Interventricular Mechanical Asynchrony in Pulmonary Arterial Hypertension. Left-to-Right Delay in Peak Shortening Is Related to Right Ventricular Overload and Left Ventricular Underfilling

Objectives: The purpose of this study was to explore in pulmonary arterial hypertension (PAH) whether the cause of interventricular asynchrony lies in onset of shortening or duration of shortening. Background: In PAH, leftward ventricular septal bowing (LVSB) is probably caused by a left-to-right (L-R) delay in myocardial shortening. Methods: In 21 PAH patients (mean pulmonary arterial pressure 55 ± 13 mm Hg and electrocardiogram-QRS width 100 ± 16 ms), magnetic resonance imaging myocardial tagging (14 ms temporal resolution) was applied. For the left ventricular (LV) free wall, septum, and right ventricular (RV) free wall, the onset time (T_onset) and peak time (T_peak) of circumferential shortening were calculated. The RV wall tension was estimated by the Laplace law. Results: The T_onset was 51 ± 23 ms, 65 ± 4 ms, and 52 ± 22 ms for LV, septum, and RV, respectively. The T_peak was 293 ± 58 ms, 267 ± 22 ms, and 387 ± 50 ms for LV, septum, and RV, respectively. Maximum LVSB was at 395 ± 45 ms, coinciding with septal overstretch and RV T_peak. The L-R delay in T_onset was -1 ± 16 ms (p = 0.84), and the L-R delay in T_peak was 94 ± 41 ms (p < 0.001). The L-R delay in T_peak was not related to the QRS width but was associated with RV wall tension (p < 0.05). The L-R delay in T_peak correlated with leftward septal curvature (p < 0.05) and correlated negatively with LV end-diastolic volume (p < 0.05) and stroke volume (p < 0.05). Conclusions: In PAH, the L-R delay in myocardial peak shortening is caused by lengthening of the duration of RV shortening. This L-R delay is related to LVSB, decreased LV filling, and decreased stroke volume.