Speckle-tracking-derived strain and strain-rate analysis: a technique for the evaluation of early alterations in right ventricle systolic function in patients with systemic sclerosis and normal pulmonary artery pressure


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Abstract

Background and aimSystemic sclerosis is associated with pulmonary artery hypertension. Speckle-tracking-derived strain and strain rate may be a diagnostic tool to detect early changes in right ventricular function, before pulmonary artery hypertension development. Our aim was to assess whether speckle-tracking-derived strain and strain-rate parameters may detect right ventricular early alterations in patients with systemic sclerosis with normal pulmonary systolic artery pressure (PAP).MethodsSeventeen asymptomatic patients with systemic sclerosis and 22 controls were enrolled. A complete two-dimensional echo with speckle-tracking-derived longitudinal strain and strain rate of the basal right ventricular free wall and interventricular septum was performed.ResultsMedian age was 56 years (43.8–71.5) in the systemic sclerosis group and 48.5 years (32–56.5) in the control group. No differences in conventional left ventricular parameters, tissue Doppler indexes, or in tricuspid annular plane systolic excursion were found. Patients with systemic sclerosis had higher levels of peak tricuspid regurgitation velocity and less respiratory collapse in the inferior vena cava. There were no differences in the speckle-tracking-derived strain and strain-rate parameters measured at the level of the basal interventricular septum and in the strain values measured at the level of the basal lateral right ventricular free wall. Nevertheless, a significant increase of the longitudinal strain rate measured at the basal lateral free wall of the right ventricle was found in patients with systemic sclerosis when compared with controls [−5.5 (−6.4–−2.6)/s vs. −1.8 (−3.9–−1.4)/s; P = 0.014].ConclusionSpeckle-tracking-derived longitudinal strain rate is useful to detect early right ventricular function changes in patients with systemic sclerosis with normal pulmonary systolic artery pressure levels. This alteration may preclude pulmonary artery hypertension development and reflect an adaptive response to higher levels of pulmonary systolic artery pressure.

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