Abstract

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – EU funding. Main funding source(s): EU’s Horizon 2020 research and innovation program under the Marie Sklodowska-Curie Background There is no consensus on which haemodynamic marker should be used to quantify acute response to cardiac resynchronization therapy (CRT) during implantation of the device. CRT has been shown to acutely reduce left ventricular (LV) end systolic as well as end-diastolic volume (EDV), precluding the use of preload dependent markers such as LV maximum pressure rise (dP/dtmax). Purpose As resynchronization will abolish the uncoordinated regional early systolic contractions of the LV, it will shorten the time to maximal pressure rise and aortic valve opening. For this reason, the purpose of this study was to investigate if duration from the time-point of ventricular pacing to dP/dtmax is less preload dependent and a better marker of acute response to CRT than dP/dtmax by comparing how the 2 markers reflected LV function during different CRT configurations. Methods LV pressure by micromanometer and volume by sonomicrometry were measured in 6 anaesthetized canines with left bundle branch block. Transient caval constrictions were performed to vary preload. Preload dependency of the 2 markers was compared by normalizing their values and calculating their relations to EDV. In 4 of the animals, biventricular pacing was performed at 3 different pacing sites with variations in atrioventricular delays that provided a range of response to CRT. To correct for acute changes in preload by CRT, stroke volume (SV) at identical EDV found from transient caval constrictions, were assessed and used as reference to grade improved LV function. Linear regression analysis was used to assess the correlation of both the duration of the preejection phase and dP/dtmax with SV. Results The duration of the preejection phase varied less with changes in preload compared to dP/dtmax: the slopes of their relation to EDV were -0.6 ± 0.7 %/ml and 4.8 ± 2.1 %/ml (p = 0.004), respectively. Turning CRT on, acutely reduced EDV from 74 ± 16 to 69 ± 17 ml (p < 0.001) at the best pacing configuration. For the different pacing sites and settings, there was a consistent relation in all animals where the preejection phase shortened as SV increased (average r2 = 0.75) (Figure A). dP/dtmax showed no clear relation to SV (average r2 = 0.22) and included cases with both negative and positive slopes (Figure B). Conclusions The duration of the preejection phase correlated with changes in LV function induced by CRT while dP/dtmax performed poorly as preload was changed. Hence, the novel timing parameter was less preload dependent and may be a better marker for assessing acute response to CRT. Abstract Figure.

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