TY - JOUR
T1 - A mechanism for immediate reduction in mitral regurgitation after cardiac resynchronization therapy
T2 - Insights from mechanical activation strain mapping
AU - Kanzaki, Hideaki
AU - Bazaz, Raveen
AU - Schwartzman, David
AU - Dohi, Kaoru
AU - Sade, L. Elif
AU - Gorcsan, John
N1 - Funding Information:
Dr. Gorcsan was supported in part by the National Institutes of Health award K24 HL04503-01 and American Heart Association National Grant-in-Aid no. 0050587N.
PY - 2004/10/19
Y1 - 2004/10/19
N2 - We tested the hypothesis that an immediate reduction in mitral regurgitation (MR) after cardiac resynchronization therapy (CRT) results from improved coordinated timing of the papillary muscle insertion sites, using the novel approach of mechanical activation strain mapping. Heart failure patients with left bundle branch block often benefit acutely from CRT; however, the role and mechanism of reduction of MR are unclear. Twenty-six consecutive patients undergoing CRT with at least mild MR were studied (ejection fraction 24 ± 6%; QRS duration 168 ± 30 ms). Echocardiographic Doppler and strain imaging was performed immediately before and the day after CRT, as well as in 10 normal control subjects. Mechanical activation sequence maps were constructed using longitudinal strain from 12 basal and mid-LV sites, with color codingof time-to-peak strain. Mitral regurgitation by the volumetric method consistently decreased after CRT: regurgitant volume from 40 ± 20 ml to 24 ± 17 ml and regurgitant fraction from 40 ± 12% to 25 ± 14% (both: p < 0.001 vs. baseline). Normal controls had uniform segmental time-to-peak strain, with a difference of only 12 ± 8 ms between all segments. In contrast, CRT patients at baseline had a 106 ± 74 ms time delay between papillary muscle insertion sites (p < 0.001 vs. normal). This interpapillary muscle time delay shortened after CRT to 39 ± 43 ms (p < 0.001 vs. baseline) and was significantly correlated with reductions in mitral regurgitant fraction (r = 0.77, p < 0.001). Cardiac resynchronization therapy significantly and immediately reduced MR. Improved coordinated timing of mechanical activation of papillary muscle insertion sites appears to be a mechanistic contributor to immediate MR reduction by CRT.
AB - We tested the hypothesis that an immediate reduction in mitral regurgitation (MR) after cardiac resynchronization therapy (CRT) results from improved coordinated timing of the papillary muscle insertion sites, using the novel approach of mechanical activation strain mapping. Heart failure patients with left bundle branch block often benefit acutely from CRT; however, the role and mechanism of reduction of MR are unclear. Twenty-six consecutive patients undergoing CRT with at least mild MR were studied (ejection fraction 24 ± 6%; QRS duration 168 ± 30 ms). Echocardiographic Doppler and strain imaging was performed immediately before and the day after CRT, as well as in 10 normal control subjects. Mechanical activation sequence maps were constructed using longitudinal strain from 12 basal and mid-LV sites, with color codingof time-to-peak strain. Mitral regurgitation by the volumetric method consistently decreased after CRT: regurgitant volume from 40 ± 20 ml to 24 ± 17 ml and regurgitant fraction from 40 ± 12% to 25 ± 14% (both: p < 0.001 vs. baseline). Normal controls had uniform segmental time-to-peak strain, with a difference of only 12 ± 8 ms between all segments. In contrast, CRT patients at baseline had a 106 ± 74 ms time delay between papillary muscle insertion sites (p < 0.001 vs. normal). This interpapillary muscle time delay shortened after CRT to 39 ± 43 ms (p < 0.001 vs. baseline) and was significantly correlated with reductions in mitral regurgitant fraction (r = 0.77, p < 0.001). Cardiac resynchronization therapy significantly and immediately reduced MR. Improved coordinated timing of mechanical activation of papillary muscle insertion sites appears to be a mechanistic contributor to immediate MR reduction by CRT.
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U2 - 10.1016/j.jacc.2004.07.036
DO - 10.1016/j.jacc.2004.07.036
M3 - Article
C2 - 15489094
AN - SCOPUS:5644236575
SN - 0735-1097
VL - 44
SP - 1619
EP - 1625
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 8
ER -