Value of Layer-Specific Strains in Hypertrophied Myocardium of Aortic Stenosis from Comparison with Hypertrophy Cardiomyopathy

Abstract

Intrinsic myocardial mechanics may have different patterns due to different etiologies of myocardial hypertrophy. We used layer-specific strain to compare the hypertrophied myocardium between hypertrophic cardiomyopathy (HCM) and aortic stenosis (AS) individuals. We searched for the differences in strain distribution and clinical implications for these patients. Comprehensive echocardiography were performed in 3 groups of 172 consecutive patients with HCM, 129 participants with moderate to severe AS and 79 healthy controls. Left ventricular (LV) layer-specific deformation parameters were obtained by two-dimensional speckle tracking echocardiography, including longitudinal strain of both sub-endocardial and sub-epicardial myocardium. The transmural strain gradient was defined as the strain difference between sub-endocardial and sub-epicardial myocardium. We further divided AS patients into two subgroups according to the median level of transmural longitudinal strain gradient. In comparison of the layer-specific myocardial deformation parameters between the HCM and AS groups, hypertrophied myocardium from the AS group had better sub-epicardial myocaridial (¬¬-13.5±3.5% vs -11.6±3.5%, p<0.001) and sub-endocardial myocardial longitudinal strain (-18.0±4.4% vs -15.3±4.3%, p<0.001), and higher transmural longitudinal strain gradient (4.5±1.3% vs 3.6±1.2%, p<0.001). Both diseased groups had significantly reduced layer-specific longitudinal strains than the healthy controls (sub-endocardial: -21.20±3.7%, sub-epicardial: -16.7±3.0%, both p <0.001 ). The transmural longitudinal strain gradient of the AS group revealed no significant difference from the healthy controls (4.49±1.3 % vs 4.51±1.0 %, p = 0.996 ), whereas there was significant reduction from the HCM group (3.61±1.2 % vs 4.51±1.0%, p < 0.001). This transmural gradient difference still remained significant after being adjusted for global longitudinal strain, age, gender, LV mass index, and average early mitral filling velocity to early annular velocity ratio (E/E’) (p<0.001) in multivariate analysis. There were no valvular severity differences in the two AS subgroups, but the subgroup with lower transmural longitudinal gradient had significant lower LV ejection fraction (62.8 ± 12.2% vs. 70.4 ± 7.5%, p < 0.001) and higher average E/E’ (20.6 ± 10.7 vs. 15.9 ± 7, p = 0.004). Hypertrophied myocardium in AS patients not only had better longitudinal strain at sub-epicardial and sub-endocardial myocardium, but also presented with more preserved transmural longitudinal strain gradient when compared to those of the HCM group. The loss of preserving adequate transmural longitudinal strain gradient might reflect intrinsic myocardial dysfunction in AS.