TY - JOUR
T1 - Usefulness of Three-Dimensional Speckle Tracking Strain to Quantify Dyssynchrony and the Site of Latest Mechanical Activation
AU - Tanaka, Hidekazu
AU - Hara, Hideyuki
AU - Saba, Samir
AU - Gorcsan, John
N1 - Funding Information:
The authors are grateful for the support of the entire staff of the echocardiography and electrophysiology laboratories of the University of Pittsburgh Presbyterian University Hospital, Pittsburgh, Pennsylvania.
PY - 2010/1/15
Y1 - 2010/1/15
N2 - Previous methods to quantify dyssynchrony could not determine regional 3-dimensional (3-D) strain. We hypothesized that a novel 3-D speckle tracking strain imaging system can quantify left ventricular (LV) dyssynchrony and site of latest mechanical activation. We studied 64 subjects; 54 patients with heart failure were referred for cardiac resynchronization therapy (CRT) with an ejection fraction 25 ± 6% and QRS interval 165 ± 29 ms and 10 healthy volunteer controls. The 3-D speckle tracking system determined radial strain using a 16-segment model from a pyramidal 3-D dataset. Dyssynchrony was quantified as maximal opposing wall delay and SD in time to peak strain. The 3-D analysis was compared to standard 2-dimensional (2-D) strain datasets and site of 3-D latest mechanical activation, not possible by 2D was quantified. As expected, dyssynchrony in patients on CRT was significantly greater than in controls (maximal opposing wall delay 316 ± 112 vs 59 ± 12 ms and SD 124 ± 48 vs 28 ± 11 ms, p <0.001 vs normal). The 3-D opposing wall delay was closely correlated with 3-D 16-segment SD (r = 0.95) and 2-D mid-LV strain (r = 0.83) and SD (r = 0.85, all p values <0.001). The 3-D site of the latest mechanical activation was most commonly midposterior (26%), basal posterior (22%), midlateral (20%), and basal lateral (17%). Eleven patients studied after CRT demonstrated improvements in 3-D synchrony (300 ± 124 to 94 ± 37 ms) and ejection fraction (24 ± 6% to 31 ± 7%, p <0.05). In conclusion, 3-D speckle tracking can successfully quantify 3-D dyssynchrony and site the latest mechanical activation. This approach may play a clinical role in management of patients on CRT.
AB - Previous methods to quantify dyssynchrony could not determine regional 3-dimensional (3-D) strain. We hypothesized that a novel 3-D speckle tracking strain imaging system can quantify left ventricular (LV) dyssynchrony and site of latest mechanical activation. We studied 64 subjects; 54 patients with heart failure were referred for cardiac resynchronization therapy (CRT) with an ejection fraction 25 ± 6% and QRS interval 165 ± 29 ms and 10 healthy volunteer controls. The 3-D speckle tracking system determined radial strain using a 16-segment model from a pyramidal 3-D dataset. Dyssynchrony was quantified as maximal opposing wall delay and SD in time to peak strain. The 3-D analysis was compared to standard 2-dimensional (2-D) strain datasets and site of 3-D latest mechanical activation, not possible by 2D was quantified. As expected, dyssynchrony in patients on CRT was significantly greater than in controls (maximal opposing wall delay 316 ± 112 vs 59 ± 12 ms and SD 124 ± 48 vs 28 ± 11 ms, p <0.001 vs normal). The 3-D opposing wall delay was closely correlated with 3-D 16-segment SD (r = 0.95) and 2-D mid-LV strain (r = 0.83) and SD (r = 0.85, all p values <0.001). The 3-D site of the latest mechanical activation was most commonly midposterior (26%), basal posterior (22%), midlateral (20%), and basal lateral (17%). Eleven patients studied after CRT demonstrated improvements in 3-D synchrony (300 ± 124 to 94 ± 37 ms) and ejection fraction (24 ± 6% to 31 ± 7%, p <0.05). In conclusion, 3-D speckle tracking can successfully quantify 3-D dyssynchrony and site the latest mechanical activation. This approach may play a clinical role in management of patients on CRT.
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U2 - 10.1016/j.amjcard.2009.09.010
DO - 10.1016/j.amjcard.2009.09.010
M3 - Article
C2 - 20102925
AN - SCOPUS:73149108250
SN - 0002-9149
VL - 105
SP - 235
EP - 242
JO - American Journal of Cardiology
JF - American Journal of Cardiology
IS - 2
ER -