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Left ventricular systolic torsion correlates global cardiac performance during dyssynchrony and cardiac resynchronization therapy

Lamia, B and Tanabe, M and Tanaka, H and Kim, HK and Gorcsan, J and Pinsky, MR (2011) Left ventricular systolic torsion correlates global cardiac performance during dyssynchrony and cardiac resynchronization therapy. American Journal of Physiology - Heart and Circulatory Physiology, 300 (3). ISSN 0363-6135

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Abstract

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 ± 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), and reduced SV, stroke work (SW), and dP/dtmax compared with RA (21 ± 5 vs. 17 ± 5 ml, 252 ± 61 vs. 151 ± 64 mJ, and 2,063 ± 456 vs. 1,603 ± 424 mmHg/s, respectively, P < 0.05). CRTa improved torsion, SV, SW, and dP/dtmax compared with RV pacing (7.7 ± 4.7°, 23 ± 3 ml, 240 ± 50 mJ, and 1,947 ± 647 mmHg/s, respectively, P < 0.05), whereas CRTfw did not (5.1 ± 3.6°, 18 ± 5 ml, 175 ± 48 mJ, and 1,699 ± 432 mmHg/s, respectively, P < 0.05). LV torsion changes covaried across conditions with SW (y = 0.94x+12.27, r = 0.81, P < 0.0001) and SV (y = 0.66x+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). Thus, we conclude that LV torsion is primarily altered by dyssynchrony, and CRT that restores LV performance also restores torsion. © 2011 the American Physiological Society.


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Details

Item Type: Article
Status: Published
Creators/Authors:
CreatorsEmailPitt UsernameORCID
Lamia, B
Tanabe, M
Tanaka, H
Kim, HKhyk11@pitt.eduHYK11
Gorcsan, Jgorcsan@pitt.eduGORCSAN
Pinsky, MRpinsky@pitt.eduPINSKY0000-0001-6166-700X
Date: 1 March 2011
Date Type: Publication
Journal or Publication Title: American Journal of Physiology - Heart and Circulatory Physiology
Volume: 300
Number: 3
DOI or Unique Handle: 10.1152/ajpheart.00177.2010
Schools and Programs: School of Medicine > Critical Care Medicine
Refereed: Yes
ISSN: 0363-6135
PubMed Central ID: PMC3064300
PubMed ID: 21169399
Date Deposited: 22 Mar 2012 20:53
Last Modified: 30 Jan 2020 16:55
URI: http://d-scholarship.pitt.edu/id/eprint/11362

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