Haemodynamic effects of changes in atrioventricular and interventricular delay in cardiac resynchronisation therapy show a consistent pattern: analysis of shape, magnitude and relative importance of atrioventricular and interventricular delay. Issue 11 (18th May 2006)

• Record Type: Journal Article
• Authors: Whinnett, Z I; Davies, J E R; Willson, K; Manisty, C H; Chow, A W; Foale, R A; Wyn Davies, D; Hughes, A D; Mayet, J; Francis, D P
• Is Part Of: Heart. Volume 92:Issue 11(2006)
• Page Start: 1628
• Page End: 1634
• Publication Date: 2006-05-18
• Subjects: AV, atrioventricular -- CARE-HF, Cardiac Resynchronization-Heart Failure -- COMPANION, Comparison of Medical Therapy, Pacing and Defibrillation in Chronic Heart Failure -- NYHA, New York Heart Association -- SBP, systolic blood pressure -- SBPrel, relative change in systolic blood pressure -- VV, interventricular; Heart -- Diseases -- Treatment -- Periodicals; Cardiology -- Periodicals; 616.12
• DOI: 10.1136/hrt.2005.080721
• Languages: English
• ISSNs: 1355-6037

Abstract

Abstract : Objective: To assess the haemodynamic effect of simultaneously adjusting atrioventricular (AV) and interventricular (VV) delays. Method: 35 different combinations of AV and VV delay were tested by using digital photoplethysmography (Finometer) with repeated alternations to measure relative change in systolic blood pressure (SBPrel ) in 15 patients with cardiac resynchronisation devices for heart failure. Results: Changing AV delay had a larger effect than changing VV delay (range of SBPrel 21 v 4.2 mm Hg, p < 0.001). Each had a curvilinear effect. The curve of response to AV delay fitted extremely closely to a parabola (average R 2 = 0.99, average residual variance 0.8 mm Hg 2 ). The response to VV delay was significantly less curved (quadratic coefficient 67 v 1194 mm Hg/s 2, p = 0.003) and therefore, although the residual variance was equally small (0.8 mm Hg 2 ), the R 2 value was 0.7. Reproducibility at two months was good, with the SD of the difference between two measurements of SBPrel being 2.5 mm Hg for AV delay (2% of mean systolic blood pressure) and 1.5 mm Hg for VV delay (1% of mean systolic blood pressure). Conclusions: Changing AV and VV delays results in a curvilinear acute blood pressure response. This shape fits very closely to a parabola, which may be valuable information in developing a streamlined clinical protocol. VV delay adjustment provides an additional, albeit smaller, haemodynamic benefit to AV optimisation.