Improvement of left ventricular wall synchronization with multisite ventricular pacing in heart failure: a prospective study using Doppler tissue imaging

Abstract

We sought to assess right, left and biventricular pacing effects on myocardial function by using pulsed-Doppler tissue imaging (DTI) and automated border detection (ABD) techniques which provide electromechanical delay (EMD) assessment of the different left ventricular walls. Methods: 15 patients (67"7 years) with drug-resistant primitive dilated cardiomyopathy and QRSG140 ms received a pacemaker for multisite ventricular pacing. Echocardiography was performed after 1 month of biventricular pacing (BVP). Echocardiographic measurements were recorded during spontaneous rhythm (SpR), right ventricular pacing (RVP), left ventricular pacing (LVP) and BVP. Results: LV ejection fraction was statistically similar between the four rhythms. BVP showed a significant EMD decrease for the lateral LV wall vs. SpR, RVP and even LVP. LVP resulted in significantly longer aortic pre-ejection time vs. BVP while the EMD temporal dispersion (time between the shortest regional EMD and the longest one) was similar in the two modes. Conclusions: BVP and LVP substantially reduce the EMD temporal dispersion of the four LV walls, but with a longer aortic pre-ejection time for LVP. In RVP, LVP and BVP, the septal LV wall is always activated later than during SpR. BVP and LVP are associated with a mitral regurgitation reduction.

Visualization of the site of the onset of ventricular depolarization by acceleration mode “Tissue Doppler Imaging” technique

“…However, the localization of the abnormal onset or regional delay of the RV and LV walls is better visualized in the apical 4-and 2-chamber views, because these views allows simultaneous visualization of almost all segments of the ventricle. Likewise, studies with TDI to identify responders of CRT reported that 4-chamber view is the best window for the assessment of regional wall delay [12][13][14][15]. In our study, observers correctly identified the origin of ventricular activation; particularly in apical 4-chamber view because this view was the most appropriate window for the distinction between basal septal and apical part of the ventricular depolarization.…”

“…Recently, TDI has gained its acceptance to identify potential CRT responders in patients with chronic heart failure and prolonged QRS complexes [12][13][14][15]. LV systolic asynchrony due to the delayed regional contraction is known to play an important role in LV dysfunction.…”

“…Especially LV lateral wall delay has been reported to predict a positive response to CRT. Although, various TDI techniques including pulsed wave TDI [13], color TDI velocity mode [14], tissue synchronization imaging [15] have been tested for identification of potential responders to CRT, based on the assessment of inter-and intraventricular dyssynchrony, standardized evaluation criteria have not yet been provided. However, these previous studies and our study with acceleration mode support the usefulness of TDI technique to determine normal and abnormal ventricular activation and to assess the contraction sequence non-invasively…”

“…Several studies reported the ability of the color-coded TDI (velocity or acceleration map) or pulsed-wave TDI modalities to localize the site of the accessory atrioventricular pathways and to evaluate the results of radiofrequency ablation [6][7][8][9][10][11]. Furthermore, recent studies have suggested a potential role of TDI technique to identify regional wall delay and predict improvement of systolic function or LV reverse remodeling after cardiac resynchronization therapy (CRT) in patients with chronic heart failure and a wide QRS complex [12][13][14][15]. Relatively few studies have examined the feasibility of color-coded TDI modality for evaluating the origin of myocardial activation in response to electrical excitation.…”

Echocardiographic evaluation of cardiac dyssynchrony

“…In diastole, two negative deflections are recorded, the Ea and Aa waves, corresponding to early rapid filling and atrial contraction, respectively. From these recordings, two different time intervals may be measured: the electromechanical delay, from QRS onset to S wave onset (17,28), and the electrosystolic delay, from QRS onset to peak systolic contraction (29) (Figure 5). A delay of more than 40 ms between opposite LV walls for each of these intervals is indicative of dyssynchrony, whereas normal subjects display values of approximately 20 ms (17).…”