New insights into mitral heart valve prolapse after chordae rupture through fluid–structure interaction computational modeling

• Type of Material: Article
• Authors: Andres Caballero, Emory University; Wenbin Mao, Emory University; Raymond McKay, Hartford Hospital; Charles Primiano, Hartford Hospital; Sabet Hashim, Emory University; Wei Sun, Emory University
• Language: English
• Date: 2018-11-23
• Publisher: Nature Research (part of Springer Nature): Fully open access journals
• Publication Version: Final Published Version
• Copyright Statement: Copyright © The Author(s) 2018
• License: Creative Commons Attribution 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1038/s41598-018-35555-5
• Title of Journal or Parent Work: Scientific Reports
• ISSN: 2045-2322
• Volume: 8
• Start Page: 17306
• End Page: 17306
• Grant/Funding Information: Andrés Caballero is in part supported by a Fulbright-Colciencias Fellowship.; This work was supported in part by the NIH HL104080 and HL127570 grants.; Wenbin Mao is in part supported by an American Heart Association Post-doctoral Fellowship 15POST25910002.
• Keywords: biomedical engineering; translational research; valvular disease
• Research Categories: Health Sciences, Medicine and Surgery; Engineering, Biomedical

Abstract

Mitral valve (MV) dynamics depends on a force balance across the mitral leaflets, the chordae tendineae, the mitral annulus, the papillary muscles and the adjacent ventricular wall. Chordae rupture disrupts the link between the MV and the left ventricle (LV), causing mitral regurgitation (MR), the most common valvular disease. In this study, a fluid-structure interaction (FSI) modeling framework is implemented to investigate the impact of chordae rupture on the left heart (LH) dynamics and severity of MR. A control and seven chordae rupture LH models were developed to simulate a pathological process in which minimal chordae rupture precedes more extensive chordae rupture. Different non-eccentric and eccentric regurgitant jets were identified during systole. Cardiac efficiency was evaluated by the ratio of external stroke work. MV structural results showed that basal/strut chordae were the major load-bearing chordae. An increased number of ruptured chordae resulted in reduced basal/strut tension, but increased marginal/intermediate load. Chordae rupture in a specific scallop did not necessarily involve an increase in the stress of the entire prolapsed leaflet. This work represents a further step towards patient-specific modeling of pathological LH dynamics, and has the potential to improve our understanding of the biomechanical mechanisms and treatment of primary MR.