Alternans decay of postextrasystolic potentiation in human left ventricle.
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 cardiomyopathy. Their LV Emax decayed consistently in alternans within the first several PES beats. These Emax alternans decays resemble those reported in canine LVs. This finding suggests for the first time the applicability of the same organ-level RF assessment method developed for canine hearts to human hearts.
Tanabe
Masaki
M
First Department of Internal Medicine, Mie University School of Medicine, Tsu, 514-8507 Japan. hsuga@ri.ncvc.go.jp
Onishi
Katsuya
K
Dohi
Kaoru
K
Ito
Masaaki
M
Nakano
Takeshi
T
Suga
Hiroyuki
H
D000818:Animals; D004285:Dogs; D004562:Electrocardiography; D006329:Heart Conduction System / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology*; D006801:Humans; D013045:Species Specificity; D018487:Ventricular Dysfunction, Left / Q000150:complications / Q000175:diagnosis* / Q000503:physiopathology*; D018879:Ventricular Premature Complexes / Q000150:complications / Q000175:diagnosis* / Q000503:physiopathology*