Background
Cardiac resynchronisation therapy(CRT) may exert its beneficial hemodynamic effect by improving ventricular synchrony and improving atrioventricular(AV) timing.
Aims
To establish the relative importance of the mechanisms through which CRT improves cardiac function and explore the potential for additional improvements with improved ventricular resynchronisation.
Methods
We performed simulations using the CircAdapt haemodynamic model and performed haemodynamic measurements while adjusting AV delay, at low and high heart rates, in 87 patients with CRT devices. We assessed QRS duration, presence of fusion and haemodynamic response.
Results
The simulations suggest intrinsic PR interval and the magnitude of reduction in ventricular activation determine the relative importance of the mechanisms of benefit. For example, if PR interval is 201ms and LV activation time is reduced by 25ms (typical for current CRT methods) then AV delay optimisation is responsible for 69% of overall improvement. Reducing LV activation time by an additional 25ms produced an additional 2.6mmHg increase in BP (30% of effect size observed with current CRT).
In the clinical population, ventricular fusion significantly shortened QRS duration (∆-27±23ms, P <0.001), and, improved SBP (mean 2.5 mmHg increase). Ventricular Fusion was present in 69% of patients, yet in 40% of patients with fusion, shortening AV delay (to a delay where fusion was not present) produced the optimal haemodynamic response.
Conclusions
Improving LV preloading by shortening AV delay is an important mechanism through which cardiac function is improved with CRT. There is substantial scope for further improvement if methods for delivering more efficient ventricular resynchronisation can be developed.