Study of Mitral stenosis in resting and exercised heart using ABAQUS™

Anand Mohan for providing his valuable guidance, comments and suggestions throughout the course of the project. Our use of the Living Heart Human Model was under an agreement between Dassault Systemes and IIT Hyderabad. Simulations were also performed for cardiac function in mitral stenosis during exercise, but LHHM predictions neither quantitatively nor qualitatively matched data indicating further improvement of the model.

The right side of the heart consists of the right atrium and the right ventricle separated by the tricuspid valve. Similarly, the left side consists of the left atrium and the left ventricle separated by the mitral valve. Cardiovascular diseases (CVDs) account for nearly 25% of deaths per year in India [Prabhakaran et al., 2005].

Repair or replacement of heart valves is the predominant way of treating such diseases. Mitral stenosis (MS) is defined as a narrowing of the mouth of the mitral valve, which provides blood flow between the left atrium and the left ventricle. The blocked valve causes a build-up of pressure and volume in the left atrium that keeps oxygenated blood from the lungs, leading to backflow of fluid to fill the lungs, making the patient feel tired or short of breath.

In the case of the (adult/pediatric) human heart, a versatile computational model of the heart should be able to provide the simulated results for normal function, various pathologies and also cardiac function during the implementation of devices such as pacemakers, left ventricular assist devices (LVADs) etc.

Living Heart Human Model

The advantage of devices designed and tested on a computer model reduces animal experiments for functional evaluation of prototypes [Chandran, 2010]. Computer models of the heart that are commercially available or under development for academic use include the Human Living Heart Model (LHHM) - an initiative of Dassault Systemes. We currently have a license for LHHM (in 2.0 beta) - and we'll briefly describe its features below.

The advantages and disadvantages associated with this choice compared to other models available in the literature are discussed in the Literature Review (section 2). The predicted results from these combined models are in good agreement with clinical data for certain parameters of the adult cardiac cycle. Furthermore, the parameters and properties of each of these models can be changed for a particular heart condition, and the simulations can be run, which then provide the results that can be analyzed for research purposes.

In this study, we evaluate the performance of LHHM (v 2.0 beta) in simulating heart function in the case of mitral stenosis and in predicting the pressure-volume behavior observed during exercise in the case of mitral stenosis by comparing it with clinical data for the same. The study design first includes the validation of LHHM predictions (in 2.0 beta) for cardiac performance under normal physiological conditions and during exercise. We then compare the predictions of the LHHM model for cases of mitral stenosis under both normal physiological and exercise conditions.

2.Literature Survey

Computational Models of Heart and Valve Function

Effects of Mitral Stenosis (MS)

Fluid-structure interaction modeling was not taken into account in this model. This model cannot say anything about the local concentration areas, but it can resolve the overall distortion. It was observed that there was a slight increase in end-diastolic volume and end-systolic volume, which led to a decrease in stroke volume, thus reducing cardiac output. It has also been hypothesized that in MS the thickening of the valve leaflets and the fibrosis of the cordae tendineae convert the valve into a rigid cylinder [Grant, 1953], impairing its movement and leading to dysfunction of the left ventricular wall.

It is also noted that there are abnormal increases in diastolic pressure for a given increase in diastolic volume, indicating reduced left ventricular compliance [Feigenbaum et al., 1966], but this effect is noted to not significantly reduce cardiac output.

Effect of exercise on heart function

3.Problem Formulation

• Simulation of Normal Heart
• Simulation of Mitral Stenosis under resting conditions
• Validation: Heart Function in Healthy Heart (Resting)
• Prediction: Heart Function in Severe Mitral Stenosis case (Resting)
• Prediction: Heart Function in Mitral Stenosis (Resting): Multiple cases ([Gorlin et.al, 1951])
• Prediction: Heart Function in Mitral Stenosis (Exercise)

We simulated a case of severe mitral stenosis with a mitral valve area of ​​1 cm2 (normal value). When the surface of the mitral valve decreases below 2 cm2 (moderate type of MS), the valve causes an obstruction of blood flow in the left ventricle [Gorlin and Gorlin, 1951; Dexter, 1952]. Gorlin et.al, 1951] observed that the symptoms of mitral stenosis can be attributed mainly to pulmonary congestion (congestion in the lungs).

Pulmonary congestion is caused by changes in circulation resulting from the narrowing of the mitral valve. Data for mean pulmonary arterial pressure (measured at the base of the pulmonary artery at the exit of the right ventricle) and mean pulmonary capillary pressure (measured at the entrance to the left atrium near the exit of the pulmonary vein) were reported for all patients both at rest and during exercise.

In our study, we obtained the LHHM predictions for pulmonary arterial pressure and pulmonary capillary pressure at rest for all eight patients. The comparison of the mean pulmonary arterial pressure and pulmonary capillary pressure are results from [Gorlin et.al 1951] (referred to as Gorlin et al. in table), and LHHM (v2.0 beta) are tabulated below in Table 4.2. However, the model performs much better and captures both quantitative and qualitative trends of data for pulmonary capillary pressure (Fig. 4.6).

This can be attributed to the fact that pulmonary capillary pressure is measured much closer to the mitral valve than pulmonary arterial pressure, thus showing the error due to the modeling to a lesser extent. Based on their observations, they concluded that the pulmonary capillary pressure increased with the increase in mitral valve blood flow and pulmonary arterial pressure increased due to the increase in pulmonary capillary pressure along with an increase in blood velocity flow in some incidents . Pulmonary arterial resistance which is the difference between pulmonary arterial pressure and pulmonary capillary pressure over cardiac output showed no consistent change with exercise.

The simulations were performed for 5 cardiac cycles in both cases and the mean values ​​for pulmonary arterial pressure, pulmonary capillary pressure and the difference between both pulmonary pressures are collected and reported. Pulmonary arterial pressure (PAP) and pulmonary capillary pressure (PCP) should increase during exercise compared to resting values. The difference between pulmonary arterial pressure and pulmonary capillary pressure should not change significantly during exercise than at rest.

We can therefore conclude that the use of LHHM (v2.0 beta) for the study of mitral stenosis is only limited to resting states and not during exercise. Furthermore, predictions of LHHM (v2.0 beta) are better at locations close to the mitral valve than at locations further away.

Figure 3.1 Effective exchange area (MV area) - Normal Heart

5.Conclusions

Future Work

For this purpose, we can include pulmonary constraints in the model, as this can increase the accuracy of the model, since the function of the heart extends to the pulmonary region. Further studies, similar to the one in this thesis, can compare LHHM predictions with clinical data for other pathologies such as Mitral regurgitation, Aortic stenosis, Myocardial Infarction (Heart Attack), etc., and new treatment techniques can also be tested for those pathologies.

6.References

Gradient currents and variational principles for cardiac electrophysiology: towards efficient and robust numerical simulations of cardiac electrical activity. Left atrial and left ventricular function in healthy children and young adults assessed by three-dimensional echocardiography.