Dispersion of monophasic action potential durations and activation times during atrial pacing, ventricular pacing, and ventricular premature stimulation in canine ventricles

• Published in: Cardiovascular research 1983-03, Vol.17 (3), p.152-161
• Main Authors: KUO, CHIEN-SUU, AMLIE, JAN PEDER, MUNAKATA, KAZUO, REDDY, C PRATAP, SURAWICZ, BORYS
• Format: Article
• Language: English
• Subjects: Action Potentials; Animals; Atrial Function; Cardiac Pacing, Artificial; dispersion of ventricular repolarisation; Dogs; Electric Stimulation; Electrocardiography; Heart - physiology; monophasic action potentials; Time Factors; Ventricular Function; ventricular premature complex
• ISSN: 0008-6363; 1755-3245
• DOI: 10.1093/cvr/17.3.152

We studied dispersion of repolarisation and the components of dispersion during atrial pacing (AP), ventricular pacing (VP), and programmed ventricular premature stimulation (VPS) using six simultaneously recorded monophasic action potentials (MAP's) from ventricular surface in nine open-chest dogs. Varitions in MAP duration (MAPD) caused no changes in the configuration of strength-interval curves. During AP, maximum dispersion (MD) between any two of six sites averaged 32± 10 ms, consisting of 27 ± 10 ms MAPD and 4±9 ms activation time (AT) differences; during VP, MD averaged 77± 16 ms, consisting of 7± 15 ms MAPD and 70± 13 ms AT differences. Maximum dispersion in the earliest ventricular premature complexes (VPC) averaged 97 ± 16 ms: the difference between this value and the MD during VP was due to an increase in MAPD difference without significant change in AT difference. Dispersion during VPS exceeded dispersion during AP by 5 to 70 ms at 61 of 68 pairs of adjacent sites separated by 1.5 to 2.0 cm; the greatest increases were due to added contributions of MAPD and AT differences. Greatest dispersion between any two of six sites during VPS occurred in the early VPC, ie, at coupling intervals (CI) ≤30 ms following effective refractory period (ERP), but at the adjacent sites the timing of greatest dispersion during VPS varied, occurring at about one half of the sites at CI within 40 to 220 ms following ERP. Our results show that the MD during AP is due predominantly to MAPD difference, during VP predominantly to AT difference, and that prematurity increases the contribution of MAPD differences to dispersion from an average of 9% during VP to an average of 25%. No spontaneous repetitive activity occurred during VPS on the surface of the left ventricle using 2 ms stimuli of strength up to 40 mA.