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Abstract
Objective To investigate the prognostic value of left atrial volume index (LAVI) in patients with moderate to severe aortic regurgitation (AR) and bicuspid aortic valve (BAV).
Methods 554 individuals (45 (IQR 33–57) years, 80% male) with BAV and moderate or severe AR were selected from an international, multicentre registry. The association between LAVI and the combined endpoint of all-cause mortality or aortic valve surgery was investigated with Cox proportional hazard regression analyses.
Results Dilated LAVI was observed in 181 (32.7%) patients. The mean indexed aortic annulus, sinus of Valsalva, sinotubular junction and ascending aorta diameters were 13.0±2.0 mm/m2, 19.4±3.7 mm/m2, 16.5±3.8 mm/m2 and 20.4±4.5 mm/m2, respectively. After a median follow-up of 23 (4–82) months, 272 patients underwent aortic valve surgery (89%) or died (11%). When compared with patients with normal LAVI (<35 mL/m2), those with a dilated LAVI (≥35 mL/m2) had significantly higher rates of aortic valve surgery or mortality (43% and 60% vs 23% and 36%, at 1 and 5 years of follow-up, respectively, p<0.001). Dilated LAVI was independently associated with reduced event-free survival (HR=1.450, 95% CI 1.085 to 1.938, p=0.012) after adjustment for LV ejection fraction, aortic root diameter, LV end-diastolic diameter and LV end-systolic diameter.
Conclusions In this large, multicentre registry of patients with BAV and moderate to severe AR, left atrial dilation was independently associated with reduced event-free survival. The role of this parameter for the risk stratification of individuals with significant AR merits further investigation.
- aortic regurgitation
- bicuspid aortic valve
- aortic valve insufficiency
- echocardiography
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Footnotes
Twitter @bogdan_popescu1, @PPibarot
Contributors All authors contributed to the conception and the design of the study. SCB, FF and VD analysed the data; all authors contributed to interpretation of the data. Drafting of the manuscript was done by SCB, FF and VD; the manuscript was critically revised by all authors. In addition, all authors gave final approval and agreed to be accountable for all aspects of the work ensuring integrity and accuracy.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests The Department of Cardiology of the Leiden University Medical Center received research grants from Abbott Vascular, Bayer, Bioventrix, Medtronic, Biotronik, Boston Scientific, GE Healthcare and Edwards Lifesciences. JJB and NAM received speaking fees from Abbott Vascular. VD received speaker fees from Abbott Vascular, Medtronic, Edwards Lifesciences, MSD and GE Healthcare. PP received funding from Edwards Lifesciences and Medtronic for echocardiography core lab analyses with no personal compensation. The remaining authors have nothing to disclose.
Provenance and peer review Not commissioned; externally peer reviewed.
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