Left bundle branch block and mortality in patients with acute heart failure syndrome: a substudy of the EFICA cohort.

AIMS: In patients with chronic heart failure (CHF), left bundle branch block (LBBB) is associated with an increased risk of cardiovascular mortality. We aimed to investigate the association of LBBB with short- and long-term outcome in patients discharged after a de novo episode of acute heart failure (AHF) or AHF complicating a mild CHF. METHODS AND RESULTS: Patients with no history of New York Heart Association class III and IV CHF, who were admitted for a severe AHF episode and enrolled in the prospective observational EFICA study (n = 403), were included. Left bundle branch block prevalence was 16%. Patients with LBBB had a higher prevalence of dilated cardiomyopathy (23 vs. 10%, P < 0.005), a higher percentage of AHF episodes without identified precipitating factor (15 vs. 2%, P < 0.001), and were less likely to present increased markers of cardiac injury (41 vs. 56%, P = 0.04). The 4-week mortality was 24.8% with no difference between LBBB and no LBBB patients. Left bundle branch block was however an independent predictor of 1-year mortality in the 4-week survivors [hazards ratio (95% confidence interval) = 2.01 (1.12-3.64), P = 0.02]. CONCLUSION: Long-term outcome of patients surviving a severe episode of de novo AHF or AHF complicating a mild CHF is worsened by LBBB. These patients may constitute a subgroup at high risk in whom specific therapeutic solutions should be investigated.

Left bundle branch block as a risk factor for progression to heart failure.

The prevalence of conduction disturbances, particularly left bundle branch block (LBBB), is strongly correlated with age and with the presence of cardiovascular disease. LBBB has been reported to affect approximately 25% of the heart failure (HF) population and it is likely that the deleterious role of such conduction disorders in the progression to HF has been underestimated. The purpose of this article is to review the data from the literature indicating that LBBB may have a causative role, mediated through the resulting intra-ventricular asynchrony, in the deterioration of cardiac function and the development of cardiac remodelling and HF. It also aims to address the potential for future clinical therapies for this conduction disorder.

Clinical efficacy of cardiac resynchronization therapy using left ventricular pacing in heart failure patients stratified by severity of ventricular conduction delay.

OBJECTIVES: We assessed the clinical efficacy of single-site left ventricular (LV) pacing and determined the impact of baseline conduction delay severity on the magnitude of benefit. BACKGROUND: Multisite biventricular pacing can improve heart failure (HF) symptoms in patients with an intraventricular conduction delay by resynchronizing abnormal ventricular contractions and improving LV systolic function. METHODS: Eighty-six patients with at least New York Heart Association functional class II HF, chronic LV systolic dysfunction, normal sinus rhythm, and a QRS interval over 120 ms were implanted for atrial-synchronized LV pacing. The single-blinded, randomized, controlled, crossover study stratified patients 1:1 by the baseline QRS interval into long (QRS >150 ms) and short (QRS 120 to 150 ms) groups, which were compared during a three-month period of active (univentricular) pacing and a three-month period of inactive (ventricular inhibited) pacing. The primary end point was peak oxygen consumption (VO(2)) followed by anaerobic threshold, distance walked in 6 min, and quality-of-life questionnaire score. PATIENTS: Twelve patients were withdrawn before randomization and 17 could not complete both study periods. The short QRS group did not improve in any end point with active pacing. For the long QRS group, peak VO(2) increased 2.46 ml/min/kg (p < 0.001), the anaerobic threshold increased 1.55 ml/min/kg (p < 0.001), the distance walked in 6 min increased 47 m (p = 0.024), and the quality-of-life score improved 8.1 points (p = 0.004). CONCLUSIONS: Left ventricular pacing significantly improves exercise tolerance and quality of life in patients with chronic HF, LV systolic dysfunction, and a QRS interval over 150 ms.

Echocardiographic quantification of left ventricular asynchrony predicts an acute hemodynamic benefit of cardiac resynchronization therapy.

OBJECTIVES: We sought to determine whether radial left ventricular (LV) asynchrony in patients with heart failure predicts systolic function improvement with cardiac resynchronization therapy (CRT). BACKGROUND: We quantified LV wall motion by echocardiography to correlate the effects of CRT on LV systolic function with wall motion synchrony. METHODS: Thirty-four patients underwent echocardiographic phase analysis of LV septal and lateral wall motion and hemodynamic testing before CRT. Phase relationships were measured by the difference between the lateral (Phi(L)) and septal (Phi(S)) wall motion phase angles: Phi(LS) = Phi(L) - Phi(S). The absolute value of Phi(LS) was used as an order-independent measure of synchrony: the absolute value Phi(LS) = the absolute value of Phi(L) - Phi(S). RESULTS: Three phase relationships were identified (mean +/- SD): type 1 (n = 4; peak positive LV pressure [dP/dt(max)] 692 +/- 310 mm Hg/s; Phi(LS) = 5 +/- 6 degrees, synchronous wall motion); type 2 (n = 17; dP/dt(max) 532 +/- 148 mm Hg/s; Phi(LS) = 77 +/- 33 degrees, delayed lateral wall motion); and type 3 (n = 13; dP/dt(max) 558 +/- 154 mm Hg/s; Phi(LS) = -115 +/- 33 degrees, delayed septal wall motion, triphasic). A large absolute value of Phi(LS) predicted a larger increase in dP/dt(max) with CRT (r = 0.74, p < 0.001). Sixteen patients were studied during right ventricular (RV), LV and biventricular (BV) pacing. Cardiac resynchronization therapy acutely reduced the absolute value of Phi(LS) from 104 +/- 41 degrees (OFF) to 86 +/- 45 degrees (RV; p = 0.14 vs. OFF), 71 +/- 50 degrees (LV; p = 0.001 vs. OFF) and 66 +/- 42 degrees (BV; p = 0.001 vs. OFF). A reduction in the absolute value of Phi(LS) predicted an improvement in dP/dt(max) in type 2 patients for LV (r = 0.87, p = 0.005) and BV CRT (r = 0.73, p = 0.04). CONCLUSIONS: Echocardiographic quantification of LV asynchrony identifies patients likely to have improved systolic function with CRT. Improved synchrony is directly related to improved hemodynamic systolic function in type 2 patients.

Left ventricular dysfunction is associated with prolonged average ventricular fibrillation cycle length in patients with implantable cardioverter defibrillators.

OBJECTIVES: In cellular studies, ventricular refractoriness (ERP) is prolonged in heart failure (CHF), but clinical evidence is lacking. The average ventricular fibrillation cycle length (VFCL) has been shown to correlate with local ERP. We hypothesized that the VFCL increases with left ventricular (LV) dysfunction. Therefore, we evaluated intracardiac VFCL recorded by implantable defibrillators (ICD) in patients with and without LV dysfunction. METHODS: We analyzed intracardiac VFCL recorded by sensing leads of Ventak MINI (Guidant) ICD in 49 patients (35 men; age 54 +/- 13 years; 25 (51%) with coronary artery disease; mean LV ejection fraction (EF) 41 +/- 17%, range 76-10) from the European Ventak MINI Investigator Group. No patients were receiving antiarrhythmic drugs, including beta-blockers. Mean and median VFCL were obtained at predischarge testing during first charge time (4.5 +/- 2.7 s, range 1.4-11). RESULTS: Mean median VFCL was 186 +/- 21ms (range 150-230 ms). Patients with LVEF >/= 50% (n = 14) had shorter median VFCL than patients with LVEF < 50% (n = 35), (171 +/- 14 vs. 191 +/- 20 ms; p = 0.002). Median VFCL correlated with LVEF (r = -0.41; p = 0.003) and age (r = 0.28, p = 0.04), but was not significantly associated with charge time and defibrillation threshold at implant. Similar results occurred with mean VFCL. In multiple linear regression and correlation models, only LVEF% was a significant predictor (p < 0.05 for all models) of median VFCL. CONCLUSIONS: LV dysfunction prolongs averaged VFCL in patients at risk for malignant ventricular arrhythmias who have implantable cardioverter defibrillators. This phenomenon might be related to alterations in the ventricular refractory period.