Right bundle branch block in patients with heart failure. Is it associated with worse cardiac function on MRI and an adverse prognosis?

Abstract

Introduction: Prolonged QRS duration has been associated with an adverse outcome in patients with heart failure (HF), but the contribution of QRS morphology is unclear. Methods: Outpatients attending a community HF service between 2000 and 2010 who had cardiac magnetic resonance imaging (CMRI) were included in this analysis. HF was defined as the presence of symptoms or signs, associated with objective evidence of cardiac dysfunction: either a left ventricular ejection fraction (LVEF) <50% or a raised amino-terminal pro-brain natriuretic peptide (NT-proBNP) >125 pg/ml. QRS duration >120 msec was grouped as left (LBBB), right bundle branch block (RBBB) or indeterminate ventricular conduction delay (IVCD) by ECG criteria. Results: Heart failure was confirmed in 878 patients, and 323 had QRS>120 msec. Comparing patients with LBBB, those with RBBB had a lower right ventric-ular ejection fraction (RVEF-RBBB: 47 (37-57), IVCD: 48 (42-56), LBBB: 51 (42-60) %; p=0.041), greater RV mass (RBBB: 53 (41-73), IVCD: 49 (41-61), LBBB: 45 (36-56) g; p<0.001), higher plasma NTproBNP (RBBB: 2013 (668-3763), IVCD:1044 (416-2737), LBBB:1158 (582-2194) pg/ml, p=0.046), more signs of peripheral congestion and higher prevalence of atrial fibrillation. During a median follow up of 1302 days (IQ range 742-2253), 271 patients died. Compared with patients who had QRS <120 msec, RBBB (HR 1.7; 95% CI: 1.1-2.5, p= 0.011) and indeterminate morphologies (HR 1.7; 95% CI: 1.1-2.6, p= 0.016) were associated with an adverse outcome, but LBBB was not. In a multivariable Cox regression model including MRI data, neither QRS duration nor morphology were independently associated with an adverse outcome. Conclusions: In patients with chronic HF with or without a reduced LVEF and QRS> 120 msec, RBBB morphology identifies patients with more severe bi-ventricular dysfunction on cardiac MRI and a poorer prognosis. Background: Hypertrophic Cardiomyopathy (HCM) is a common genetic disorder with a wide variability in anatomic and clinical expression. However, data on Papillary Muscles (PMs) are scarce. Therefore, we aimed to analyze PMs characteristics by magnetic resonance imaging in a HCM population. Methods: We retrospectively evaluated 50 HCM patients (pts) who performed Cardiac Magnetic Resonance (CMR) in our institution, between 2008 and 2012. All pts had preserved Left Ventricular Ejection Fraction (LVEF) and were on sinus rhythm. Cine and Delayed Enhancement (DE) images were acquired on a 3T scanner and analyzed using a commercial workstation. All statistics analyses were performed using SPSS 20.0 version. Results: HCM pts were predominantly male (66%), with a mean age 47±18 years. Fifty-eight percent were in NYHA class I and the remaining in NYHA class II. The most common morphological presentation was septal HCM (68%) followed by apical HCM (14%). LV outflow gradient ≥30 mmHg was present only in 9 pts. LVEF (70±6%) and LV volumes (VTD=80±15 ml/m 2 ; VTS=24±7ml/m 2) were in the normal range. Right ventricular EF was 63±6%. In the majority of pts LV wall mass (LVWM) was increased (107±45g/m 2). The maximal LV Wall Thickness (LVWT) was 20±6mm, with hypertrophy involving 6±4 segments. Hypertrabecu-lation was also a common feature (32%), but a non-compacted/compacted my-ocardium ratio >2.3 was found only in 6 pts (involving ≤2 segments). Eighty-four percent of pts had DE in LV wall, mainly in the hypertrophied segments and with a focal pattern (60%). The RV insertions points also represent a common location (62%). Subendocardial or transmural DE occurred only in 9 pts. We identified > 2 PMs in two cases. The mean PMs mass was 6±2g/m 2 , slightly higher in PMs in anterior location. We found a significant correlation between PMs mass and LVWM (rho 0.64, p<0.0001), maximal LVWT (p=0.01) and the number of hyper-trophied segments (rho 0.55, p<0.0001). PMs DE was present in 34% of the pts, with equal distribution to PMs and in one case confined to them. There was no correlation between PMs DE and the numbers of segments with DE in LV wall. Finally, pts with PMs DE had significantly increased PMs mass compared with other pts (7±3 vs 5±2g/m 2 , p=0.04). Conclusions: In our population, PMs hypertrophy paralleled that of the LV wall and DE was identified in a significant proportion of pts. These findings suggest PMs enrolment in the cardiomyopathic process of HCM with potencial clinical consequences in some pts.