Why the study?
Extracellular potassium concentration might modify electrophysiological properties in the border zone of ischemic myocardium, but its effects on depolarization and repolarization characteristics across the ischemic-normal border required evaluation.
In a rat model of acute ischemia/reperfusion, low-normal potassium levels (<4.7 mM) promoted the formation of an electrophysiological border zone and increased reperfusion extrasystolic burden.
Answers are grounded in this paper and cite their sources.
Supports further investigation of potassium effects on ischemic borders; hypothesis-generating and should not change clinical practice.
Extracellular potassium concentration might modify electrophysiological properties in the border zone of ischemic myocardium. We evaluated the depolarization and repolarization characteristics across the ischemic–normal border under [K + ] variation. Sixty-four-lead epicardial mapping was performed in 26 rats ([K + ] 2.3–6.4 mM) in a model of acute ischemia/reperfusion. The animals with [K + ] < 4.7 mM (low–normal potassium) had an ischemic zone with ST-segment elevation and activation delay, a border zone with ST-segment elevation and no activation delay, and a normal zone without electrophysiological abnormalities. The animals with [K + ] >4.7 mM (normal-high potassium) had only the ischemic and normal zones and no transitional area. Activation–repolarization intervals and local conduction velocities were inversely associated with [K + ] in linear regression analysis with adjustment for the zone of myocardium. The reperfusion extrasystolic burden (ESB) was greater in the low–normal as compared to normal-high potassium animals. Ventricular tachycardia/fibrillation incidence did not differ between the groups. In patch-clamp experiments, hypoxia shortened action potential duration at 5.4 mM but not at 1.3 mM of [K + ]. IK(ATP) current was lower at 1.3 mM than at 5.4 mM of [K + ]. We conclude that the border zone formation in low–normal [K + ] was associated with attenuation of IK(ATP) response to hypoxia and increased reperfusion ESB.
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Bernikova et al. (2023) studied this question.
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