Connection between Magnesium Deficiency, Coronary Vasospasm & Endothelial Injury

“...Two vicious cycles generating ischaemia and injury
The aetiology of coronary vasospasm is not fully understood. Only a 40-60% reduction in luminal diameter for 1 h is required to produce arterial endothelial damage and thrombosis.[9] Coronary vasospasm secondary to frequent rises in catecholamine concentrations that result from very long endurance exercise, together with high shear stress[9] and turbulence,[9] could be responsible for endothelial injury. In dogs, submaximum exercise raises catecholamine concentration sufficiently to increase alpha-adrenergic coronary vasoconstrictor tone. [10]
This vasospasm in turn could be responsible for the focal necrosis that leads to the focal fibrosis of the myocardium.[11] A potential vicious cycle might be set up between coronary vasospasm, endothelial injury, and reduction or loss of endothelium-derived relaxing factor[12]" Since acute severe myocardial ischaemia caused by high concentrations of catecholamines induces release of catecholamines from the adrenal medulla and myocardial nerve endings, there is the potential for a second vicious cycle.[13] By impairing left ventricular function, both cycles could have been responsible for the exercise-induced pulmonary oedema described above. Both runners had had similar symptoms while completing ultramarathons the previous year.[6]
With acute hypoxia during high-altitude marathons[7] run without acclimatisation[14] an imbalance betweeen myocardial oxygen supply and demand might be exacerbated by high concentrations of catecholamines[15] and by respiratory alkalosis,[14] both of which are conducive to coronary vasospasm.[10,16] Increased myocardial oxygen demand[13] occurs because of a high rate-pressure product resulting from hypoxia,[14] and exposure to cold. Both hypoxia and cold compound rises in catecholamine concentrations.[17]

Magnesium deficiency and thrombogenesis
Magnesium ion deficiency is a further possible complication of long exercise,[18-20] some deficiency may still be present 3 months later.[18] The mechanism is not clear, but may be partly due to removal of free magnesium ions from the circulation by chelation with catecholamine-induced free fatty acids.[19] Exposure to heat also contributes to magnesium ion deficiency.[20] This deficiency increases release of catecholamines,[21] increases the potential for coronary vasospasm,[22] potentiates the vasoconstrictor action of catecholamines,[22] and—in combination with catecholamine infusions or stress—sensitises animals to myocardial necrosis.[23] Magnesium ion deficiency may precipitate a hypercoagulable state,[23] which may be aggravated by residual increased catecholamines (conducive to platelet aggregation and thrombin generation),[24] the increase in catecholamine concentration may persist until the second day after a marathon.[25] It is noteworthy that in a group of 20 patients with vasospastic (variant) angina Goto et al [26] showed that almost half had magnesium ion deficiency that is often unrecognised.[19,21,26] ...”

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