months.
                Magnesium was well tolerated, with no significant adverse effects and no change in blood pressure or pulse rate. Laboratory and electrocardiographic variables did not differ significantly between placebo- and magnesium-treated groups. Serum magnesium rose from 0.76 mmol/L to 1.42 mmol/L over 24 hours and remained significantly higher than in the placebo group at 48 hours. Thirty percent of magnesium-treated and 40% of placebo-treated patients were dead or disabled (Barthel Index score < 60) at 3 months (P = .42). There was a decrease in the number of early deaths in the magnesium-treated group (P = .066, log-rank test).
                Magnesium sulfate is well tolerated after acute stroke and has no deleterious hemodynamic effects at this dose. Further trials are required to determine efficacy.
In view of the poor quality of included trials and the heterogeneity between trials, the evidence in favour of a causal association between magnesium supplementation and blood pressure reduction is weak and is probably due to bias. This is because poor quality studies generally tend to over-estimate the effects of treatment. Larger, longer duration and better quality double-blind placebo controlled trials are needed to assess the effect of magnesium supplementation on blood pressure and cardiovascular outcomes.