{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,22]],"date-time":"2025-10-22T02:58:53Z","timestamp":1761101933327},"reference-count":46,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2011,3]]},"abstract":"<jats:p> Left ventricular (LV) systolic torsion is a primary mechanism contributing to stroke volume (SV). We hypothesized that change in LV torsion parallels changes in global systolic performance during dyssynchrony and cardiac resynchronization therapy (CRT). Seven anesthetized open chest dogs had LV pressure-volume relationship. 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. Simultaneous RV-LV free wall and RV-LV apex pacing (CRTfw and CRTa, respectively) 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 the apical and basal rotation. RA pacing had minimal dyssynchrony (52 \u00b1 36 ms). RV pacing induced dyssynchrony (189 \u00b1 61 ms, P &lt; 0.05). CRTa decreased dyssynchrony (46 \u00b1 36 ms, P &lt; 0.05 vs. RV pacing), whereas CRTfw did not (110 \u00b1 96 ms). Torsion during baseline RA was 6.6 \u00b1 3.7\u00b0. RV pacing decreased torsion (5.1 \u00b1 3.6\u00b0, P &lt; 0.05 vs. control), and reduced SV, stroke work (SW), and dP\/d t<jats:sub>max<\/jats:sub> compared with RA (21 \u00b1 5 vs. 17 \u00b1 5 ml, 252 \u00b1 61 vs. 151 \u00b1 64 mJ, and 2,063 \u00b1 456 vs. 1,603 \u00b1 424 mmHg\/s, respectively, P &lt; 0.05). CRTa improved torsion, SV, SW, and dP\/d t<jats:sub>max<\/jats:sub> compared with RV pacing (7.7 \u00b1 4.7\u00b0, 23 \u00b1 3 ml, 240 \u00b1 50 mJ, and 1,947 \u00b1 647 mmHg\/s, respectively, P &lt; 0.05), whereas CRTfw did not (5.1 \u00b1 3.6\u00b0, 18 \u00b1 5 ml, 175 \u00b1 48 mJ, and 1,699 \u00b1 432 mmHg\/s, respectively, P &lt; 0.05). LV torsion changes covaried across conditions with SW ( y = 0.94 x+12.27, r = 0.81, P &lt; 0.0001) and SV ( y = 0.66 x+0.91, r = 0.81, P &lt; 0.0001). LV dyssynchrony changes did not correlate with SW or SV ( r = \u22120.12, P = 0.61 and r = 0.08, P = 0.73, respectively). Thus, we conclude that LV torsion is primarily altered by dyssynchrony, and CRT that restores LV performance also restores torsion. <\/jats:p>","DOI":"10.1152\/ajpheart.00177.2010","type":"journal-article","created":{"date-parts":[[2010,12,17]],"date-time":"2010-12-17T23:03:01Z","timestamp":1292626981000},"page":"H853-H858","source":"Crossref","is-referenced-by-count":12,"title":["Left ventricular systolic torsion correlates global cardiac performance during dyssynchrony and cardiac resynchronization therapy"],"prefix":"10.1152","volume":"300","author":[{"given":"Bouchra","family":"Lamia","sequence":"first","affiliation":[{"name":"Department of Critical Care Medicine, University of Pittsburgh Medical Center, Pittsburgh; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masaki","family":"Tanabe","sequence":"additional","affiliation":[{"name":"Cardiovascular Institute, University of Pittsburgh, Pittsburgh, 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