Abstract
Aim of the present study was to describe the left ventricular longitudinal strain (LS) in all myocardial layers in patients with severe aortic stenosis (AS), preserved left ventricular ejection fraction (LVEF) in different LV geometry and to compare LS analysis before and early after acute LV unloading provided by transcatheter aortic valve implantation (TAVI). 68 patients were enrolled. LS was measured from the endocardial layer (Endo-LS), epicardial layer (Epi-LS) and full thickness of myocardium (Transmural-LS) before and after TAVI. Patients were divided in two groups accordingly with relative wall thickness (RWT): concentric LV hypertrophy (cLVH) vs eccentric LV hypertrophy (eLVH). Less impaired values of LS at baseline were observed, in all layers, in patients with cLVHas compared to patients with eLVH (Endo-LS was − 13.2 ± 2 vs − 11.1±3 %, p = 0.041; Epi-LS was − 11.8 ± 1.8 vs − 9.9 ± 3 %, p = 0.043; Transmural-LS was − 12.3 ± 1.8 vs − 10.49 ± 3.3 %, p = 0.02, respectively). A significant improvement in endocardial LS (Endo-LS) after TAVI was detected only in cLVH(− 13 ± 2 vs − 14 ± 2, p = 0.011). Our findings documented that concentric LVH had better basal strain function and showed a better myocardial recovery after TAVI compared to eLVH.
Highlights
In patients with aortic stenosis (AS), left ventricular hypertrophy (LVH) is considered to be an adaptive response to the increased afterload [1, 2]
Analysis included the collection of clinical characteristics and 2D/3D echocardiographic features, such as LV volumes indexed for body surface area (BSA), and ejection fraction (LVEF), LV mass, LV diastolic function, right ventricular (RV) dimension and function and RV-longitudinal strain (LS)
Patients were divided in two groups, to relative wall thickness (RWT) measurement. concentric LV hypertrophy (cLVH) was more represented than eccentric LV hypertrophy (eLVH) in our study population (46 patients, 68%, vs. 22 patients, 32%)
Summary
In patients with aortic stenosis (AS), left ventricular hypertrophy (LVH) is considered to be an adaptive response to the increased afterload [1, 2]. LVH reduces systolic wall stress and helps to preserve LV ejection fraction (LVEF), but it may lead to some long term adverse consequences such as myocardial fibrosis, diastolic filling impairment and LV dysfunction [3]. Different types of LVH have been previously described. Gaasch and Zile [4], identified four groups of LV geometry, based on the estimation of LV mass and LV relative wall thickness (RWT). Multilayer strain analysis in AS revealed that LS may be impaired in all myocardial layers (sub-endocardial, sub-epicardial and transmural), independently from LV shape [9]. Acute myocardial contractility response after afterload removal in different LV geometry has been not exhaustively described
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