Image-based, whole-system hemodynamic modeling of mitral regurgitation and its impact on the right ventricular function

TL;DR

This study uses 3D and 0D models to explore how mitral regurgitation affects right ventricular function and cardiovascular hemodynamics.

Contribution

A novel integration of 3D left heart and 0D whole-system models to analyze mitral regurgitation's impact on the right ventricle.

Findings

Progressive mitral regurgitation increases right ventricular afterload and risks dysfunction despite preserved contractility.

Left-heart metrics and MR severity indices do not fully reflect right ventricular impairment.

Direct assessment of right ventricular structure and function is crucial for evaluating mitral regurgitation risk.

Abstract

Mitral regurgitation (MR) is a common valvular disease associated with complications such as pulmonary hypertension, atrial fibrillation, and heart failure. However, its full impact on the cardiovascular system, especially on right heart function, is not yet fully understood. Understanding this relationship is important because the right ventricle (RV) is critical for maintaining cardiovascular function. Dysfunction of the RV, which may be contributed by conditions like MR, is strongly associated with poor clinical outcomes. Despite its importance, comprehensively studying MR's effect on the RV has been challenging due to the complex, interdependent nature of cardiovascular dynamics, limited patient data, and the difficulty in synthesizing disparate information to clarify the left heart-right heart connection.

The primary goal of this study is to investigate the effects of MR on cardiovascular hemodynamics and RV function by integrating 3D models of the left heart with a closed-loop 0D models of the entire cardiovascular system. We further conduct detailed analyses using patient-specific models to explore how various system modifications impact the RV, providing insights into the nuanced effects of MR on the right heart.

This analysis provides several clinically relevant insights. First, progressive MR markedly increases RV afterload and predisposes the RV to dysfunction, even when intrinsic RV contractility is preserved or enhanced. Second, MR-specific severity indices and left-heart metrics alone fail to capture the true burden on the right heart; RV impairment can progress despite stable or only modestly changing MR descriptors. Finally, these findings highlight the need to incorporate direct assessment of RV structure and function into the evaluation of MR, as RV vulnerability plays a critical role in determining patient risk and guiding management decisions.

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