LAYER-SPECIFIC STRAIN RESPONSE FOLLOWING ACUTE PRESSURE UNLOADING IN SEVERE AORTIC STENOSIS

Abstract

The left ventricular (LV) wall is composed of endocardial, mid-myocardial, and epicardial layer and each myocardial layer have different vulnerability to ischemia and pressure overload. However, the effects of pressure unloading after transcatheter aortic valve replacement (TAVR) or aortic valve replacement (AVR) on the mechanics of three myocardial layers are largely unknown in patient with severe aortic stenosis (AS). The present study evaluated change in LV biomechanics, layer-by-layer, following acute pressure unloading in patients with severe AS. In twenty-eight consecutive patients with severe AS who underwent TAVR, LV peak global longitudinal and circumferential strains of the endocardial, mid-myocardial and epicardial layers were evaluated using multilayer speckle tracking echocardiography before, one week after, one month and one year after TAVR. The LV multilayer strains of thirty-three patients with severe AS who underwent AVR and performed echocardiography at one year after AVR were also evaluated retrospectively. Longitudinal and circumferential strains were significantly highest in the endocardial layer and lowest in the epicardial layer at baseline. At one month following TAVR, longitudinal strain significantly improved in all layers compared with the baseline (endocardium (%) -16.7 ± 3.8 vs. -18.6 ± 3.3, P = 0.01; mid-myocardium -14.4 ± 3.2 vs. -16.2 ± 3.5, P < 0.01; epicardium -12.4 ± 2.8 vs. -13.6 ± 2.6, P = 0.01), whereas LV ejection fraction and circumferential strain remained unchanged. Importantly, only those with LV hypertrophy (LVH) (n =19) demonstrated improved longitudinal strain than without LVH (n=9) (Figure 1). The improvement in longitudinal strain was more prominent in the endocardial layer, which was evident even at an early time point (1 week) after TAVR. At one year following TAVR, longitudinal strain also significantly improved in all layers compared with the baseline, particularly in patient with LVH. Interestingly, at one year following AVR, longitudinal strain revealed significant improvement in all layers only in patient with LVH. LV longitudinal strain significantly improved in all three layers following acute pressure unloading, which was most prominent in patients with the greatest degree of LVH. The earliest improvements after relief of LV pressure overload following the procedure was observed in the endocardial layer. Evaluation of multilayer strain may provide new insights into the pathophysiology of pressure unloading in aortic stenosis as well as in LV mechanics in the future.