• Wieneke Vlastra, Thomas P W van den Boogert, Thomas Krommenhoek, BronzwaerAnne-Sophie G TAGTDepartment of Internal Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands.Laboratory for Clinical Cardiovascular Physiology, Center for Heart Failure Research, Academic Medical Center, University of Ams, Henk J M M Mutsaerts, Hakim C Achterberg, Esther E Bron, Wiro J Niessen, MajoieCharles B L MCBLMDepartment of Radiology and Nuclear Medicine, Amsterdam University Medical Centers, Location AMC and VUmc, University of Amsterdam, Amsterdam, The Netherlands., Aart J Nederveen, Jan Baan, Johannes J van Lieshout, Jan J Piek, R Nils Planken, HenriquesJosé P SJPSDepartment of Clinical and Experimental Cardiology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam, Heart Center, Amsterdam, The Netherlands., and Ronak Delewi.
• Department of Clinical and Experimental Cardiology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam, Heart Center, Amsterdam, The Netherlands.
• Int J Cardiovasc Imaging. 2019 Nov 1; 35 (11): 2123-2133.

AbstractChronic silent brain infarctions, detected as new white matter hyperintensities on magnetic resonance imaging (MRI) following transcatheter aortic valve implantation (TAVI), are associated with long-term cognitive deterioration. This is the first study to investigate to which extent the calcification volume of the native aortic valve (AV) measured with cardiac computed tomography angiography (CTA) predicts the increase in chronic white matter hyperintensity volume after TAVI. A total of 36 patients (79 ± 5 years, median EuroSCORE II 1.9%, Q1-Q3 1.5-3.4%) with severe AV stenosis underwent fluid attenuation inversion recovery (FLAIR) MRI < 24 h prior to TAVI and at 3 months follow-up for assessment of cerebral white matter hyperintensity volume (mL). Calcification volumes (mm3) of the AV, aortic arch, landing zone and left ventricle were measured on the CTA pre-TAVI. The largest calcification volumes were found in the AV (median 692 mm3) and aortic arch (median 633 mm3), with a large variation between patients (Q1-Q3 482-1297 mm3 and 213-1727 mm3, respectively). The white matter hyperintensity volume increased in 72% of the patients. In these patients the median volume increase was of 1.1 mL (Q1-Q3 0.3-4.6 mL), corresponding with a 27% increase from baseline (Q1-Q3 7-104%). The calcification volume in the AV predicted the increase of white matter hyperintensity volume (Δ%), with a 35% increase of white matter hyperintensity volume, per 100 mm3 of AV calcification volume (SE 8.5, p < 0.001). The calcification volumes in the aortic arch, landing zone and left ventricle were not associated with the increase in white matter hyperintensity volume. In 72% of the patients new chronic white matter hyperintensities developed 3 months after TAVI, with a median increase of 27%. A higher calcification volume in the AV was associated with a larger increase in the white matter hyperintensity volume. These findings show the potential for automated AV calcium screening as an imaging biomarker to predict chronic silent brain infarctions.

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