Interventricular mechanical asynchrony in pulmonary arterial hypertension: left-to-right delay in peak shortening is related to right ventricular overload and left ventricular underfilling

Abstract

ObjectivesThe 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.BackgroundIn PAH, leftward ventricular septal bowing (LVSB) is probably caused by a left-to-right (L-R) delay in myocardial shortening.MethodsIn 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 (Tonset) and peak time (Tpeak) of circumferential shortening were calculated. The RV wall tension was estimated by the Laplace law.ResultsThe Tonset was 51 ± 23 ms, 65 ± 4 ms, and 52 ± 22 ms for LV, septum, and RV, respectively. The Tpeak 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 Tpeak. The L-R delay in Tonset was −1 ± 16 ms (p = 0.84), and the L-R delay in Tpeak was 94 ± 41 ms (p < 0.001). The L-R delay in Tpeak was not related to the QRS width but was associated with RV wall tension (p < 0.05). The L-R delay in Tpeak 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).ConclusionsIn 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