Background: In patients with ischemic heart failure undergoing cardiac resynchronization therapy (CRT) the underlying myocardial substrate at the left ventricle (LV) pacing site may affect CRT response. However, the effect of delivering the pacing stimulus remote, adjacent to or over LV transmural scar tissue (TST) identified by echocardiography is still unknown. Methods: First, 35 patients with healed myocardial infarction (57 ± 11 years) were prospectically studied to demonstrate the capability of echocardiographic end-diastolic wall thickness (EDWT) to identify LV-TST as defined by delayed enhancement magnetic resonance imaging (DE-MRI). Subsequently, in 136 patients (65 ± 10 years) who underwent CRT, EDWT was retrospectively evaluated at baseline. The LV catheter placement was defined over, adjacent to and remote from TST if pacing was delivered at a scarred segment, at a site 1 segment adjacent to or remote from scarred segments. CRT response was defined as LV end-systolic volume (ESV) decrease by at least 10% after 6 months. Results: A EDWT ≤ 5 mm identified TST at DE-MRI with 92% sensitivity and 96% specificity. In the 76 CRT responders, less overall and posterolateral TST segments and more segments paced remote from TST areas were found. At the multivariate regression analysis, the number of TST segments and scar/pacing relationship showed a significant association with CRT response. Conclusions: In addition to LV global scar burden, CRT response relates also to the myocardial substrate underlying pacing site as evaluated by standard echocardiography. This information may expand the role of echocardiography to guide pacing site avoiding pacing at TST areas. © 2011 Elsevier Ireland Ltd.
Pacing transmural scar tissue reduces left ventricle reverse remodeling after cardiac resynchronization therapy
Citro R;
2013-01-01
Abstract
Background: In patients with ischemic heart failure undergoing cardiac resynchronization therapy (CRT) the underlying myocardial substrate at the left ventricle (LV) pacing site may affect CRT response. However, the effect of delivering the pacing stimulus remote, adjacent to or over LV transmural scar tissue (TST) identified by echocardiography is still unknown. Methods: First, 35 patients with healed myocardial infarction (57 ± 11 years) were prospectically studied to demonstrate the capability of echocardiographic end-diastolic wall thickness (EDWT) to identify LV-TST as defined by delayed enhancement magnetic resonance imaging (DE-MRI). Subsequently, in 136 patients (65 ± 10 years) who underwent CRT, EDWT was retrospectively evaluated at baseline. The LV catheter placement was defined over, adjacent to and remote from TST if pacing was delivered at a scarred segment, at a site 1 segment adjacent to or remote from scarred segments. CRT response was defined as LV end-systolic volume (ESV) decrease by at least 10% after 6 months. Results: A EDWT ≤ 5 mm identified TST at DE-MRI with 92% sensitivity and 96% specificity. In the 76 CRT responders, less overall and posterolateral TST segments and more segments paced remote from TST areas were found. At the multivariate regression analysis, the number of TST segments and scar/pacing relationship showed a significant association with CRT response. Conclusions: In addition to LV global scar burden, CRT response relates also to the myocardial substrate underlying pacing site as evaluated by standard echocardiography. This information may expand the role of echocardiography to guide pacing site avoiding pacing at TST areas. © 2011 Elsevier Ireland Ltd.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
