Ventricular interaction rather than electrical resynchronisation determines haemodynamic response to cardiac resynchronisation therapy in dyssynchronous heart failure

Abstract

Purpose: It is still unclear why left ventricular and biventricular pacing (LVP and BiVP, respectively) have comparative positive effects on haemodynamic function of patients with dyssynchronous heart failure (HF). To enhance understanding of the working mechanism of cardiac resynchronisation therapy (CRT), we assessed haemodynamic and local electromechanical consequences of LVP in comparison to BiVP. Methods: Haemodynamic response to LVP and BiVP (%-change LVdP/dtmax) was measured in 6 dogs with HF and left-bundle branch block (LBBB) and in 40 HF patients with QRS-width ≥120ms, followed by computer simulations of local myofibre mechanics during LVP and BiVP in the failing heart with LBBB. Pacing-induced changes of electrical activation were measured in dogs using contact mapping and in patients using a noninvasive multielectrode epicardial electrocardiographic mapping technique. Results: LVP and BiVP similarly increased LVdP/dtmax in dogs (p=0.33) and in patients (p=0.93), but only BiVP significantly decreased electrical dyssynchrony (Figure). In the simulations, LVP and BiVP increased total ventricular myofibre work to the same extent (Figure). While the LVP-induced increase was entirely due to enhanced right ventricular (RV) myofibre work, the BiVP-induced increase was due to enhanced myofibre work of both the LV and RV. Overall, LVdP/dtmax correlated better with total ventricular myofibre work than with LV or RV myofibre work alone. ![Figure][1] Conclusions: Experimental, human, and computational data support the similarity of haemodynamic response to LVP and BiVP, despite differences in electrical dyssynchrony. The simulations provide the novel insight that, through ventricular interaction, the RV myocardium importantly contributes to the improvement in LV pump function induced by CRT. [1]: pending:yes