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European Journal of Heart Failure 2009 11(9):863-871; doi:10.1093/eurjhf/hfp107
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Septal rebound stretch reflects the functional substrate to cardiac resynchronization therapy and predicts volumetric and neurohormonal response

Bart W.L. De Boeck1,*, Arco J. Teske1, Mathias Meine1, Geert E. Leenders1, Maarten J. Cramer1, Frits W. Prinzen2 and Pieter A. Doevendans1

1 Department of Cardiology, University Medical Centre Utrecht, Heidelberglaan 100 3584 CX, Utrecht, The Netherlands
2 Department of Physiology, University of Maastricht, Maastricht, The Netherlands

* Corresponding author. Tel: +31 88 755 6176, Fax: +31 30 251 6396, Email: b.w.l.deboeck{at}umcutrecht.nl


   Abstract

Aims: To develop a novel myocardial deformation index that is highly sensitive to the effect of cardiac resynchronization therapy (CRT) and that can be used to predict response to CRT.

Methods and results: Before and 6.5 ± 2.3 months after implantation of a CRT device, longitudinal shortening and stretch were timed and quantified by speckle tracking echocardiography in a cohort of 62 patients. Distinction was made between systolic total stretch (STS; all systolic stretch) and systolic rebound stretch (SRS; only systolic stretch following initial shortening). Systolic total stretch and SRS could be measured in all wall segments in 41 of 62 patients. Septal SRS quantification was possible in all 62 patients and was performed by a blinded observer. Cardiac resynchronization therapy reduced STS (–55 ± 30%) but reduced SRS (–77 ± 21%) significantly more (P < 0.01). The largest amount of baseline SRS and the largest reductions in SRS (–90 ± 22%) were found in the septum. Reductions in local SRS were paralleled by increases in local systolic shortening that were twice as large (r = 0.79), thereby strongly improving septal function. Baseline values of septal SRS correlated with reductions in left ventricular end-systolic volume index ({Delta}LVESVi; r = 0.62) and brain-type natriuretic peptide (BNP) ({Delta}log10BNP; r = 0.57). Septal SRS was an independent predictor of CRT response in linear regression analysis and predicted {Delta}LVESVi of ≥15% with a sensitivity and specificity of 81% at ROC analysis (areas under the curve 0.89 ± 0.04).

Conclusion: Septal rebound stretch appears to be a sensitive and practical diagnostic criterion to quantify the functional substrate amenable to CRT and to predict response.

Key Words: Heart failure • Resynchronization therapy • Physiology • Echocardiography • Remodelling

Received June 18, 2009; Accepted July 8, 2009


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