Key result
Heat stress triggers severe myocardial injury, ECG abnormalities, and increased susceptibility to ventricular arrhythmias.
Why the study?
Heat stress has been linked to arrhythmias and cardiomyocyte injury, but the specific molecular mechanisms and effective intervention strategies remain unclear.
Heat stress promotes myocardial injury and ventricular arrhythmias through mitochondrial dysfunction, providing insights into potential molecular mechanisms and intervention targets.
BACKGROUND: With global warming, extreme summer heat has led to a higher morbidity and mortality of heat stroke (HS). Although heat stress has been linked to arrhythmias and cardiomyocyte injury, the specific molecular mechanisms and effective intervention strategies remain to be clarified. METHOD: We retrospectively collected clinical data from HS patients. A rat HS model was established, and the underlying mechanisms were investigated using biochemical and electrophysiological approaches, combined with proteomics and metabolomics analyses of myocardial tissues and cells. In vivo and in vitro intervention experiments were performed using the mitochondrial reactive oxygen species (ROS) scavenger MitoTEMPO and calcineurin inhibitor (FK506). RESULTS: Heat stress caused severe myocardial injury and electrocardiographic abnormalities in HS patients. HS rats exhibited increased susceptibility to ventricular arrhythmias (VAs), manifested by prolonged action potential duration (APD), increased Ca CONCLUSION: Heat stress triggers mitochondrial dysfunction through a Ca
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Xiang et al. (2026) studied Heat stroke. Heat stress was evaluated on Myocardial injury and ventricular arrhythmias. Heat stress caused severe myocardial injury and electrocardiographic abnormalities in heat stroke patients and increased susceptibility to ventricular arrhythmias in rat models.
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