Left Ventricular Lead Electrical Delay Is a Predictor of Mortality in Patients With Cardiac Resynchronization Therapy.

BACKGROUND: Electric left ventricular lead position, assessed by the electric delay from the beginning of the QRS complex to the local LV electrogram (QLV), was found in previous studies to be a strong predictor of short-term response to cardiac resynchronization therapy. We hypothesized that suboptimum electric position of the left ventricular lead is associated with an excess of heart failure events and mortality. METHODS AND RESULTS: We analyzed the clinical outcome of patients with left bundle branch block or intraventricular conduction delay treated with cardiac resynchronization therapy at our institution during 9 years. Baseline clinical characteristics, QLV/QRS duration (QLV ratio) at cardiac resynchronization therapy implant, and data about heart failure hospitalization and mode of death were collected in 329 patients who were followed for a period of 3.3±1.9 years. Of them, 83 were hospitalized for heart failure and 83 died. Event rates for all-cause mortality, cardiac mortality, noncardiac mortality, heart failure mortality, and sudden death were 25.2%, 14.9%, 10.3%, 12.2%, and 2.1%, respectively. Patients with a QLV ratio ≤0.70 had significantly worse event-free survival for all study end points--hazard ratio, 1.6; 95% confidence interval, 1.0 to 2.4; P=0.05 for heart failure hospitalization; hazard ratio, 2.9; 95% confidence interval, 1.6 to 5.5; P=0.001 for heart failure mortality; hazard ratio, 1.8; 95% confidence interval, 1.1 to 2.7; P=0.01 for cardiac mortality; and hazard ratio, 2.1; 95% confidence interval, 1.2 to 3.7; P=0.01 for all-cause mortality. In multivariable analysis, QLV ratio ≤0.70 remained associated with all study end points. CONCLUSIONS: Electric left ventricular lead position in cardiac resynchronization therapy patients was a significant predictor of heart failure hospitalization and mortality.

Left ventricular mechanical activity detected by impedance recording.

AIMS: Recording and analysing impedance fluctuation along the cardiac cycle in the right (RV) and left ventricles (LV). METHODS AND RESULTS: During a biventricular (BiV) implantation procedure, impedance was sequentially derived between the atrial ring electrode and either electrode (tip or ring) of the RV lead [transvalvular impedance (TVI)], and between the atrial ring and either the tip or ring electrode of a coronary sinus lead, positioned in a cardiac vein [left ventricle impedance (LVI)]. The LVI signal was also recorded by the implanted pacemaker at the 1 day and 3 months follow-ups. With intrinsic conduction, TVI showed an average increase of 53 +/- 29 ohm during ventricular systole, whereas at the same time, LVI decreased by 45 +/- 21 ohm (25 and 23 patients, respectively, out of 28 tested cases). Transvalvular impedance and LVI displayed a similar time course, which appeared to be related to the systolic timing in the RV and LV. Both LVI amplitude and duration decreased as a function of the cardiac rate. The LVI deflection started immediately after LV stimulation, and often anticipated the R-wave sensing after contralateral pacing. At the 3-month follow-up, LVI amplitude was decreased in 70% of cases and increased in the remainder, with a non-significant average change of -5 +/- 85% with respect to the acute recordings. CONCLUSION: Transvalvular impedance properties are consistent with the assumption of an inverse relationship with RV volume. Though LVI requires a different physical interpretation, the waveform duration might reflect the timing of LV myocardial contraction. In this hypothesis, the relationship between TVI and LVI could provide insight into the effects of BiV pacing on mechanical synchronization.