Left ventricular lead electrical delay predicts response to cardiac resynchronization therapy

Harvard University, Cambridge, Massachusetts, United States
Heart Rhythm (Impact Factor: 4.92). 11/2006; 3(11):1285-92. DOI: 10.1016/j.hrthm.2006.07.034
Source: PubMed

ABSTRACT Intracardiac electrograms can be used to guide left ventricular (LV) lead placement during implantation of cardiac resynchronization therapy (CRT) devices. Although attempts often are made to ensure that the LV lead is positioned at a site of maximal electrical delay, information on whether this is useful in predicting the acute hemodynamic response and long-term clinical outcome to CRT is limited.
The purpose of this study was to assess the ability of intracardiac (electrogram) measurements made during LV lead placement in patients undergoing CRT for predicting acute hemodynamic response and long-term clinical outcome to CRT.
Seventy-one subjects with standard indications for CRT underwent electrogram measurements and echocardiograms performed in the acute phase of this study. The LV lead electrical delay was measured intraoperatively from the onset of the surface ECG QRS complex to the onset of the sensed electrogram on the LV lead, as a percentage of the baseline QRS interval. Echocardiographic assessment of the hemodynamic response to CRT was measured as an intra-individual percentage change in dP/dt over baseline (DeltadP/dt, derived from the mitral regurgitation Doppler profile) with CRT on and off. dP/dt was measurable in 48 subjects, and acute responders to CRT were defined as those with DeltadP/dt >or=25%. Long-term response was measured as a combined endpoint of hospitalization for heart failure and/or all cause mortality at 12 months. Time to the primary endpoint was estimated by the Kaplan-Meier method, with comparisons made using the log rank test.
LV lead electrical delay correlated weakly with DeltadP/dt of the combined group (n = 48, r = 0.311, P = .029) but was strongly correlated with DeltadP/dt in the nonischemic subgroup (n = 20, r = 0.48, P = .027). LV lead electrical delay (%) was significantly longer in acute responders (69.6 +/- 23.9 vs 31.95 +/- 11.57, P = .002) among patients with nonischemic cardiomyopathy. A reduced LV lead electrical delay (<50% of the QRS duration) was associated with worse clinical outcome within the entire cohort (hazard ratio: 2.7, 95% confidence interval: 1.17-6.68, P = .032) as well as when stratified into ischemic and nonischemic subgroups.
Measuring LV lead electrical delay is useful during CRT device implantation because it may help predict hemodynamic response and long-term clinical outcome.

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    • "presence of scarring) may impact the electrical activation pattern and explain our findings. A long electrical delay may represent either delayed overall electrical activation of that segment or slow conduction through a region of LV scar [8] [9]. Our findings seem to suggest that a large variability in LV activation exists among CRT candidates, although the conventional lateral or postero-lateral LV segments might be preferred for lead positioning, as they are generally areas of late activation. "
    International journal of cardiology 01/2014; 172(2). DOI:10.1016/j.ijcard.2013.12.206 · 6.18 Impact Factor
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    • "Furthermore, one previous electrophysiological study using electro-anatomical mapping found great variability in the electrical and hemodynamic variables (16). Other investigators have used information extracted from electrodes inserted into the ventricles (during and after CRT) in an attempt to correlate the electrical data with both hemodynamic information and the clinical evolution of patients (17-19). "
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    ABSTRACT: Few studies have evaluated cardiac electrical activation dynamics after cardiac resynchronization therapy. Although this procedure reduces morbidity and mortality in heart failure patients, many approaches attempting to identify the responders have shown that 30% of patients do not attain clinical or functional improvement. This study sought to quantify and characterize the effect of resynchronization therapy on the ventricular electrical activation of patients using body surface potential mapping, a noninvasive tool. This retrospective study included 91 resynchronization patients with a mean age of 61 years, left ventricle ejection fraction of 28%, mean QRS duration of 182 ms, and functional class III/IV (78%/22%); the patients underwent 87-lead body surface mapping with the resynchronization device on and off. Thirty-six patients were excluded. Body surface isochronal maps produced 87 maximal/mean global ventricular activation times with three regions identified. The regional activation times for right and left ventricles and their inter-regional right-to-left ventricle gradients were calculated from these results and analyzed. The Mann-Whitney U-test and Kruskall-Wallis test were used for comparisons, with the level of significance set at p≤0.05. During intrinsic rhythms, regional ventricular activation times were significantly different (54.5 ms vs. 95.9 ms in the right and left ventricle regions, respectively). Regarding cardiac resynchronization, the maximal global value was significantly reduced (138 ms to 131 ms), and a downward variation of 19.4% in regional-left and an upward variation of 44.8% in regional-right ventricular activation times resulted in a significantly reduced inter-regional gradient (43.8 ms to 17 ms). Body surface potential mapping in resynchronization patients yielded electrical ventricular activation times for two cardiac regions with significantly decreased global and regional-left values but significantly increased regional-right values, thus showing an attenuated inter-regional gradient after the cardiac resynchronization therapy.
    Clinics (São Paulo, Brazil) 07/2013; 68(7):986-991. DOI:10.6061/clinics/2013(07)16 · 1.42 Impact Factor
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    • "Similar to our study, Singh et al [16]. analyzed clinical response after one year of CRT in patients with LBBB pattern. "
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    ABSTRACT: Considerable proportion of patients does not respond to the cardiac resynchronization therapy (CRT). This study investigated clinical relevance of left ventricular electrode local electrogram delay from the beginning of QRS (QLV). We hypothesized that longer QLV indicating more optimal lead placement in the late activated regions is associated with the higher probability of positive CRT response. We conducted a retrospective, single-centre analysis of 161 consecutive patients with heart failure and LBBB or nonspecific intraventricular conduction delay (IVCD) treated with CRT. We routinely intend to implant the LV lead in a region with long QLV. Clinical response to CRT, left ventricular (LV) reverse remodelling (i.e. decrease in LV end-systolic diameter - LVESD ≥10%) and reduction in plasma level of NT-proBNP >30% at 12-month post-implant were the study endpoints. We analyzed association between pre-implant variables and the study endpoints. Clinical CRT response rate reached 58%, 84% and 92% in the lowest (≤105 ms), middle (106-130 ms) and the highest (>130 ms) QLV tertile (p < 0.0001), respectively. Longer QRS duration (p = 0.002), smaller LVESD and a non-ischemic cardiomyopathy (both p = 0.02) were also univariately associated with positive clinical CRT response. In a multivariate analysis, QLV remained the strongest predictor of clinical CRT response (p < 0.00001), followed by LVESD (p = 0.01) and etiology of LV dysfunction (p = 0.04). Comparable predictive power of QLV for LV reverse remodelling and NT-proBNP response rates was observed. LV lead position assessed by duration of the QLV interval was found the strongest independent predictor of beneficial clinical response to CRT.
    BMC Cardiovascular Disorders 05/2012; 12(1):34. DOI:10.1186/1471-2261-12-34 · 1.50 Impact Factor
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