New interpretation of systolic time intervals from active cross-bridge model
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Updated: Nov 6, 2026

Simultaneous Brightfield, Fluorescence, and Optical Coherence Tomographic Imaging of Contracting Cardiac Trabeculae Ex Vivo
Published on: October 2, 2021
1Department of Medicine, Dokkyo University School of Medicine, Tochigi, Japan.
Abstract:
Using an active cross-bridge model proposed by the authors, it has been established theoretically that cross-bridge activation rate (Ka) of the left ventricular myocardium, which might correspond to the rate of binding of Ca2+ with troponin C, is approximately expressed as a simple formula: Ka = 3/electromechanical systole (sec-1), although no definitive biological proof has yet been provided for the equation. One hundred eighteen patients without significant cardiac disease and 6 patients who had atrioventricular block with a permanent pacemaker were evaluated to determine the Ka value of the normal human left ventricular myocardium (test 1), and to examine the effect of changes in heart rate (test 2) as well as afterloading (test 3) or dobutamine infusion (test 4) on Ka. The pacing rate was increased from 50 to 110 beats/min at 20-beat increments in test 2. Arterial pressure was elevated by angiotensin II infusion in test 3, and 7 subjects received a continuous dobutamine infusion in test 4. The Ka value was found to be related to heart rate, to be increased by dobutamine infusion, and to be decreased by myocardial lengthening due to afterloading. Dependence of Ka on heart rate appeared to result from changes in myocardial length. The Ka value corrected for heart rate (Kac) had an average variation of only 4.6%, and was unrelated to age or myocardial length in individual subjects. Thus, the Kac value of normal human left ventricular myocardium appears to be nearly constant between individuals but to be increased by catecholamine infusion or myocardial shortening.
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