TRICUSPID AND MITRAL REGURGITATION Mitral Annular Elasticity Determines Severity of Regurgitation in Barlow’s Mitral Valve Disease Karl-Andreas Dumont, MD, PhD, Hans Martin Dahl Aguilera, MSc, Robert Persson, MD, Victorien Prot, MSc, PhD, John-Peder Escobar Kvitting, MD, PhD, and Stig Urheim, MD, PhD, Oslo, Trondheim, and Bergen, Norway Objectives: Barlow’s mitral valve disease with late systolic mitral regurgitation provides diagnostic and thera- peutic challenges. The mechanisms of the regurgitation are still unclear. We hypothesized that the onset and the severity of late systolic regurgitation are determined by annulus dynamics and the mechanical stresses imposed by the left ventricle. Methods: Ten patients with Barlow’s mitral valve disease and mitral annulus disjunction (MAD) were compared with 10 healthy controls. Resting blood pressure was measured, and transthoracic three-dimensional echo- cardiography was analyzed using a holographic display that allows tracking and measurements of mitral annulus surface area (ASA) throughout the cardiac cycle. A novel annulus elastance index (dASA/dP) was calculated between aortic valve opening and onset of mitral regurgitation. Severity of MAD was quantified as the disjunction index (mm degree). Leaflet coaptation area was calculated using a finite element model. Results: Peak systolic ASAs in controls and patients were 9.3 6 0.6 and 21.1 6 3.1 cm 2 , respectively (P < .001). In patients, the ASA increased rapidly during left ventricular ejection, and onset of mitral regurgitation coincided closely with peak upslope of annulus area change (dASA/dt). The finite element model showed a close association between rapid annulus displacement and coaptation area deficit in Barlow’s mitral valve disease. Systolic annulus elastance index (0.058 6 0.036 cm 2 /mm Hg) correlated strongly with disjunction index (r = 0.91, P < .0001). More- over, regurgitation volume showed a positive correlation with systolic blood pressure (r = 0.80, P < .01). Conclusion: The present pilot study supports the hypothesis that annulus dilatation may accentuate mitral valve regurgitation in patients with Barlow’s mitral valve disease. A novel annulus elastance index may predict the severity of mitral valve regurgitation in selected patients. (J Am Soc Echocardiogr 2022;35:1037-46.) Keywords: Barlow, Mitral annulus, Mitral regurgitation, Finite element, Disjunction Barlow’s mitral valve disease is characterized by bileaflet myxomatous thickening of the mitral valve, excessive valve tissue with billowing of the leaflets, and late systolic prolapse of diseased segments. The severely dilated annulus enlarges with flattening of the saddle-shaped configuration and subsequent mid-late systolic regurgitation. 1-4 Concomitant affection of the tricuspid valve also seems to show some specific features. 5 In the normal beating heart, important conformational changes of the mitral annulus take place in the late diastole and isovolumetric contraction phases, thus preventing flow reversal during ventricular systole. The mitral annulus conforms into a saddle shape and con- tracts like a sphincter during ventricular systole to enhance leaflet coaptation. These annulus dynamics are important for a balanced dis- tribution of the mechanical stresses imposed by the left ventricle (LV) on the mitral valve. 6-8 Annulus dynamics in functional and degenerative mitral regurgi- tation have been thoroughly studied for parameters such as saddle shape and annular dimensions. 9-13 The annulus in Barlow’s mitral valve disease, in contrast to fibroelastic deficiency and functional mitral regurgitation, is often larger and more dynamic. Furthermore, the concomitant mitral annulus disjunction (MAD) that is often found in Barlow patients exaggerates annular dysfunction. 14,15 The mechanisms of late systolic regurgitation in Barlow’s mitral valve disease, however, are still undetermined due to the complex three-dimensional (3D) dynamics of the mitral valve apparatus. From the Department of Cardiothoracic Surgery, Oslo University Hospital, Rikshospitalet (K.-A.D., J.-P.E.K.), Oslo; Department of Structural Engineering, Faculty of Engineering Science, Norwegian University of Science and Technology (H.M.D.A., V.P.), Trondheim; and Department of Heart Disease, Haukeland University Hospital and University of Bergen (R.P., S.U.), Bergen, Norway. Conflicts of Interest: None. Reprint requests: Karl-Andreas Dumont, MD, PhD, Department of Cardiothoracic Surgery, Oslo University Hospital, Rikshospitalet, Oslo, Norway (E-mail: kardum@ ous-hf.no). 0894-7317 Copyright 2022 by the American Society of Echocardiography. Published by Elsevier Inc. This is an open access article under the CC BY license (http:// creativecommons.org/licenses/by/4.0/). https://doi.org/10.1016/j.echo.2022.07.001 1037
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