The extent of left ventricular (LV) dyssynchrony might not be comparable between right ventricular pacing-induced left bundle branch block (RV-LBBB) and idiopathic LBBB (iLBBB), despite the morphologic analogy on the electrocardiogram. The objectives of the present study were to elucidate the differences in the LV dyssynchrony index (LVdys) between RV-LBBB and iLBBB, and to assess the prognostic implication of LV dyssynchrony. The conventional echocardiographic parameters, LVdys, and LV end-systolic wall stress were evaluated in 20 healthy volunteers and 21 patients with iLBBB and 20 with RV-LBBB with preserved LV systolic function. Three types of LVdys were evaluated: LVdys-6, LVdys-2, and LVdys-standard deviation. The patients were clinically followed up for about 3 years. The prevalence of LV dyssynchrony was not rare in those with either iLBBB or RV-LBBB, but it was more prevalent in the patients with iLBBB than in those with RV-LBBB. The patients with iLBBB had greater LVdys than those with RV-LBBB (84 ± 55 vs 55 ± 50 for LVdys-6, 51 ± 49 vs 31 ± 40 for LVdys-2, 37 ± 24 vs 24 ± 22 for LVdys-standard deviation in iLBBB vs RV-LBBB). LVdys displayed significant correlations with QRS duration, LV volumes, LV ejection fraction, LV end-systolic wall stress, and mitral inflow E/mitral annular E′ velocity ratio. Multivariate logistic regression analysis showed that the LV end-diastolic volume and LV end-systolic wall stress were independent determinants of the presence of LV dyssynchrony. During follow-up, no cardiovascular death or hospitalization for heart failure was reported in either group. In conclusion, despite similarities in electrocardiographic morphology, the extent of LV dyssynchrony were greater in patients with iLBBB, with LV preload and afterload the main determinants. No association was found between the presence of LV dyssynchrony and prognosis.
The activation pattern of right ventricular (RV) pacing has been postulated to be similar to that of left bundle branch block (LBBB). RV pacing can induce an abnormal left ventricular (LV) electrical activation sequence with an electrocardiographic manifestation of LBBB, leading to LV dyssynchrony. LV dyssynchrony by RV pacing is associated with deleterious effects on LV systolic function, asymmetrical hypertrophy, redistribution of the cardiac mass, chronic LV remodeling, and mitral regurgitation. Despite similarities in QRS morphology, a paucity of data is available regarding the difference in the extent of LV dyssynchrony between intrinsic LBBB (iLBBB) and RV pacing-induced LBBB (RV-LBBB), especially in patients with preserved LV ejection fraction. In addition, the prognostic effect of LV dyssynchrony in patients with LBBB is still elusive. Therefore, we sought to compare mechanical dyssynchrony between patients with iLBBB and those with RV-LBBB, and to clarify the contribution made by LV mechanical dyssynchrony on the outcome using novel 2-dimensional speckle tracking-derived LV dyssynchrony indexes (LVdys).
Methods
A total of 53 patients (25 patients with iLBBB and 28 with RV-LBBB) were the initial candidates for the present study. Of the 53 patients, 12 were excluded from the final analysis because of inadequate echocardiographic image quality for 4, the presence of coronary artery disease in 2, consent withdrawal by 2, a change in the pacing mode by 2, and unreliable off-line speckle tracking analysis for 2 patients. For comparison purposes, 20 normal healthy subjects were invited to participate as controls. Accordingly, the data from 61 subjects (age 56 ± 12 years, 25 men) were finally analyzed: 20 normal volunteers (group 1), 21 patients with idiopathic iLBBB (group 2), and 20 patients with RV-LBBB (group 3). All subjects provided written informed consent before study enrollment.
The diagnostic criteria of LBBB were as follows: QRS duration >120 ms, presence of wide, notched, or slurred R waves in the left precordial leads, the absence of Q waves on precordial leads, and the presence of monophasic QS in leads V 1 and V 2 . In group 3, the clinical indication for pacemaker implantation was complete atrioventricular block not accompanied by the presence of coronary artery disease. The pacemaker lead was placed at the RV apex in all patients, which was confirmed by chest radiography. A total of 18 patients had a DDD mode pacemaker implanted, and 2 patients had a VVI mode pacemaker implanted. All 41 patients recruited were free of any congenital or valvular heart disease, and all had a LV ejection fraction of >45%. Invasive coronary angiography was performed to rule out the presence of significant coronary artery disease in all members of groups 2 and 3. The mean duration of RV apical pacing in group 3 was 978 ± 334 days (at least >1 year) at enrollment. The Institutional Review Board of our hospital approved the study protocol.
Transthoracic echocardiograms were obtained using commercially available equipment (Vivid 7, GE Medical Systems, Milwaukee, Wisconsin). The appropriateness of patients for inclusion was determined on the basis of the 2-dimensional echocardiographic image quality. Those with technically inappropriate image quality were excluded at this stage. From the echocardiogram, the LV end-diastolic and end-systolic wall thicknesses, LV end-diastolic and end-systolic volume, and LV ejection fraction using the modified biplane Simpson method, pulsed-wave Doppler examination of the mitral inflow, and pulsed-wave tissue Doppler imaging at the medial mitral annulus were measured. From the mitral inflow Doppler signals, the early transmitral inflow velocity (E), late transmitral inflow velocity (A), and deceleration time of E velocity were determined. Standard M-mode and 2-dimensional images were obtained during end-expiratory breath hold for better image acquisition and stored in cineloop format from 3 consecutive beats.
Because systemic vascular resistance was reported to be an unreliable index of LV afterload, we calculated the LV end-systolic wall stress as a reliable representative of LV afterload. LV end-systolic wall stress was calculated using the following formula :
LV end − systolic wall stress = ( Pes ) [ Des ( Hes ) ( 1 + Hes / Des ) ] ( 0.34 )
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