Magnesium in coronary artery disease.

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.