Clinical InvestigationAortic StenosisPrognostic Value of Left Atrial Strain in Aortic Stenosis: A Competing Risk Analysis
Graphical abstract
Section snippets
Study Population
Participants were from the prospective, multicenter Singapore Assessment of Valvular Insufficiency and Obstruction Using Biomarkers (SAVIOUR) study.19 They had moderate or severe AS (peak transaortic jet velocity [Vmax] ≥ 3.0 m/sec or aortic valve area [AVA] by the continuity equation ≤ 1.2 cm2), no or minimal symptoms (New York Heart Association [NYHA] functional class I or II), LVEF ≥ 50%, and no more than moderate aortic or mitral regurgitation. Informed consent was obtained. The study
Results
Among 173 patients (age, 69 ± 11 years; 55% men; aortic Vmax, 404 ± 78 cm/sec; mean pressure gradient, 40 ± 17 mm Hg; indexed AVA, 0.56 ± 0.13 cm2/m2), median LA reservoir strain (LASr), LA conduit strain (LAScd), and LA contractile strain (LASct) were 27% (IQR, 22%-32%), 12% (IQR, 8%-15%), and 16% (IQR, 13%-18%), respectively. Baseline characteristics, echocardiographic parameters, and median biomarker levels by primary outcome are shown in Table 1. Over a median follow-up period of 2.7 years
Summary of Key Findings
We present compelling data supporting a role for LA strain in the prognostic evaluation of largely asymptomatic patients with moderate to severe AS and preserved LVEF (Graphical Abstract). In competing risk analyses, LA deformation indices consistently outperformed those of AS hemodynamics and LV myocardial response, including LV GLS, and were independent of established clinical risk factors and NT-proBNP, a widely applied guideline-endorsed biomarker,1 in predicting adverse outcomes. LAScd <
Conclusion
In largely asymptomatic patients with moderate or severe AS and preserved LVEFs, LA strain was a stronger prognosticator of adverse clinical outcomes than other key echocardiographic indices and offered additive predictive value to clinical risk markers and plasma NT-proBNP. LAScd < 6%, LASr < 20%, and LASct < 12% identified patients at higher risk for adverse outcomes.
Acknowledgments
The contributions of all clinical staff members, study coordinators, technicians, and patients who assisted with this study are duly acknowledged.
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This study was funded by the National Medical Research Council of Singapore (NMRC/CG/NUHCS/2010, NMRC/CG12Aug14, and NMRC/CGAug16C006), which was not involved in the conduct of the study.
Dr Ewe has received personal fees from Medtronic, Edwards Lifesciences, and Abbott Medical, outside the submitted work. Dr Ding has received personal and speaker fees from GE and Phillips and nonfinancial support from Phillips, outside the submitted work; Dr Richards has received grants from the National Medical Research Council (NMRC) of Singapore; is a long-term collaborator with Roche Diagnostics, the provider of assays central to this submission; and has received support in kind, grants, and speaker’s honoraria from and participated on advisory boards for Roche Diagnostics. Dr Ling has received grants from the National Medical Research Council of Singapore, during the conduct of the study.