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Updated: May 12, 2026
Transthoracic Speckle Tracking Echocardiography for the Quantitative Assessment of Left Ventricular Myocardial Deformation
Published on: October 20, 2016
Ventricular function and dyssynchrony quantified by speckle-tracking echocardiography in patients with acute and
Kazuhide Ichikawa1, Kaoru Dohi, Emiyo Sugiura
1Department of Cardiology and Nephrology, Mie University Graduate School of Medicine, Tsu, Japan.
Background:
The aim of this study was to noninvasively investigate right ventricular and left ventricular (LV) adaptation to right ventricular pressure overload in patients with acute pulmonary thromboembolism (APTE) and chronic pulmonary artery hypertension (CPAH).
Methods:
Thirty-seven patients with APTE, 36 patients with CPAH, and 33 controls were retrospectively enrolled. Myocardial deformation and wall motion were analyzed using speckle-tracking strain and displacement imaging echocardiography in the right and left ventricles. The standard deviation of the heart rate-corrected intervals from QRS onset to peak systolic strain and peak systolic displacement (PSD) for the six segments was used to quantify right ventricular and LV mechanical dyssynchrony (peak systolic strain dyssynchrony and PSD dyssynchrony). The myocardial performance index in both ventricles was also evaluated.
Results:
The APTE and CPAH groups had reduced ventricular performance (LV myocardial performance index, 0.40 ± 0.10, 0.66 ± 0.18 [P < .05 vs controls], and 0.58 ± 0.19 [P < .05 vs controls] in the control, APTE, and CPAH groups, respectively) and large mechanical dyssynchrony (LV longitudinal PSD dyssynchrony, 58 ± 41 msec, 119 ± 49 msec [P < .05 vs controls], and 83 ± 37 msec [P < .05 vs controls and the APTE group] in the control, APTE, and CPAH groups, respectively) in both ventricles. Multiple regression analysis indicated that LV longitudinal PSD dyssynchrony in the APTE group and the LV eccentricity index in the CPAH group were independent determinants of LV myocardial performance index.
Conclusions:
Pathophysiologic mechanisms that regulate ventricular performance vary depending on whether the ventricles are exposed to acute or chronic right ventricular pressure overload.
