AIMS: This study was performed to determine whether or not the kinetics of action potential duration restitution during double premature stimuli (S3) differ from that during single premature stimuli (S2) in the human intact right ventricle. METHODS AND RESULTS: A monophasic action potential (MAP) was simultaneously recorded from the right ventricular apex (RVA) and outflow tract (RVOT) during programmed ventricular pacing in 11 patients with symptomatic bradyarrhythmias (five males, six females, mean age 58 years). In the five most recent patients, the RV pressure and its dp/dt were also obtained during the protocol. A substantial difference in the restitution of the MAP duration (MAPD) between S2 and S3 was observed at short diastolic intervals (< l00 ms), that is, the restitution curve of S2 showed an early biphasic pattern (upward hump), while such a phenomenon was not seen during the restitution of S3. All the quantitative parameters of MAPD restitution representing its kinetics were significantly greater in S3 than S2. Maximum attainable dispersion of repolarization between the two MAPs was significantly greater during S3 than S2 (76 +/- 17 vs 59 +/- 17 ms, P<0.05) and was mainly caused by the difference in the MAPD difference, thus by the difference in the restitution kinetics of S2 and S3. The dp/dt of the RV pressure was significantly greater during S3 than S2 for all diastolic intervals tested. CONCLUSION: It was concluded that similar to previously reported canine experimental studies, the APD restitution of S3 is substantially different from that of S2 in the human intact ventricle (endocardium).
AIMS: This study was performed to determine whether or not the kinetics of action potential duration restitution during double premature stimuli (S3) differ from that during single premature stimuli (S2) in the human intact right ventricle. METHODS AND RESULTS: A monophasic action potential (MAP) was simultaneously recorded from the right ventricular apex (RVA) and outflow tract (RVOT) during programmed ventricular pacing in 11 patients with symptomatic bradyarrhythmias (five males, six females, mean age 58 years). In the five most recent patients, the RV pressure and its dp/dt were also obtained during the protocol. A substantial difference in the restitution of the MAP duration (MAPD) between S2 and S3 was observed at short diastolic intervals (< l00 ms), that is, the restitution curve of S2 showed an early biphasic pattern (upward hump), while such a phenomenon was not seen during the restitution of S3. All the quantitative parameters of MAPD restitution representing its kinetics were significantly greater in S3 than S2. Maximum attainable dispersion of repolarization between the two MAPs was significantly greater during S3 than S2 (76 +/- 17 vs 59 +/- 17 ms, P<0.05) and was mainly caused by the difference in the MAPD difference, thus by the difference in the restitution kinetics of S2 and S3. The dp/dt of the RV pressure was significantly greater during S3 than S2 for all diastolic intervals tested. CONCLUSION: It was concluded that similar to previously reported canine experimental studies, the APD restitution of S3 is substantially different from that of S2 in the human intact ventricle (endocardium).