Assessment of left atrial-left ventricular-arterial coupling using 2-dimensional speckle tracking echocardiography.

by 2D-STE, and investigated the effect of cardiovascular risk factors on LA-LV-arterial coupling.1 In their multivariate linear regression analysis, peak early diastolic LV longitudinal strain rate (SR-LVe) and E/e’/S-LAs were independent predictors related to abdominal aortic stiffness in patients with cardiovascular risk factors. On the other hand, only age contributed to abdominal aortic stiffness in the control subjects. The authors state that the subendocardial LA and LV layers in the longitudinal direction, and the intima and media of large artery are simultaneously impaired by cardiovascular risk factors in subclinical patients. In addition, they also state that LA and LV myocardial fibrosis and medial degeneration of the abdominal aorta might be important mechanisms of impaired LA-LV-arterial coupling.1 For the detection of myocardial fibrosis, cardiac magnetic resonance imaging (MRI) is the reference method. Late gadolinium-enhanced MRI (LGE-MRI) can detect small subendocardial infarction with high spatial resolution compared with myocardial single-photon-emission computed tomography (SPECT).13 There are some comparative studies of strain measurement by 2D-STE and cardiac MRI. As for the evaluation of LV myocardial scar, LV myocardial strain evaluation by 2D-STE can detect segments with myocardial infarction, and global LV strain is closely associated with infarct size on LGEMRI.14 In regard to the assessment of myocardial fibrosis in the LA, Oakes et al reported a method that uses LGE-MRI for assessing LA wall enhancement, which is presumed to be fibrosis.15 They also showed that LA wall fibrosis on LGE-MRI is inversely related to LA strain and the strain rate measured by 2D-STE. As cardiac MRI is useful for tissue characterization, a comparative study with cardiac MRI might be of value to investigate whether or not the fibrotic process is associated with abnormal LA-LV-Ao coupling. In addition, as the current authors point out, further interventional study is required to clarify whether angiotensin II receptor blockers and statin treatment have a beneficial effect for patients with abnormal LALV-arterial coupling.