Mechanism of postextrasystolic potentiation in the right ventricle

The mechanism of postextrasystolic potentiation (PESP) has been studied in the left ventricle in humans; however, this phenomenon has not been evaluated in the right ventricle. Accordingly, 18 sinus beats were compared to postextrasystolic beats during the same cineventriculogram using simultaneous high-fidelity right ventricular (RV) and pulmonary artery pressures and cast-validated biplane cineventriculographic volumes in normal patients. The increase in cycle length was 22 ± 12% (standard deviation) in the postextrasystolic beats. Right ventricular ejection fraction increased from 61 ± 10 to 68 ± 4% (p < 0.001) and RV stroke volume increased from 99 ± 18 to 128 ± 20 ml (p < 0.001) due to an increase in RV end-diastolic volume (165 ± 34 to 189 ± 30 ml, p < 0.001) as RV end-systolic volume (65 ± 24 to 61 ± 17 ml, difference not significant) and RV end-systolic pressure (16 ± 7 to 17 ± 6 mm Hg, difference not significant) remained unchanged. Despite an increase in RV systolic pressure from 29 ± 7 to 31 ± 7 mm Hg (p < 0.01) and an increase in RV end-diastolic pressure from 8 ± 4 to 10 ± 5 mm Hg (p < 0.001), RV +dPdtmax did not change (318 ± 102 to 294 ± 82 mm Hg/s, difference not significant). However, the difference between pulmonary artery diastolic pressure and RV end-diastolic pressure decreased from control (10 ± 4 mm Hg) to postextrasystolic beat (5 ± 3 mm Hg, range 0 to 10, p < 0.001) and dPdtmax occurred after pulmonic valve opening in 14 of 15 beats where simultaneous high-fidelity pulmonary artery pressure was recorded. These data indicate that the mechanism of PESP in the right ventricle may result from a preload-dependent mechanism rather than enhanced contractility because end-diastolic volume and stroke volume increase as end-systolic volume is unchanged. In the right ventricle peak +dPdtmax cannot be used as an index of contractility because developed pressure is small and dPdtmax is not isovolumic.