Bloom S
Magnesium. 1986;5(3-4):154-64.
The death rate due to myocardial infarction appears to vary with dietary consumption of Mg. This could be due to effects on atherosclerosis, coronary artery spasm, altered pathogenesis of myocardial infarction, increased vulnerability to arrhythmia, or some combination of these. Mg deficiency (MD) has been found to increase the severity of a coronary occlusive event in terms of the amount of necrosis produced by a given occlusion. MD is also associated with increased likelihood of arrhythmia development. In addition, reduced extracellular magnesium concentration (Mgo) is associated with contraction of vascular smooth muscle that may be the equivalent of arterial spasm. In hamsters, MD leads to fibrinoid necrosis thought to be secondary to Ca overload. These 3 effects: coronary artery spasm, cardiac arrhythmia, and increased vulnerability to myocardial necrosis following coronary occlusion, may all be dependent on changes in myocardial and vascular smooth muscle electrolyte metabolism that follow from the reduced Mgo that is associated with MD.
心肌梗死的死亡率似乎随镁的膳食摄入量而变化。这可能是由于对动脉粥样硬化、冠状动脉痉挛、心肌梗死发病机制改变、心律失常易感性增加或这些因素的某种组合产生的影响。已发现镁缺乏（MD）会根据给定闭塞产生的坏死量增加冠状动脉闭塞事件的严重程度。MD还与心律失常发生的可能性增加有关。此外，细胞外镁浓度（Mgo）降低与血管平滑肌收缩有关，这可能等同于动脉痉挛。在仓鼠中，MD会导致纤维蛋白样坏死，认为这是继发于钙超载的结果。这三种效应：冠状动脉痉挛、心律失常以及冠状动脉闭塞后心肌坏死易感性增加，可能都取决于与MD相关的Mgo降低所导致的心肌和血管平滑肌电解质代谢变化。
