Influence of aortic elastic properties on pulse pressure changes induced by rapid ventricular pacing

Abstract

The mechanism of aortic pulse pressure decline induced by acute rapid ventricular pacing remains incompletely understood. It has been ascribed to changes in stroke volume or aortic compliance. This becomes more complicated by the dependence of aortic compliance on the level of the mean aortic pressure as well as the aortic wall properties. To test the role of such mechanical factors, aortic pressure-diameter hemodynamics, derived from simultaneous tip-micromanometer aortic pressure recordings and high-fidelity ultrasonic intravascular aortic diameter recordings, were measured in 15 normal subjects during and after abrupt cessation of rapid ventricular pacing (up to 160 bpm). Immediately after terminating the pacing, diastolic aortic pressure declined (−9%, from 87.4 ± 1.2 to 79.5 ± 1.7 mmHg,P< 0.0001) while systolic aortic pressure increased (+19%, from 109.5 ± 1.6 to 130.1 ± 2.8 mmHg,P< 0.0001). Thus, pulse pressure increased from 22.1 ± 2.2 to 50.6 ± 3.1 mmHg,P< 0.0001. To quantify systolic and diastolic aortic pressure differences we compared the first postpaced beat (a) and the last paced beat (b). To estimate what the aortic pressure would have been for the paced beats had the aortic diameter differences due to the different heart rate not occurred we calculated the theoretical pressure of the paced beat P_b=E_b·D_a, where E_b was the instantaneous aortic elastance of the paced beat and D_a was the aortic diameter for the postpaced beat. The corrected pressure difference was then calculated by the following: ΔP_cor=(D_a·E_b)−P_a. It was found that systolic ΔP_cor was 25% of systolic ΔP_raw and diastolic ΔP_cor was 89% of diastolic ΔP_raw. ΔP_raw was the pressure difference between paced and spontaneous beat measured from the raw data. ΔP_cor indicates the portion of ΔP_raw that results from a change in aortic stiffness as a consequence of viscous behavior or aorto-ventricular coupling. These data indicate that the majority of diastolic pressure decline after pacing was terminated, may reflect a change in aortic stiffness while the majority of systolic pressure rise, and may be attributable to differences in hemodynamics alone.