BACKGROUND: Up to 50% of patients do not respond to Cardiac Resynchronization Therapy (CRT). Recent work has focused on quantifying mechanical dyssynchrony and left ventricular scar. Septal reverse-mismatch (R-MM) (reduced FDG uptake vs perfusion) has been observed in patients with cardiomyopathy and prolonged QRS duration. We hypothesized that a greater quantity of septal R-MM would indicate a greater potential for reversibility of the cardiomyopathy, when the dyssynchrony is improved with CRT. Therefore, this study's objective was to assess whether greater septal R-MM pattern predicts response to CRT. METHODS AND RESULTS: Forty-nine patients had pre-implant Rubidium-82 and Fluorine-18-fluorodeoxyglucose PET scanning. Total and regional left ventricular scar size and extent of R-MM were calculated. Response to CRT was defined as ≥10% improvement in left ventricular end-systolic volume or ≥5% absolute ejection fraction improvement. In the non-ischemic cardiomyopathy subset non-responders had significantly less septal R-MM than responders (13.1% compared to 27.1%, P = .012). There were correlations between the extent of septal R-MM and the increase in ejection fraction (r = 0.692, P = .0004) and reduction in left ventricular end-systolic volume (r = -0.579, P = .004). For each 5% absolute increase in extent of septal R-MM the odds ratio of being a responder was 2.17 (95% CI 1.15, 4.11, P = .017). Extent of septal R-MM displayed high sensitivity and specificity (area under curve = 0.855, P = .017) to predict response. CONCLUSIONS: In patients with non-ischemic cardiomyopathy, greater extent of septal glucose metabolic R-MM pattern, predicted response to CRT. This parameter may be useful for identifying patients who benefit from CRT.
BACKGROUND: Up to 50% of patients do not respond to Cardiac Resynchronization Therapy (CRT). Recent work has focused on quantifying mechanical dyssynchrony and left ventricular scar. Septal reverse-mismatch (R-MM) (reduced FDG uptake vs perfusion) has been observed in patients with cardiomyopathy and prolonged QRS duration. We hypothesized that a greater quantity of septal R-MM would indicate a greater potential for reversibility of the cardiomyopathy, when the dyssynchrony is improved with CRT. Therefore, this study's objective was to assess whether greater septal R-MM pattern predicts response to CRT. METHODS AND RESULTS: Forty-nine patients had pre-implant Rubidium-82 and Fluorine-18-fluorodeoxyglucose PET scanning. Total and regional left ventricular scar size and extent of R-MM were calculated. Response to CRT was defined as ≥10% improvement in left ventricular end-systolic volume or ≥5% absolute ejection fraction improvement. In the non-ischemic cardiomyopathy subset non-responders had significantly less septal R-MM than responders (13.1% compared to 27.1%, P = .012). There were correlations between the extent of septal R-MM and the increase in ejection fraction (r = 0.692, P = .0004) and reduction in left ventricular end-systolic volume (r = -0.579, P = .004). For each 5% absolute increase in extent of septal R-MM the odds ratio of being a responder was 2.17 (95% CI 1.15, 4.11, P = .017). Extent of septal R-MM displayed high sensitivity and specificity (area under curve = 0.855, P = .017) to predict response. CONCLUSIONS: In patients with non-ischemic cardiomyopathy, greater extent of septal glucose metabolic R-MM pattern, predicted response to CRT. This parameter may be useful for identifying patients who benefit from CRT.
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