Interventricular mechanical asynchrony in pulmonary arterial hypertension

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.