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Published on: August 18, 2016
Insights
Magnesium plays a crucial role in coronary artery disease, influencing arteriosclerosis and myocardial function. Supplementation may offer benefits, particularly in managing ventricular arrhythmias and acute myocardial infarction.
Area of Science:
- Cardiology
- Biochemistry
- Pathophysiology
Background:
- Coronary artery disease (CAD) involves complex mechanisms including arteriosclerosis, coronary spasm, and myocardial dysfunction.
- Magnesium's role in cardiovascular health is increasingly recognized, with implications for various aspects of CAD.
Purpose of the Study:
- To review the multifaceted role of magnesium in the pathogenesis and management of coronary artery disease.
- To synthesize experimental and human evidence regarding magnesium's impact on arteriosclerosis, coronary spasm, myocardial function, acute myocardial infarction, and ventricular arrhythmias.
Main Methods:
- Literature review of experimental studies (animal models) and human epidemiological/retrospective studies.
- Analysis of magnesium's effects on arterial smooth muscle reactivity, myocardial mitochondria, and tissue magnesium levels during ischemia/infarction.
Main Results:
- Magnesium depletion exacerbates atherogenic effects, while supplementation shows a retarding effect.
- Low magnesium enhances arterial smooth muscle reactivity and may initiate coronary spasm; high magnesium suppresses it.
- Experimental magnesium deficiency disrupts myocardial mitochondria but does not directly cause cardiac failure.
- Ischemic or infarcted myocardium loses magnesium, potentially leading to ventricular arrhythmias.
- Magnesium-depleted hearts show larger necrotic areas after coronary occlusion.
- Serum magnesium levels fall in acute myocardial infarction, possibly due to lipolysis.
- Parenteral magnesium can treat ventricular fibrillation in CAD, irrespective of baseline serum levels.
Conclusions:
- Magnesium status is a significant factor in coronary artery disease development and progression.
- Magnesium plays a protective role against arteriosclerosis and coronary spasm.
- Magnesium management is crucial for mitigating risks associated with acute myocardial infarction and ventricular arrhythmias in CAD patients.
Abstract:
Magnesium in coronary artery disease is reviewed with regard to its role in the pathogenesis of arteriosclerosis, coronary spasm, myocardial function, acute myocardial infarction and ventricular arrhythmias. Experimentally, magnesium depletion potentiates and supplementation retards the effect of atherogenic diets. Evidence from human studies is circumstantial. Reactivity of arterial smooth muscle is enhanced by low and suppressed by high magnesium media. Evidence that magnesium depletion may initiate coronary spasm is provided by dog and retrospective human studies. Although experimental magnesium deficiency disrupts myocardial mitochondria, there are no studies which show that magnesium deficiency will lead to cardiac failure or that replacement will improve cardiac function. It is known that an infarcted or ischaemic myocardium loses magnesium and this may be the basis for ventricular arrhythmias. Coronary occlusion in a previously magnesium-depleted heart will result in a larger area of necrosis and ischaemia. The fall in serum magnesium in acute myocardial infarction is probably due to the formation of soap in fat cells undergoing catecholamine lipolysis. Ventricular fibrillation in coronary artery disease will respond to parenteral magnesium, even in the presence of normal serum concentrations.
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