Introduction. Left ventricular (LV) systolic torsion is a primary mechanism contributing to stroke volume. We hypothesized that change in LV torsion parallels changes in global systolic performance during dyssynchrony and cardiac resynchronization therapy (CRT). Methods. Seven anesthetized open-chest dogs had LV pressure-volume relations. Apical, basal and mid-LV cross-sectional echocardiographic images were studied by speckle tracking analysis. Right atrial (RA) pacing served as control. Right ventricular (RV) pacing simulated left bundle branch block (LBBB). Simultaneous RV-LV free wall and RV-LV apex pacing (CRTfw and CRTa) modeled CRT. Dyssynchrony was defined as the time difference in peak strain between earliest and latest segments. Torsion was calculated as the maximum difference between apical and basal rotation. Results. RA pacing had minimal dyssynchrony (52±36 ms). RV pacing induced dyssynchrony (189±61 ms, p<0.05). CRTa decreased dyssynchrony (46±36 ms, p<0.05 vs. RV pacing) whereas CRTfw did not (110±96 ms). Torsion during baseline RA was 6.6±3.7°. RV pacing decreased torsion (5.1±3.6°, p<0.05 vs. control), reduced stroke volume (SV), stroke work (SW), and dP/dtmax compared to RA (21±5 vs. 17±5 mL, 252±61 vs. 151±64 mJ, and 2063±456 vs. 1603±424 mm Hg⋅s-1, respectively, p<0.05). CRTa improved torsion, SV, SW and dP/dtmax compared to RV pacing (7.7±4.7°, 23±3 mL, 240±50 mJ and 1947±647 mm Hg⋅s-1, respectively, p<0.05) whereas CRTfw did not (5.1±3.6°, 18±5 mL, 175±48 mJ 1699±432 mm Hg⋅s-1, respectively, p<0.05). LV torsion changes co-varied across conditions with SW (y=0.94x+12.27, r=0.81, p<0.0001) and stroke volume (y = 0.66 x+0.91, r = 0.81, p<0.0001). LV dyssynchrony changes did not correlate with SW or SV (r=-0.12, p=0.61 and r=0.08, p=0.73 respectively). Conclusions. LV torsion is primarily altered by dyssynchrony and CRT that restores LV performance also restores torsion.
- animal model
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