Key result
In non-diabetic rat hearts with non-uniform contraction, transient elevation of glucose from 150 to 400 mg/dL increased the velocity of Ca2+ waves and arrhythmia susceptibility by activating CaMKII.
Why the study?
Stress hyperglycemia in non-diabetic acute coronary syndrome patients correlates with mortality, but whether transient glucose elevation affects arrhythmia susceptibility in non-diabetic hearts with non-uniform contraction was unexamined.
Transient glucose elevation increases arrhythmia susceptibility in non-diabetic rat trabeculae via CaMKII activation, likely through O-GlcNAcylation.
No immediate clinical implications; leaves open CaMKII as arrhythmia target in human hyperglycemia.
BACKGROUND: In non-diabetic patients with acute coronary syndrome, stress hyperglycemia occasionally occurs and is related to their mortality. Whether transient elevation of glucose affects arrhythmia susceptibility in non-diabetic hearts with non-uniform contraction was examined. METHODS AND RESULTS: waves and the number of triggered action potentials. In addition, in the presence of 1 μmol/L autocamtide-2 related inhibitory peptide or 50 μmol/L diazo-5-oxonorleucine, the elevation of glucose did not increase the number of triggered action potentials. Furthermore, the elevation of glucose by adding L-glucose did not increase their number. CONCLUSIONS: waves by activating CaMKII,probably through glycosylation with O-linked β-N-acetylglucosamine, thereby increasing arrhythmia susceptibility.
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Handoh et al. (2020) studied Non-uniform contraction in non-diabetic myocardium (model for acute coronary syndrome). Transient elevation of glucose vs. 150 mg/dL glucose was evaluated on Velocity of Ca2+ waves and number of spontaneous action potentials (arrhythmias) triggered by electrical stimulation (p=<0.05). In non-diabetic rat hearts with non-uniform contraction, transient elevation of glucose from 150 to 400 mg/dL increased the velocity of Ca2+ waves and arrhythmia susceptibility by activating CaMKII.
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