Impact of severe aortic stenosis on layer-specific longitudinal strain and its prognostic value

European Heart Journal(2019)

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摘要
Abstract Background Global longitudinal strain (GLS) was used to detect early myocardial dysfunction in patients with aortic stenosis (AS), however few data are currently available on the different susceptibility of specific myocardial layer to increased wall stress and its prognostic role. The present study sought to investigate the relationship between changes in LV multilayer strain and the clinical outcome of patients with severe AS and preserved left ventricle ejection fraction (LVEF). Methods We included in the analysis 211 patients (56% males, mean age 73±12 years old) with severe AS and LVEF≥50%, divided in symptomatic (n=114) and asymptomatic group (n=97), and 50 controls matched for age and sex. Patients with moderate-to-severe concomitant valvulopathy and inadequate acoustic windows for evaluation by speckle tracking analysis were excluded. Clinical, demographic and resting echocardiographic data were recorded, including quantification of 2D GLS, subendocardial LS and subepicardial LS. Results Symptomatic patients had increased LV wall thickness and LV mass index than asymptomatic ones (p<0.001), higher transaortic mean pressure gradients (48±14 vs 44±13 mmHg, p=0.004), and lower aortic valve areas (0.42±0.09 vs 0.45±0.08 cm2/m2, p<0.017). GLS was significantly lower in patients with AS compared to controls, especially in symptomatic group (17.9±3.4 vs 19.1±3.1 vs 20.7±2.1%, p<0.001 in symptomatic, asymptomatic and control groups respectively) suggesting an early, subtle, myocardial dysfunction. In particular, the analysis of layer-specific myocardial deformation revealed a marked difference in both the subendocardial LS (20.1±4.9 vs 21.7±4.2 vs 23.4±2.5%, p<0.001) and subepicardial LS (15.8±3.1 vs 16.8±2.8 vs 18.3±1.8%, p<0.001). At multivariable logistic regression analysis, subendocardial LS was independently associated to symptoms (OR=1.148, p=0.014), together with indexed left atrial volume (OR=1.035, p=0.007) and LV concentric remodelling (OR=2.429, p=0.031). During a mean follow up of 38 months (IQ range 18–60 months), 12 patients with asymptomatic severe AS had a cardiovascular (CV) death. The presence of a subendocardial LS <22% at baseline was associated with a higher rate of CV events at 3 and 5-year follow-up (19% vs 5% at 3-year follow-up, and 22% vs 8% at 5-year follow-up, respectively; log-rank p=0.044). Conclusion In patients with severe AS, LS impairment involves all myocardial layers and is more prominent in the advanced phases of the disease. In this setting, the subendocardial LS appears to be independently associated to symptoms than subepicardial LS. In asymptomatic patients, a reduced value of subendocardial LS is associated with higher CV mortality at 3- and 5-year follow-up.
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