Lack of Association Between Left Ventricular Dyssynchrony and The Development of Cardiomyopathy in Patients with Left Bundle Branch Block and Initially Preserved Left Ventricular Ejection Fraction

Background Left bundle branch block (LBBB) causes left ventricular (LV) dyssynchrony that can lead to a subsequent cardiomyopathy (CMP). Objectives Among patients with LBBB and an initially preserved LV ejection fraction (EF), we evaluated the relationship between LV dyssynchrony assessed by echocardiography and the future development of LV systolic dysfunction. Methods Subjects were taken from a database of LBBB patients with an initially preserved LVEF (≥45%) without clinically relevant coronary disease or other identifiable cause of CMP. From the initial echocardiogram obtained after diagnosis of LBBB in which the LVEF was preserved, we compared LVEF and LV dimensions in patients who maintained a preserved LVEF (pEF - N=40) with those who developed LV systolic dysfunction (EF≤40%; subsequent CMP - N=28) over a mean follow up period of 58.0±37.8 mos. We also quantified dyssynchrony from this echocardiogram using two methods: 1) time delay between the earliest peak septal and peak posterior wall contraction by M-mode; and 2) time difference between peak posterior wall contraction and onset of transmitral E-wave on pulsed-wave Doppler, for which a value above zero indicates significant dyssynchrony. Results (data are means±sd) There were no significant differences among clinical variables (including age, gender, and other comorbidities). Echocardiographic data are shown in the table below. The subsequent CMP group exhibited a slightly lower mean LVEF compared to the pEF group with the LV end diastolic diameters (LVEDD) and end systolic diameters (ESD) being correspondingly and significantly increased. However, we observed no statistically significant differences with either measure of dyssynchrony. Conclusions Among LBBB patients with an initially preserved LVEF, the degree of LV dyssynchrony assessed through these two echocardiographic measures was not different between those who maintained a preserved EF versus those who developed a subsequent CMP. These data indicate that dyssynchrony itself does not predict future LV systolic dysfunction in patients with patients with LBBB, and support the notion that the mechanisms contributing to LBBB-associated cardiomyopathy are complex and perhaps not driven by dyssynchrony alone. Left bundle branch block (LBBB) causes left ventricular (LV) dyssynchrony that can lead to a subsequent cardiomyopathy (CMP). Among patients with LBBB and an initially preserved LV ejection fraction (EF), we evaluated the relationship between LV dyssynchrony assessed by echocardiography and the future development of LV systolic dysfunction. Subjects were taken from a database of LBBB patients with an initially preserved LVEF (≥45%) without clinically relevant coronary disease or other identifiable cause of CMP. From the initial echocardiogram obtained after diagnosis of LBBB in which the LVEF was preserved, we compared LVEF and LV dimensions in patients who maintained a preserved LVEF (pEF - N=40) with those who developed LV systolic dysfunction (EF≤40%; subsequent CMP - N=28) over a mean follow up period of 58.0±37.8 mos. We also quantified dyssynchrony from this echocardiogram using two methods: 1) time delay between the earliest peak septal and peak posterior wall contraction by M-mode; and 2) time difference between peak posterior wall contraction and onset of transmitral E-wave on pulsed-wave Doppler, for which a value above zero indicates significant dyssynchrony. (data are means±sd) There were no significant differences among clinical variables (including age, gender, and other comorbidities). Echocardiographic data are shown in the table below. The subsequent CMP group exhibited a slightly lower mean LVEF compared to the pEF group with the LV end diastolic diameters (LVEDD) and end systolic diameters (ESD) being correspondingly and significantly increased. However, we observed no statistically significant differences with either measure of dyssynchrony. Among LBBB patients with an initially preserved LVEF, the degree of LV dyssynchrony assessed through these two echocardiographic measures was not different between those who maintained a preserved EF versus those who developed a subsequent CMP. These data indicate that dyssynchrony itself does not predict future LV systolic dysfunction in patients with patients with LBBB, and support the notion that the mechanisms contributing to LBBB-associated cardiomyopathy are complex and perhaps not driven by dyssynchrony alone.