RV Dyssynchrony by Speckle Tracking Strain in Pulmonary Arterial Hypertension: Will This Outcome Variable Take Root?

SEE PAGE 642 T he pressure overload of pulmonary arterial hypertension (PAH) predisposes the right ventricle (RV) to hypertrophy, dilation, and reduced pump function. Alterations in RV functional indexes such as tricuspid annular plane excursion, fractional area change, and tissue Doppler myocardial velocity have been shown to have prognostic significance in PAH (1). With the advent of strain and strain rate imaging, a decrement in RV strain indexes has also been noted in PAH patients. Data from extensive investigations concerning left ventricular dyssynchrony suggest that defining dyssynchrony descriptors of the RV may be a productive approach to understanding RV dysfunction in PAH. Interventricular and RV intraventricular dyssynchrony have been described in PAH (2–4). The interventricular delay noted due to later peak RV myocardial shortening and the ensuing delayed onset of RV diastolic relaxation lead to reduced left ventricular function by adverse diastolic interaction. Electrophysiological studies have also shown that in PAH, the RV, which completes activation and repolarization later than the left ventricle, exaggerates this delay. Unloading of the left ventricle, typical of PAH, also leads to its atrophic remodeling. Within the RV itself there is electromechanical dyssynergy in the contraction of the free wall and septum. Both tissue Doppler imaging and speckle tracking algorithms have been used to study intraventricular dyssynchrony in PAH (5,6). RV dyssynchrony in PAH strongly correlates with the extent of