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A systematic review and meta-analysis of prospective studies that comprised 313,041 individuals and 11,995 cardiovascular diseases, 7534 ischemic heart diseases, and 2686 fatal ischemic heart disease events found that higher serum levels of magnesium were significantly associated with a lower risk of cardiovascular disease, and higher dietary magnesium intakes (up to approximately 250 mg/day) were associated with a significantly lower risk of ischemic heart disease caused by a reduced blood supply to the heart muscle.
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Circulating serum magnesium (per 0.2 mmol/L increment) was associated with a 30% lower risk of cardiovascular disease (RR: 0.70; 95% CI: 0.56, 0.88 per 0.2 mmol/L) and trends toward lower risks of IHD (RR: 0.83; 95% CI: 0.75, 1.05) and fatal ischemic heart disease (RR: 0.61; 95% CI: 0.37, 1.00). Dietary magnesium (per 200 mg/day increment) was not significantly associated with cardiovascular disease (RR: 0.89; 95% CI: 0.75, 1.05) but was associated with a 22% lower risk of ischemic heart disease (RR: 0.78; 95% CI: 0.67, 0.92). The association of dietary magnesium with fatal ischemic heart disease was nonlinear (p < 0.001), with an inverse association observed up to a threshold of ~250 mg/day (RR: 0.73; 95% CI: 0.62, 0.86), compared with lower intakes . ½Û´Ä·ìÀ¶¥Þ¥°¥Í¥·¥¦¥à¡Ê0.2mmol / LÁý²Ã¤¢¤¿¤ê¡Ë¤Ï¿´·ì´É¼À´µ¤Î¥ê¥¹¥¯¤ò30¡óÄã²¼¤µ¤»¡¢¤½¤·¤Æ¡¢µõ·ìÀ¿´¼À´µ(IHD)¤ÈÃ×̿Ū¤Êµõ·ìÀ¿´¼À´µ¤ËØí´µ¤¹¤ë¥ê¥¹¥¯¤ò²¼¤²¤ë·¹¸þ¤¬¤¢¤ê¤Þ¤¹¡£
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¿©»ö¤Ë¤è¤ë¥Þ¥°¥Í¥·¥¦¥à¤ÈÃ×̿Ūµõ·ìÀ¿´¼À´µ¤È¤Î´ØÏ¢¤ÏľÀþ¤Ç¤Ï¤Ê¤¯¡¢¤è¤êÄ㤤ÀݼèÎ̤ËÈæ³Ó¤¹¤ë¤È¡¢µÕÁê´Ø¡ÊµÕÈæÎã¡Ë¤ÏÌó250 mg /Æü¤ÎïçÃÍ¡Êʬ´ôÅÀ¡Ë¤Þ¤Ç´Ñ»¡¤µ¤ì¤Þ¤·¤¿¡£ ¡Ê£±Æü¤Ë¿©»ö¤Ë´ó¤ë¥Þ¥°¥Í¥·¥¦¥à¤ÎÀݼèÎ̤¬¶Ë¾¯Î̤ξì¹ç¡¢¸ú²Ì¤¬Ìµ¤¤¤È¸À¤¦¤³¤È¡£¡Ë In a monocentric, controlled, double-blind study, 79 patients with severe congestive heart failure (NYHA IV) under optimal medical cardiovascular treatment were randomised to receive either magnesium orotate (6000 mg for 1 month, 3000 mg for about 11 months, n = 40) or placebo (n = 39). Both groups were comparable in demographic data, duration of heart failure and pre- and concomitant treatment. After mean treatment duration of 1 year (magnesium orotate: 364.1 +/¡Ý 14.7 days, placebo: 361.2 +/¡Ý 12.7 days) the survival rate was 75.7% compared to 51.6% under placebo (p < 0.05). Clinical symptoms improved in 38.5% of patients under magnesium orotate, whereas they deteriorated in 56.3% of patients under placebo (p < 0.001) . ñ¿´ÂÐ¾ÈÆó½ÅÌÕ¸¡»î¸³¡ÊÃ𣱡ˤǡ¢ºÇŬ¤Ê°å³ØÅª¿´·ì´É¼£ÎŤò¼õ¤±¤Æ¤¤¤ë½Å¾Éݵ·ìÀ¿´ÉÔÁ´¡ÊNYHA IV¡Ë´µ¼Ô79¿Í¤ËÂФ·¡¢Ìµºî°Ù¤Ç¡¢40¿Í¤ËÂФ·¤Æ¤Ï¥ª¥í¥Á¥ó»À¥Þ¥°¥Í¥·¥¦¥à¤ò1¥ö·î6000 mg¤Î¥±¡¼¥¹¤ÈÌó11¥ö·î3000 mg¤Î¥±¡¼¥¹¤Ëʬ¤±ÅêÍ¿¤·¡¢»Ä¤ê¤Î39¿Í¤ËÂФ·¤Æ¤ÏÀ®Ê¬¤òÁ´¤¯´Þ¤Þ¤Ê¤¤µ¶Ìô¡Ê¥×¥é¥»¥Ü¡Ë¤òÅêÍ¿¤·¤Þ¤·¤¿¡£
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Magnesium orotate may be used as adjuvant therapy in patients on optimal treatment for severe congestive heart failure, increasing survival rate and improving clinical symptoms and patient¡Çs quality of life.
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A meta-analysis of seven prospective trials with a total of 241,378 participants observed a modest but statistically significant inverse association between magnesium intake and risk of stroke. An intake increment of 100 mg Magnesium/day was associated with an 8% reduction in risk of total stroke (combined RR: 0.92; 95% CI: 0.88, 0.97). Magnesium intake was inversely associated with risk of ischemic stroke (RR: 0.91; 95% CI: 0.87, 0.96) but not intracerebral hemorrhage (RR: 0.96; 95% CI: 0.84, 1.10) or subarachnoid hemorrhage (RR: 1.01; 95% CI: 0.90, 1.14) . In an updated meta-analyses of prospective studies to date, the combined RR of total stroke was 0.87 (95% CI: 0.83, 0.92) for a 100 mg/day increase in magnesium intake, 0.91 (95% CI: 0.88, 0.94) for a 1000 mg/day increase in potassium intake, and 0.98 (95% CI: 0.94, 1.02) for a 300 mg/day increase in calcium intake . ¹ç·×241,378¿Í¤Î»²²Ã¼Ô¤Ë¤è¤ë7¤Ä¤ÎÁ°¸þ¤»î¸³¤Î²òÀϤǤϡ¢¥Þ¥°¥Í¥·¥¦¥àÀݼèÎ̤ÈÇ¾Â´Ãæ¤Î¥ê¥¹¥¯¤È¤Î´Ö¤ËÃæÄøÅ٤Ǥ¹¤¬Åý·×Ū¤ËͰդʵÕÁê´Ø¤ò´Ñ»¡¤·¤Þ¤·¤¿¡£¡ÊÃí¡Ë¤Ä¤Þ¤ê¡¢¥Þ¥°¥Í¥·¥¦¥à¤ò¿¤¯Àݼ褹¤ë¤È¡¢Ç¾Â´Ãæ¤Î¥ê¥¹¥¯¤¬¸º¤ë¤È¤¤¤¦¤³¤È¡£
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Magnesium sulfate is neuroprotective in preclinical models of stroke and has shown signals of potential efficacy with an acceptable safety profile when delivered early after stroke onset in humans. In a recent study, 1700 patients with suspected stroke received either intravenous magnesium sulfate or placebo, beginning within 2 h after symptom onset. Prehospital initiation of magnesium sulfate therapy was safe and allowed the start of therapy within 2 h after the onset of stroke symptoms, but it did not improve disability outcomes at 90 days .
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The frequency of cardiac arrhythmias occurring after myocardial infarction is higher in hypomagnesemic patients and can be reduced by magnesium administration. Several trials indicate that an intravenous magnesium infusion early after suspected myocardial infarction could decrease the risk of death. A meta-analysis with 2316 patients of the Leicester Intravenous Magnesium Intervention Trial (LIMIT-2) found a significant reduction in mortality in those patients who were given intravenous magnesium sulfate (8 mmol over 5 min followed by 65 mmol over 24 h) within 24 h of suspected myocardial infarction or physiological saline. By intention-to-treat analysis mortality from all causes was 7.8% in the magnesium group and 10.3% in the placebo group (2 p = 0.04), a relative reduction of 24% (95% confidence interval 1%–43%) . However, another study involving 58,050 patients with suspected myocardial infarction, (ISIS-4, Fourth International Study of Infarct Survival), showed no benefit from magnesium therapy . Also in the Magnesium in Coronaries (MAGIC) trial with 6213 patients with acute ST-elevation myocardial infarction, magnesium therapy had no benefit . Thus, the use of intravenous magnesium sulphate remains controversial. Nevertheless, magnesium therapy should be considered in those with refractory arrhythmias.
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