Alterations in Titin Properties and Myocardial Fibrosis Correlate With Clinical Phenotypes in Hemodynamic Subgroups of Severe Aortic Stenosis

Titin-isoform expression, titin phosphorylation, and myocardial fibrosis were studied in 30 patients with severe symptomatic aortic stenosis (AS). Patients were grouped into “classical” high-gradient, normal-flow AS with preserved ejection fraction (EF); “paradoxical” low-flow, low-gradient AS with...

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Detalles Bibliográficos
Autores principales: Gotzmann, Michael, Grabbe, Susanne, Schöne, Dominik, von Frieling-Salewsky, Marion, dos Remedios, Cristobal G., Strauch, Justus, Bechtel, Matthias, Dietrich, Johannes W., Tannapfel, Andrea, Mügge, Andreas, Linke, Wolfgang A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2018
Materias:
CLINICAL RESEARCH
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6059007/
https://www.ncbi.nlm.nih.gov/pubmed/30062220
http://dx.doi.org/10.1016/j.jacbts.2018.02.002
Descripción
Sumario:Titin-isoform expression, titin phosphorylation, and myocardial fibrosis were studied in 30 patients with severe symptomatic aortic stenosis (AS). Patients were grouped into “classical” high-gradient, normal-flow AS with preserved ejection fraction (EF); “paradoxical” low-flow, low-gradient AS with preserved EF; and AS with reduced EF. Nonfailing donor hearts served as controls. AS was associated with increased fibrosis, titin-isoform switch toward compliant N2BA, and both total and site-specific titin hypophosphorylation compared with control hearts. All AS subtypes revealed titin and matrix alterations. The extent of myocardial remodeling in “paradoxical” AS was no less severe than in other AS subtypes, thus explaining the unfavorable prognosis.

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