Background: Mitral valve (MV) elongation is a primary hypertrophic cardiomyopathy (HCM) phenotype and contributes to obstruction. The residual MV leaflet that protrudes past the coaptation point is especially susceptible to flow-drag and systolic anterior motion. Histopathological features of MVs in obstructive hypertrophic cardiomyopathy (OHCM), and of residual leaflets specifically, are unknown. Objectives: The purpose of this study was to characterize gross, structural, and cellular histopathologic features of MV residual leaflets in OHCM. On a cellular-level, we assessed for developmental dysregulation of epicardium-derived cell (EPDC) differentiation, adaptive endocardial-to-mesenchymal transition and valvular interstitial cell proliferation, and genetically-driven persistence of cardiomyocytes in the valve. Conclusions: MV residual leaflets in HCM were characterized by histologic findings that were likely secondary to chronic hemodynamic stress and may further increase susceptibility to systolic anterior motion.
Histopathology of the Mitral Valve Residual Leaflet in Obstructive Hypertrophic Cardiomyopathy / Troy A.L., Narula N., Massera D., Adlestein E., Castro Alvarez I., Janssen P.M.L., Moreira A.L., Olivotto I., Stepanovic A., Thomas K., Zeck B., Chiriboga L., Swistel D.G., Sherrid M.V.. - In: JACC. ADVANCES. - ISSN 2772-963X. - ELETTRONICO. - 2:(2023), pp. 100308.0-100308.0. [10.1016/j.jacadv.2023.100308]
Histopathology of the Mitral Valve Residual Leaflet in Obstructive Hypertrophic Cardiomyopathy
Olivotto I.;
2023
Abstract
Background: Mitral valve (MV) elongation is a primary hypertrophic cardiomyopathy (HCM) phenotype and contributes to obstruction. The residual MV leaflet that protrudes past the coaptation point is especially susceptible to flow-drag and systolic anterior motion. Histopathological features of MVs in obstructive hypertrophic cardiomyopathy (OHCM), and of residual leaflets specifically, are unknown. Objectives: The purpose of this study was to characterize gross, structural, and cellular histopathologic features of MV residual leaflets in OHCM. On a cellular-level, we assessed for developmental dysregulation of epicardium-derived cell (EPDC) differentiation, adaptive endocardial-to-mesenchymal transition and valvular interstitial cell proliferation, and genetically-driven persistence of cardiomyocytes in the valve. Conclusions: MV residual leaflets in HCM were characterized by histologic findings that were likely secondary to chronic hemodynamic stress and may further increase susceptibility to systolic anterior motion.
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