Pathophysiology and Current Evidence for Detection of Dyssynchrony

Cardiac dyssynchrony is divided into electrical dyssynchrony and mechanical dyssynchrony. Electrical dyssynchrony is associated with a prolonged conduction time in the ventricles resulting in a prolonged QRS duration [1]. Mechanical dyssynchrony presents the mechanical discoordination that is most often related to simultaneous contraction and stretch in different segments of the left ventricle (LV) as well as delays in the time to peak contraction from one segment to another [1]. Dyssynchrony comprises three main components: atrioventricular (AV), interventricular and intraventricular. AV dyssynchrony is a delay in the normal sequential AV contraction, due to delayed conduction through the AV node. The result is a disordered ventricular diastolic filling and a decreased LV preload that compromises stroke volume (due to the failure of the Starling mechanism) [1, 2]. AV dyssynchrony is defined by an LV filling time (LVFT) indexed to R-R interval < 40% [1, 2] (Fig. 1 [3]). Interventricular dyssynchrony and intraventricular dyssynchrony have a relatively greater effect on ventricular pump function than AV dyssynchrony. Interventricular dyssynchrony describes a sequential delay in activation between the right ventricle (RV) and LV, resulting in a lack of coordinated contraction [4]. Interventricular dyssynchrony is evaluated by the measurement of interventricular mechanical delay (IVMD), pulse wave (PW) aortic (left ventricular outflow tract, apical five-chamber view) and pulmonary (right ventricular outflow tract, parasternal short-axis view) flow velocities. It is also estimated by the calculation of the difference in time between the beginning of Q wave (ECG) and the onset of LV outflow and the time between the beginning of Q and the onset of RV outflow [1, 5]. These values represent left and right ventricular pre-ejection period (PEP). IVMD values of > 40 ms and values of LV PEP of > 140 ms are considered pathological [1, 5, 6] (Fig. 2 [3]). In left bundle branch block (LBBB), the anterior surface of the RV is the earliest to depolarize (due to rapid electrical propagation through the intact right bundle branch), and the posterolateral basal LV is mostly the latest (due to the relatively slow propagation from cell to cell). The hemodynamic consequences of dyssynchronous LV contraction are decreased stroke volume, stroke work, a slower rate of rising of LV pressure and increased LV end-systolic wall stress. Additionally, the LV end-systolic pressure-volume curve shifts to the right, indicating that the LV functions at a larger volume to recruit the Frank-Starling mechanism [1, 5, 6]. Intraventricular dyssynchrony is evaluated by M-mode,