Abstract

Background: To address the question if submassive pulmonary embolism with impairment of right ventricular (RV) function may also influence left ventricular (LV) function and especially LV rotational mehanics and segmental function three dimensional speckle tracking imaging (3D-STI) was investigated in submassive pulmonary embolism. Methods: In 15 patients with submassive pulmonary embolism (PE) and 20 healthy volunteers three dimensional speckle tracking echocardiography and standard 2D echocardiography was performed (Artida, Toshiba, Japan). Analysis of parameters of RV geometry (sphericity-index: RVSI = longitudinal-axis length/ short-axis width), function (RV fractional area change: RV-FAC and tricuspid annular plane systolic excursion: TAPSE) and pressure overload (right ventricular systolic pressure: RVSP) as well as LV rotation and peak strains (PS) of longitudinal (LS) and circumferential (CS) strain were assessed offline. Systolic dyssynchrony (SDI) was defined as standard deviation of mean from time to PS and corrected for R-R' interval. Results: RV function was reduced by 25% (RV-FAC) and RV geometry as indicated by a mean diastolic RVSI of 1.13 was altered in the PE group compared with control subjects (p< 0.05). Global systolic LV strains and LV ejection fraction were significantly reduced (p< 0.01) in PE, whereas LV lateral wall LS and CS were less affected. Interventricular LS, CS and global systolic LV rotations correlated with RVSP, systolic RVSI and RV-FAC (r= -0.72, r= -0.69, r= 0.71; for all p< 0.01). Systolic dyssynchrony of LV was higher in patients with PE compared to control persons, with a pronounced lateral wall delay (p< 0.05). Parameters of systolic dyssynchrony of LV showed significant correlation with RV function and geometry (r= 0.65 and r= 0.69; p< 0.01). Conclusions: Acute right ventricular pressure overload directly affects RV function and geometry. RV pressure overload further influences LV geometry, which impairs LV torsion and segmental LS and CS, more for the septal segments than for the free wall of the left ventricle. These findings imply that patients with submassive pulmonary embolism could be more in risk of clinical deterioration by reduced and altered LV function. This clinical relevant interplay of both ventricles may be a valuable parameter to define patients at very high risk. The mechanisms for this interesting interventricular interplay remains to be elucidated.

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