Left ventricular contraction-relaxation coupling in normal, hypertrophic, and failing myocardium quantified by speckle-tracking global strain and strain rate imaging.

OBJECTIVE

The aim of this study was to noninvasively quantify global left ventricular (LV) contraction and relaxation, and to investigate their relationship in normal, hypertrophic, and failing myocardium.

METHODS

Fifty patients with hypertensive LV hypertrophy (LVH) (LVH group), 50 patients with dilated cardiomyopathy (DCM) (DCM group), and 50 normal subjects (control group) had echocardiographic evaluations. Global LV peak systolic strain (PSS) and peak relaxation rate (PRR) during early diastole were analyzed by speckle-tracking strain and strain rate imaging in the longitudinal and circumferential directions.

RESULTS

Both global PSS and PRR were reduced in the LVH group in the longitudinal direction. In the circumferential direction, global PSS was maintained and global PRR was reduced in the LVH group. The reductions in both global PSS and PRR were more pronounced in both directions in the DCM group compared with the other 2 groups. Global PSS correlated strongest with global PRR among the clinical and echocardiographic variables, which exhibited the best fit with exponential regressions in both the longitudinal and circumferential directions in all subjects (longitudinal: y=0.15e(-0.10x), r2=0.75; circumferential: y=0.21e(-0.09x), r2=0.76, P<.01, respectively). Multiple regression analysis indicated that global PSS was the most powerful determinant of global PRR in both longitudinal and circumferential directions.

CONCLUSION

Global LV function quantified using speckle-tracking echocardiography revealed strong coupling of LV contraction to relaxation sequentially from normal to failing myocardium, regardless of their heterogeneous pathophysiology. In addition, the extent of myocardial systolic shortening was the most powerful independent contributor of LV relaxation in both the longitudinal and circumferential directions. These results strongly indicate that LV myocardial systolic contraction directly regulates its relaxation.