Bashir Y, Sneddon J F, Staunton H A, Haywood G A, Simpson I A, McKenna W J, Camm A J
Department of Cardiological Sciences, St. George's Hospital Medical School, London, United Kingdom.
Am J Cardiol. 1993 Nov 15;72(15):1156-62. doi: 10.1016/0002-9149(93)90986-m.
Magnesium deficiency frequently develops in patients with congestive heart failure and may increase susceptibility to lethal arrhythmias and sudden death via multiple pathophysiologic mechanisms. The effects of peroral magnesium supplementation were investigated in a randomized, double-blind, crossover trial involving 21 patients with stable congestive heart failure secondary to coronary artery disease. All were receiving long-term loop diuretics, and had normal renal function, and low or normal serum magnesium concentrations. Subjects alternately received enteric-coated magnesium chloride (15.8 mmol magnesium per day) and placebo for 6 weeks. Magnesium therapy increased serum magnesium from 0.87 +/- 0.07 to 0.92 +/- 0.05 mmol/liter (p < 0.05), serum potassium from 4.0 +/- 0.3 to 4.3 +/- 0.4 mmol/liter (p < 0.01) and urinary magnesium excretion from 2.82 +/- 0.96 to 4.74 +/- 2.38 mmol/24 hours (p = 0.001). There was no significant change in heart rate or Doppler cardiac index, but mean arterial pressure decreased from 91 +/- 10 to 87 +/- 10 mm Hg (p < 0.05) and systemic vascular resistance from 1,698 +/- 367 to 1,613 +/- 331 dynes s cm-5 (p = 0.047). The frequency of isolated ventricular premature complexes was reduced by 23% (95% confidence interval [CI] 6 to 37%; p < 0.02), couplets by 52% (95% CI 30 to 65%; p < 0.001) and nonsustained ventricular tachycardia episodes by 24% (95% CI 15 to 49%; p < 0.01). Plasma epinephrine decreased from 447 +/- 535 to 184 +/- 106 pg/ml (p = 0.02), but there was no corresponding change in plasma norepinephrine or heart rate variability.(ABSTRACT TRUNCATED AT 250 WORDS)
充血性心力衰竭患者常出现镁缺乏，且可能通过多种病理生理机制增加发生致命性心律失常和猝死的易感性。在一项随机、双盲、交叉试验中，对21例因冠状动脉疾病导致的稳定型充血性心力衰竭患者口服补充镁的效果进行了研究。所有患者均长期服用袢利尿剂，肾功能正常，血清镁浓度低或正常。受试者交替接受肠溶氯化镁（每天15.8 mmol镁）和安慰剂，为期6周。镁治疗使血清镁从0.87±0.07 mmol/升增至0.92±0.05 mmol/升（p<0.05），血清钾从4.0±0.3 mmol/升增至4.3±0.4 mmol/升（p<0.01），尿镁排泄量从2.82±0.96 mmol/24小时增至4.74±2.38 mmol/24小时（p = 0.001）。心率或多普勒心脏指数无显著变化，但平均动脉压从91±10 mmHg降至87±10 mmHg（p<0.05），全身血管阻力从1698±367 dynes s cm-5降至1613±331 dynes s cm-5（p = 0.047）。孤立性室性早搏的频率降低了23%（95%置信区间[CI] 6%至37%；p<0.02），成对室性早搏降低了52%（95% CI 30%至65%；p<0.001），非持续性室性心动过速发作降低了24%（95% CI 15%至49%；p<0.01）。血浆肾上腺素从447±535 pg/ml降至184±106 pg/ml（p = 0.02），但血浆去甲肾上腺素或心率变异性无相应变化。（摘要截短于250字）
