Effect of cardiac resynchronization therapy on the sequence of mechanical activation assessed by two-dimensional radial strain imaging.
Cardiac resynchronization therapy (CRT) induces left ventricular (LV) reverse remodeling by synchronizing LV mechanical activation. We evaluated changes in segmental LV activation after CRT and related them to CRT response. A total of 292 patients with heart failure (65 ± 10 years, 77% men) treated with CRT underwent baseline echocardiographic assessment of LV volumes and ejection fraction. Time-to-peak radial strain was measured for 6 midventricular LV segments with speckle-tracking strain imaging. Moreover, the time difference between the peak radial strain of the anteroseptal and the posterior segments was calculated to obtain LV dyssynchrony. After 6 months, LV volumes, segmental LV mechanical activation timings, and LV dyssynchrony were reassessed. Response to CRT was defined as ≥15% decrease in LV end-systolic volume at 6-month follow-up. Responders (n = 177) showed LV resynchronization 6 months after CRT (LV dyssynchrony from 200 ± 127 to 85 ± 86 ms; p <0.001) by earlier activation of the posterior segment (from 438 ± 141 to 394 ± 132 ms; p = 0.001) and delayed activation of the anteroseptal segment (from 295 ± 155 to 407 ± 138 ms; p <0.001). In contrast, nonresponders (n = 115) experienced an increase in LV dyssynchrony 6 months after CRT (from 106 ± 86 to 155 ± 112 ms; p = 0.001) with an earlier activation of posterior wall (from 391 ± 139 to 355 ± 136 ms; p = 0.039) that did not match the delayed anteroseptal activation (from 360 ± 148 to 415 ± 122 ms; p = 0.001). In conclusion, responders to CRT showed LV resynchronization through balanced lateral and anteroseptal activations. In nonresponders, LV dyssynchrony remains, by posterior wall preactivation and noncompensatory delayed septal wall activation.
Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands; Department of Cardiology, Centre Hospitalier de l'Université de Montréal, Montréal, Québec, Canada.
Dominique
D
Auger
Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands.
Ulas
U
Hoke
Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands.
Joep
J
Thijssen
Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands.
Elena
E
Abate
Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands.
Kai-Hang
KH
Yiu
Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands.
See Hooi
SH
Ewe
Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands.
Tomasz G
TG
Witkowski
Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands.
Darryl P
DP
Leong
Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands.
Eduard R
ER
Holman
Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands.
Nina
N
Ajmone Marsan
Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands.
Martin J
MJ
Schalij
Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands.
Jeroen J
JJ
Bax
Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands. Electronic address: v.delgado@lumc.nl.
Victoria
V
Delgado
D000368:Aged; D004452:Echocardiography / Q000379:methods*; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000628:therapy*; D006352:Heart Ventricles / Q000000981:diagnostic imaging* / Q000503:physiopathology; D006801:Humans; D008297:Male; D009204:Myocardial Revascularization / Q000379:methods*; D013318:Stroke Volume; D016896:Treatment Outcome; D016277:Ventricular Function, Left / Q000502:physiology*; D020257:Ventricular Remodeling