Myocardial Structural, Perfusion, and Metabolic Correlates of Left Bundle Branch Block Mechanical Derangement in Patients With Dilated Cardiomyopathy

Abstract

Background— Left bundle branch block (LBBB) influences on regional left ventricular (LV) structure, perfusion, and metabolism have not yet been thoroughly investigated in dilated cardiomyopathy patients. Methods and Results— Eleven dilated cardiomyopathy patients with LBBB (mean±SD age, 62±11 years; LV ejection fraction, 35±8%) and 7 dilated cardiomyopathy patients without LBBB (mean±SD age, 58±9 years; LV ejection fraction, 37±10%) were studied by cardiac magnetic resonance and positron emission tomography. The left ventricle was divided in 3 regions: septum, adjacent (anterior-inferior walls), and lateral. Regional midwall circumferential strain, maximum shortening, and strain rate were obtained from tagged cardiac magnetic resonance. The systolic stretch index was calculated as positive strain rate (stretching) divided by total strain rate. Myocardial metabolic rate of glucose and resting and hyperemic myocardial blood flow were quantified by 2-[ 18 F]fluoro-2-deoxyglucose and [ 13 N]ammonia positron emission tomography, respectively. Compared with non-LBBB patients, LBBB patients showed a highly inhomogeneous systolic deformation pattern that changed gradually, moving from a discoordinate [(systolic stretch index, 0.485 (0.284)] and poorly contracting (maximum shortening, −1.14±0.96%) septum to a coordinate [systolic stretch index, 0.002 (0.168)] and strongly contracting (maximum shortening, −13.63±2.58%) lateral region (both P <0.0001). This pattern was closely matched to the myocardial metabolic rate of glucose, disclosing lowest, intermediate, and highest values in the septum, adjacent, and lateral regions, respectively ( P <0.0001). Septal-to-lateral thickness ratio was lower in LBBB than in non-LBBB patients ( P =0.03). In both groups, the LV distribution of resting and hyperemic myocardial blood flow and myocardial blood flow reserve did not differ significantly. Conclusions— In dilated cardiomyopathy patients, the extensive LV contraction abnormalities induced by LBBB cause regional myocardial metabolic and structural remodeling, without consistent changes in blood flow.