Antonio D'Onofrio1, Salvatore Ivan Caico2, Assunta Iuliano3, Paolo Pieragnoli4, Valter Bianchi5, Daniela Orsida2, Antonio Pani6, Mario Pasqualini7, Francesca Amadori8, Ludovico Vasquez9,10, Antonello Talarico11, Chiara Minoia2, Roberto Ospizio12, Greta Merlotti12, Maurizio Malacrida12, Giuseppe Stabile3. 1. Unità Operativa di Elettrofisiologia, Studio e Terapia delle Aritmie, Monaldi, Ospedale Monaldi, Via Leonardo Bianchi 1, 80131, Naples, Italy. donofrioant1@gmail.com. 2. Ospedale Sant'Antonio Abate, Gallarate, VA, Italy. 3. Clinica Mediterranea, Naples, Italy. 4. Azienda Ospedaliera Careggi, Florence, Italy. 5. Unità Operativa di Elettrofisiologia, Studio e Terapia delle Aritmie, Monaldi, Ospedale Monaldi, Via Leonardo Bianchi 1, 80131, Naples, Italy. 6. Ospedale Manzoni, Lecco, Italy. 7. Ospedale Civile Destra Secchia, Pieve di Coriano, MN, Italy. 8. Ospedale San Francesco, Nuoro, Italy. 9. Presidio Ospedaliero "G. Fogliani", Milazzo, ME, Italy. 10. Azienda Sanitaria Provinciale di Messina, Messina, Italy. 11. Ospedale Annunziata, Cosenza, Italy. 12. Boston Scientific Italia, Milano, Italy.
Abstract
PURPOSE: Latency during left ventricle (LV) pacing has been suggested as a potential cause of ineffectual biventricular pacing. We assessed the incidence, predictors, and impact on outcome of increased LV latency in 274 patients undergoing cardiac resynchronization therapy (CRT). METHODS: On implantation, the latency interval was defined as the shortest stimulus-to-QRS onset interval in any lead of the 12-lead ECG. A stimulus-to-QRS onset interval ≥ 40 ms was used to define the presence of increased LV latency. RESULTS: Increased LV latency was observed in 55 patients (20%). On multivariate analysis, only ischemic etiology proved to be a predictor of increased LV latency. On 12-month echocardiographic evaluation, 68% patients showed a ≥ 15% decrease in LV end systolic volume (74% patients with increased LV latency, 67% patients without increased LV latency (p = 0.58). The presence of increased LV latency was not associated with a different clinical response to CRT. CONCLUSIONS: Increased LV latency occurred in almost 20% of patients undergoing CRT and was more frequent in patients with ischemic heart disease. The presence of increased LV latency does not seem to have an impact on echocardiographic or clinical response to CRT.
PURPOSE: Latency during left ventricle (LV) pacing has been suggested as a potential cause of ineffectual biventricular pacing. We assessed the incidence, predictors, and impact on outcome of increased LV latency in 274 patients undergoing cardiac resynchronization therapy (CRT). METHODS: On implantation, the latency interval was defined as the shortest stimulus-to-QRS onset interval in any lead of the 12-lead ECG. A stimulus-to-QRS onset interval ≥ 40 ms was used to define the presence of increased LV latency. RESULTS: Increased LV latency was observed in 55 patients (20%). On multivariate analysis, only ischemic etiology proved to be a predictor of increased LV latency. On 12-month echocardiographic evaluation, 68% patients showed a ≥ 15% decrease in LV end systolic volume (74% patients with increased LV latency, 67% patients without increased LV latency (p = 0.58). The presence of increased LV latency was not associated with a different clinical response to CRT. CONCLUSIONS: Increased LV latency occurred in almost 20% of patients undergoing CRT and was more frequent in patients with ischemic heart disease. The presence of increased LV latency does not seem to have an impact on echocardiographic or clinical response to CRT.
Entities:
Keywords:
Cardiac resynchronization therapy; Ischemic heart disease with left ventricular pacing; Latency; Outcome; Ventricular pacing
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