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European Heart Journal Advance Access published online on November 11, 2008
European Heart Journal, doi:10.1093/eurheartj/ehn481
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Toward understanding response to cardiac resynchronization therapy: left ventricular dyssynchrony is only one of multiple mechanisms

Chirine Parsai1,*, Bart Bijnens1,2,3, George Ross Sutherland1, Aigul Baltabaeva1, Piet Claus2, Maciej Marciniak1, Vince Paul1, Mike Scheffer4, Erwan Donal5, Geneviève Derumeaux6 and Lisa Anderson1

1 Department of Cardiology, St George’s Hospital, Blackshaw Road, SW17 0QT London, UK
2 ICREA, Universitat Pompeu Fabra (CISTIB), Barcelona, Spain
3 University of Leuven, Belgium
4 Medical Centre Rijnmond South, Rotterdam, The Netherlands
5 Hopital Pontchaillou, Rennes, France
6 Hopital Louis Pradel, Lyon, France

Received 16 April 2008; revised 2 September 2008; accepted 2 October 2008.

* Corresponding author. Tel: +44 2087251397, Fax: +44 2087254402, Email: chirineparsai{at}hotmail.com

Aim: To date, most published echocardiographic methods have assessed left ventricular (LV) dyssynchrony (DYS) alone as a predictor for response to cardiac resynchronization therapy (CRT). We hypothesized that the response is instead dictated by multiple correctable factors.

Methods and results: A total of 161 patients (66 ± 10 years, EF 24 ± 6%, QRS > 120 ms) were investigated pre- and post-CRT (median of 6 months). Reduction in NYHA Class ≥1 or LV reverse remodelling (end-systolic volume reduction ≥ 10%) defined response. Four different pathological mechanisms were identified. Group1: LVDYS characterized by a pre-ejection septal flash (SF) (87 patients, 54%). Elimination of SF (77 of 87 patients) resulted in reverse remodelling in 100%. Group 2: short-AV delay (21 patients, 13%) resolution (19 of 21 patients) resulted in reverse remodelling in 16 of 19. Group 3: long-AV delay (16 patients, 10%) resolution (14 of 16 patients) resulted in NYHA Class reduction ≥1 in 11 with reverse remodelling in five patients. Group 4: exaggerated LV–RV interaction (15 patients, 9%) reduced post-CRT. All responded clinically with fall in pulmonary artery pressure (P = 0.003) but did not volume respond. Group 5: patients with none of the above correctable mechanisms (22 patients, 14%). None responded to CRT.

Conclusion: CRT response is dictated by correction of multiple independent mechanisms of which LVDYS is only one. Long-axis DYS measurements alone failed to detect 40% of responders.

Key Words: Echocardiography • Heart failure • Cardiac resynchronization therapy

This paper was guest edited by Professor Martin J. Schalij, Leiden University Medical Center, Department of Cardiology, Albinusdreef 2, C5-P, 2300 RC, Leiden, The Netherlands.


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