Key result
Simulated mitral valve calcification significantly impaired diastolic filling and reduced stroke volume to 47.87 mL compared to 71.49 mL in the normal model, which could be compensated by increasing left ventricular filling pressure.
Why the study?
Understanding the interaction between the mitral valve and the left ventricle is critical for assessing cardiac pump function, particularly during mitral valve dysfunction.
Does pathological mitral valve dynamics (HOCM or calcification) affect left ventricular pump function and hemodynamics in a coupled MV-LV computational model?
Does pathological mitral valve dynamics (HOCM or calcification) affect left ventricular pump function and hemodynamics in a coupled MV-LV computational model?
Computational modeling demonstrates that mitral valve pathology significantly impairs left ventricular pump function, but near-normal function can be achieved in calcified valves by increasing filling pressure or myocardial contractility.
Computational models suggest hemodynamic compensation in mitral calcification; leaves open clinical translation pending human validation.
Background Understanding the interaction between the mitral valve (MV) and the left ventricle (LV) is very important in assessing cardiac pump function, especially when the MV is dysfunctional. Such dysfunction is a major medical problem owing to the essential role of the MV in cardiac pump function. Computational modelling can provide new approaches to gain insight into the functions of the MV and LV. Methods In this study, a previously developed LV–MV model is used to study cardiac dynamics of MV leaflets under normal and pathological conditions, including hypertrophic cardiomyopathy (HOCM) and calcification of the valve. The coupled LV–MV model is implemented using a hybrid immersed boundary/finite element method to enable assessment of MV haemodynamic performance. Constitutive parameters of the HOCM and calcified valves are inversely determined from published experimental data. The LV compensation mechanism is further studied in the case of the calcified MV. Results Our results show that MV dynamics and LV pump function can be greatly affected by MV pathology. For example, the HOCM case showed bulged MV leaflets at the systole owing to low stiffness, and the calcified MV was associated with impaired diastolic filling and much-reduced stroke volume. We further demonstrated that either increasing the LV filling pressure or increasing myocardial contractility could enable a calcified valve to achieve near-normal pump function. Conclusion The modelling approach developed in this study could deepen our understanding of the interactions between the MV and the LV and help in risk stratification of heart valve disease and in silico treatment planning by exploring intrinsic compensation mechanisms.
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Cai et al. (2022) studied Mitral valve disease (Hypertrophic cardiomyopathy and calcification) (n=1). Simulated hypertrophic cardiomyopathy and calcified mitral valve vs. Normal mitral valve model was evaluated on Hemodynamic performance (stroke volume, transvalvular pressure gradient, effective orifice area). Simulated mitral valve calcification significantly impaired diastolic filling and reduced stroke volume to 47.87 mL compared to 71.49 mL in the normal model, which could be compensated by increasing left ventricular filling pressure.
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