Why the study?
In pulmonary arterial hypertension, leftward ventricular septal bowing is probably caused by a left-to-right delay in myocardial shortening, but whether the cause of interventricular asynchrony lies in the onset of shortening or the duration of shortening was uncertain.
Cross-Sectional (n=21)
In pulmonary arterial hypertension, interventricular mechanical asynchrony and leftward ventricular septal bowing are driven by prolonged duration of right ventricular shortening rather than delayed onset of shortening, impairing left ventricular filling and stroke volume.
Hypothesis-generating in PAH; leaves open whether asynchrony assessment or correction alters outcomes.
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.
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Marcus et al. (2008) conducted a cross-sectional in Pulmonary arterial hypertension (n=21). Magnetic resonance imaging myocardial tagging was evaluated on Left-to-right delay in time to peak circumferential shortening (Tpeak) (MD 94 ms, p=<0.001).
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