Published in:
Open Access 01-12-2017 | Research article
Left ventricular systolic function changes in hypertrophic cardiomyopathy patients detected by the strain of different myocardium layers and longitudinal rotation
Published in: BMC Cardiovascular Disorders | Issue 1/2017
Login to get accessAbstract
Background
Impairment of left ventricular (LV) longitudinal function has an important role in hypertrophic cardiomyopathy (HCM). This research investigated an association between the longitudinal strain of different myocardial layers, longitudinal rotation and the LV systolic function of HCM patients.
Methods
The research was performed on 36 HCM patients and 36 healthy subjects. The peak systolic longitudinal strain of the subendocardial, midmyocardial, and subepicardial layers was measured using 2-dimensional speckle tracking echocardiography (2D–STE). The apical long-axis and 4- and 2- chamber views were acquired via 2D Doppler echocardiography. The curve of the longitudinal rotation was traced at 17 timepoints in the analysis of 2 cardiac cycles.
Results
Compared with healthy subjects, in HCM patients regional LV peak systolic longitudinal strain was less, not only in hypertrophied LV myocardium, but also in non-hypertrophied myocardium. The rotational degrees of the midmyocardial-septal, apex, and lateral wall of HCM patients were significantly different from that of normal subjects, as follows. In HCM patients, clockwise longitudinal rotation was found. The interventricular septum thickness at end-diastole positively correlated with the peak longitudinal systolic strain of the subendocardial, the midmyocardial, and the subepicardial layers. The area under ROC curve values for subendocardial, midmyocardial and subepicardial layers in HCM patients were 0.923, 0.938, 0.948.
Conclusion
In HCM patients, the longitudinal function was damaged, even with normal LV ejection fraction. The peak longitudinal systolic strain of the subendocardial, midmyocardial, and subepicardial layers, and the longitudinal rotation detected by 2D–STE, are very sensitive predictors of systolic function in patients with HCM.