Key result
Higher LV R-wave amplitude at implant is linked to echocardiographic response to CRT.
Why the study?
The optimal left ventricular stimulation site and the predictive value of local stimulation characteristics for response to CRT in non-ischaemic cardiomyopathy patients have not been systematically studied.
Do left ventricular stimulation characteristics at implantation predict echocardiographic response to CRT at 6 months in patients with non-ischaemic cardiomyopathy?
Cohort (n=138)
Do left ventricular stimulation characteristics at implantation predict echocardiographic response to CRT at 6 months in patients with non-ischaemic cardiomyopathy?
Higher LV R-wave amplitude at the time of CRT device implantation is associated with a favorable echocardiographic response at 6 months in patients with non-ischemic cardiomyopathy.
Stimulation characteristics at LV lead implantation may predict CRT response in non-ischaemic cardiomyopathy; hypothesis-generating and requires prospective validation.
AIMS: Although the electrical stimulation of an ischaemic tissue adversely affects the left ventricular (LV) systolic function, the optimal stimulation site in patients with non-ischaemic cardiomyopathy has not been systematically studied. We hypothesized that the local stimulation characteristics at the time of device implantation predict the response to cardiac resynchronization therapy (CRT). METHODS AND RESULTS: We measured the impedance, sensing, and capture threshold of a bipolar LV lead in 138 patients with non-ischaemic cardiomyopathy undergoing first implantation of CRT device for drug refractory heart failure. All patients underwent echocardiography at baseline and at 6 months post-implantation. An absence of favourable response to CRT was defined as <15% decrease in echocardiographic LV end-systolic volume (LVESV) at 6 months. Echocardiographic response to CRT was observed in 70% of patients. The LV lead measurements predicted neither the optimal stimulation site nor the response to CRT. Left ventricular capture threshold (1.50 ± 1.1 vs. 1.32 ± 0.8 V) and impedance (725 ± 287 vs. 720 ± 261 Ω) were similar between the responders and the non-responders. Independent of baseline LV ejection fraction or ESV, the LV R-wave amplitude at implantation was significantly higher (P = 0.0038) in responders (12.7 ± 5.2 mV) than in non-responders (9.7 ± 6.3 mV), with an area under the receiver operating characteristic curve of 0.7. CONCLUSION: Response to CRT, as determined by decrease in LVESV at 6 months, was associated with significantly higher LV R-wave amplitude at the time of device implantation.
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Deplagne et al. (2010) conducted a cohort in Non-ischaemic cardiomyopathy with drug refractory heart failure (n=138). Left ventricular R-wave amplitude at implantation vs. Lower R-wave amplitude was evaluated on Echocardiographic response to CRT (≥15% decrease in LV end-systolic volume at 6 months) (AUC 0.7, p=0.0038). Higher left ventricular R-wave amplitude at device implantation was significantly associated with echocardiographic response to CRT at 6 months (12.7 vs 9.7 mV; P=0.0038).
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