Pacing therapy for atrioventricular dromotropathy: a combined computational–experimental–clinical study

Figures

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  Figure 1. Schematic representation of the animal experimental set-up. (A) Overview of the porcine model. Pacemaker leads were transvenously inserted in the right atrial (RA) appendage and right ventricular (RV) apex and attached to the left ventricular (LV) epicardium. Complete atrioventricular (AV) block was created by radiofrequency ablation of the AV-node. The LV pressure and volume were measured using a conductance catheter and RV and left atrial (LA) pressure were measured using a cathetertip manometer. (B) Signal analysis. The first derivative of LV volume was used to calculate forward flow over the mitral valve (blue area under E and A wave) and diastolic mitral regurgitation (MR, red area). The integral of aortic flow, measured by a flow probe, was used to quantify forward stroke volume and cardiac output (purple area).

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  Figure 2. Haemodynamic effect of improving atrioventricular (AV)-coupling in pig experiments and computer simulations during biventricular pacing. (Top row) LV and LA pressures, (second row) flow, and (third row) ECG from a representative experiment. (Fourth and fifth row) Pressures and flow calculated from computer simulations.

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  Figure 3. Haemodynamic response to improving atrioventricular (AV) coupling in pig experiments and computer simulations during biventricular pacing. Relative changes in haemodynamic function by shortening AV-delay in all pig experiments (top panel) and simulations (bottom panel) when compared with a baseline PR interval of 300 ms. For the pig experiments mean±SD are presented. * indicates P < 0.05 when compared with baseline. MAP, mean arterial pressure; LAPmean, mean left atrial pressure; LVEDV, left ventricular end diastolic volume.

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  Figure 4. Effect of interventricular desynchronization on haemodynamic benefits of restoring AV-coupling. Simulation data from the protocol where restoration of AV-coupling was achieved with unchanged synchronous ventricular activation (red) or with biventricular (BiV) pacing (orange) or right ventricular (RV) pacing (purple). (A) Change in stroke volume. (B) Pressure volume loops at optimal pump function. (C) Mitral valve flow.

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  Figure 5. Haemodynamic effect of improving atrioventricular (AV)-coupling in patients. (A) Left ventricular (LV) pressure (Top row) and flow (Second row) and ECG (third row), as measured in a representative patient. Diastolic mitral regurgitation (MR) is presented in red. Absolute changes in (B) diastolic mitral forward flow, and (C) diastolic mitral regurgitant (MR) fraction when compared with baseline (AAI) in the entire cohort. In the ECG an atrial pacing spike is present in all conditions, in the biventricular paced beats the LV pacing spike is indicted by a large vertical bar which is followed 40 ms later by a small spike representing the RV stimulus. Mean ± SD are presented. *P < 0.05 when compared with baseline.

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  Figure 6. Haemodynamic effect of improving atrioventricular (AV)-coupling in patients during biventricular (BiV) and right ventricular (RV) pacing. (A) Left ventricular (LV) pressure–volume loops in a representative patient at baseline (dashed line) and at tested AV-delay settings (solid lines) during BiV pacing (left) and right ventricular pacing (right). Relative changes in stroke volume (B) and stroke work (C) when compared with baseline (AAI) for BiV (black) and RV pacing (grey) in the entire cohort. Mean ± SD are presented. *P < 0.05 when compared with baseline.