Abstract

Background: Up to 35% of patients with dyssynchrony do not respond to cardiac resynchronization therapy (CRT). This may result from suboptimal placement of the left ventricular (LV) pacing lead. Currently there is no consensus on the best parameter for the LV lead optimization or the optimal site for LV pacing. Methods: 27 patients, 13 with ischemic cardiomyopathy (ICM) and 14 with non-ischemic cardiomyopathy (NICM), who did not respond to CRT within twelve months, were studied. 19/27 patients had initial LV lead placement in the anterolateral and 8/27 in the lateral-basal segment of the LV. A new LV lead was placed in multiple sites in the coronary venous system. Acute measurements were performed with the conductance catheter to select the new LV pacing site. Change in LV stroke volume and dP/dtmax were used as a guide to optimal lead position, After implantation patients were followed clinically at 1, 3, 6 and 12 months. Echocardiography, the Minnesota Living with Heart Failure Questionnaire, and 6 min hall walk tests were completed at the baseline and 6 month intervals. Results: During acute measurements the biggest increase in stroke volume was seen in the apico lateral segment of the LV. The new apico lateral LV lead position significantly increased stroke volume (+27%, P =.01), stroke work (+45%, P =.04) reduced end-systolic volume (-5%, P =.04) and did not significantly change dP/dtmax (+5%, P =.2) when compared to the old LV lead position in all 27 patients. Long term follow up demonstrated that the acute increase in the LV stroke volume resulted in significantly better response to therapy. After 6 months all patients showed improvement in quality of life and the 6 minute hall walk test, NICM patients had significant increase in EF (+10%, P=0.05) and 12/14 decreased ES and ED volume >15%. ICM patients had worse results EF (+2%, P=0.1) and ES and ED volumes decreased in 7/13. At 12 months 4/13 patients with ICM and 2/14 with NICM died. Conclusions: In patients who are non-responders, repositioning or adding LV lead to the original CRT system with use of hemodynamic guidance significantly improved response. Mechanism of improvement was related to the increase in LV stroke volume, not the change dP/dt max. The optimal LV pacing site was lateral towards the apex in all patients. Despite the improvements the mortality in the ICM group after 12 months was high. Background: Up to 35% of patients with dyssynchrony do not respond to cardiac resynchronization therapy (CRT). This may result from suboptimal placement of the left ventricular (LV) pacing lead. Currently there is no consensus on the best parameter for the LV lead optimization or the optimal site for LV pacing. Methods: 27 patients, 13 with ischemic cardiomyopathy (ICM) and 14 with non-ischemic cardiomyopathy (NICM), who did not respond to CRT within twelve months, were studied. 19/27 patients had initial LV lead placement in the anterolateral and 8/27 in the lateral-basal segment of the LV. A new LV lead was placed in multiple sites in the coronary venous system. Acute measurements were performed with the conductance catheter to select the new LV pacing site. Change in LV stroke volume and dP/dtmax were used as a guide to optimal lead position, After implantation patients were followed clinically at 1, 3, 6 and 12 months. Echocardiography, the Minnesota Living with Heart Failure Questionnaire, and 6 min hall walk tests were completed at the baseline and 6 month intervals. Results: During acute measurements the biggest increase in stroke volume was seen in the apico lateral segment of the LV. The new apico lateral LV lead position significantly increased stroke volume (+27%, P =.01), stroke work (+45%, P =.04) reduced end-systolic volume (-5%, P =.04) and did not significantly change dP/dtmax (+5%, P =.2) when compared to the old LV lead position in all 27 patients. Long term follow up demonstrated that the acute increase in the LV stroke volume resulted in significantly better response to therapy. After 6 months all patients showed improvement in quality of life and the 6 minute hall walk test, NICM patients had significant increase in EF (+10%, P=0.05) and 12/14 decreased ES and ED volume >15%. ICM patients had worse results EF (+2%, P=0.1) and ES and ED volumes decreased in 7/13. At 12 months 4/13 patients with ICM and 2/14 with NICM died. Conclusions: In patients who are non-responders, repositioning or adding LV lead to the original CRT system with use of hemodynamic guidance significantly improved response. Mechanism of improvement was related to the increase in LV stroke volume, not the change dP/dt max. The optimal LV pacing site was lateral towards the apex in all patients. Despite the improvements the mortality in the ICM group after 12 months was high.

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