PMID: 15040853Mar 26, 2004

Alternans decay of postextrasystolic potentiation in human left ventricle

The Japanese Journal of Physiology
Masaki TanabeHiroyuki Suga

Abstract

An organ-level assessment of the total Ca2+ handled in the excitation-contraction coupling in a beating heart has been accomplished in canine left ventricles (LVs). This approach combines the intramyocardial Ca2+ recirculation fraction (RF) with the cardiac O2 consumption for the excitation-contraction coupling. The RF has conventionally been obtained from the exponential decay of the postextrasystolic (PES) potentiation of myocardial contractility. However, in canine LVs, the PES contractility in terms of Emax (end-systolic pressure-volume ratio) has been shown to decay generally in alternans under both physiological and pathological conditions. Nevertheless, the RF can be obtained from the exponential decay component in the PES Emax alternans decay. We expected that the same Ca2+ assessment could be applied to the human heart. As the first step, we investigated whether the PES Emax would decay in alternans or exponentially in patient LVs. We retrospectively analyzed 13 patient cases that had stable regular beats unexpectedly interrupted by a spontaneous extrasystole followed by a PES compensatory pause during their diagnostic examination. These patients had either mitral regurgitation, old myocardial infarction, or dilated ca...Continue Reading

References

Apr 1, 1990·Physiological Reviews·Hiroyuki Suga
Jan 1, 1994·Heart and Vessels·J ArakiHiroyuki Suga
Jan 1, 1995·The Japanese Journal of Physiology·Juichiro ShimizuHiroyuki Suga
Jul 19, 2000·American Journal of Physiology. Heart and Circulatory Physiology·Juichiro ShimizuHiroyuki Suga
Apr 16, 2003·Journal of Biomechanics·Hiroyuki Suga
Nov 11, 2003·The Japanese Journal of Physiology·Juichiro ShimizuHiroyuki Suga

Citations

Sep 13, 2013·Pacing and Clinical Electrophysiology : PACE·Takeshi KashimuraTohru Minamino

Related Concepts

Canis familiaris
Electrocardiographic Recorders
Cardiac Conduction System
Left Ventricular Structure
Ventricular Dysfunction, Left
Premature Ventricular Contractions

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