Key result
Ischemic cardiomyocyte metabolic alterations drive necrosis and ventricular arrhythmias via hyperkalemia, acidosis, and calcium overload.
Why the study?
In heart failure or myocardial ischemia, fatty acid metabolism and hypoxia-induced metabolic changes can become deleterious via oxidative stress and arrhythmogenesis. This review aims to promote an integral understanding of the molecular basis of myocardial contraction and energetic metabolism in cardiomyocytes to aid in developing future treatments for acute coronary ischemia.
Answers are grounded in this paper and cite their sources.
Does not alter ischemia or arrhythmia management; leaves open metabolic targets for prospective trials.
Cardiac muscle contraction is a strictly regulated process which conjugates a series of electrophysiological, biochemical and mechanic events, resulting in the pumping of blood to all bodily tissues.These phenomena require a very high energetic demand both for generating the necessary mechanical force, and for maintaining cellular homeostasis during the process.In the myocardium, fatty acids (FA) represent the main energy substrate, although other secondary substrates, such as glucose and ketone bodies, may also be used.Nevertheless, under certain conditions such as heart failure or myocardial ischemia, FA metabolism may become deleterious via mechanisms such as oxidative stress and arrhythmogenesis.In an ischemic milieu, various metabolic changes occur as a consequence of hypoxia, favoring cell necrosis, ventricular arrhythmias, and death.Major events in this context include an increase in extracellular K + , a decrease in pH, and accumulation of intracellular calcium.This review includes a detailed description of the molecular basis underlying myocardial contraction and energetic metabolism in cardiomyocytes, aiming to promote an integral understanding of the pathophysiology of heart ischemia.This in turn may aid in the development of future, more satisfactory alternative treatments in the management of acute coronary ischemia episodes.
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Martínez et al. (2017) conducted a review in Heart ischemia and arrhythmogenesis. Altered cardiomyocyte energetic metabolism during myocardial ischemia promotes cell necrosis and ventricular arrhythmias via extracellular K+ elevation, pH reduction, and intracellular calcium overload.
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