Key result
Magnesium deficiency combined with platelet-activating factor is linked to coronary vasospasm and young sudden cardiac death.
Why the study?
A novel hypothesis combining the roles of dietary magnesium deficiency and platelet-activating factor in coronary arterial vasospasm and sudden cardiac death in young populations was proposed but requires review and synthesis of evidence.
Answers are grounded in this paper and cite their sources.
No clinical action indicated; leaves open magnesium's role in pediatric SCD for prospective study.
Magnesium (Mg) is a co-factor for more than 500 enzymes, and is the second most abundant intracellular cation after potassium. It is vital in numerous physiological, cellular and biochemical functions and systems necessary for life. Approximately 35 years ago, our laboratory suggested that a progressive, dietary deficiency and/or metabolic induced loss of Mg from the body, beginning early in life, particularly during development of the coronary arteries, could lead to coronary arterial vasospasm, ischemic heart disease, and sudden-cardiac death (SCD). Herein, we review evidence for a brand-new, novel hypothesis which combines knowledge suggesting a combined role for hypomagnesemia and platelet-activating factor (PAF) which may provide insights into unexplained SCD in infants, children, and young adults. This review documents what takes place in the cardiovascular system when the body and its tissues are subjected to lower than normal dietary Mg intake, and also provides new evidence for a series of heretofore unknown actions of PAF that are most likely involved and/or trigger coronary arterial vasospasm in the presence of low concentrations of ionized Mg levels. The roles of vascular remodeling, NF-κB and proto-oncogenes are considered to play major roles in this hypothesis.
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Altura Bm (2016) conducted a review in Sudden Cardiac Death. Hypomagnesemia and platelet-activating factor was evaluated. Dietary magnesium deficiency combined with platelet-activating factor generation may trigger coronary arterial vasospasm, potentially leading to sudden cardiac death in infants, children, and youths.
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