Left ventricular twisting model to simulate left ventricular contraction and pressure increase during isovolumic contraction

Background: It is well known that the tremendous internal pressure build-up in the left ventricle (LV) cavity during isovolumic contraction is due to the contraction of the spirally woven myocardial fibers. Methodology and Results: In this chapter, a biomechanics model of the left-ventricle (LV) is developed to investigate the mechanism of LV pressure generation during isovolumic contraction. The LV is modeled as a fluid-filled thick-walled cylinder (with both ends closed) to simulate isovolumic contraction. We have shown that the tremendous internal cavity pressure build-up during isovolumic contraction is contributed by active torsion and compression caused by the contraction of the spirally wound myocardial fibers. We have matched the magnitude of the principal compressive stresses to the isometric myocardial fiber stresses, and then determined their orientation required for the LV model to generate the monitored pressure. In this process, we have also determined the constitutive property of the myocardial fibers, as well as magnitude of the stress generated in them and their equivalent orientation corresponding to the magnitude and direction of the principal stresses. Conclusion: The results indicate that both myocardial fiber stresses and orientations (as given by the principal stresses) vary during the isovolumic contraction phase. The most significant aspect of our work is that LV twisting is a vital mechanism for the high intra-LV cavity pressure build-up during isovolumic contraction. Additionally, we have shown that the fiber orientation (based on the principal stress’ directions) conforms to the values monitored in literature. Thus, we could conceivably employ the twist angle (derived noninvasively by MRI Tagging) as an LV contractility parameter. Significance: Using this LV Twisting model, we can determine the myocardial fibers’ orientation. This can have an important bearing on the capacity of the LV to generate adequate pressure during isovolumic contraction. By applying our model to patients, we can determine the ranges of fiber orientation in normal LVs and infarcted LVs. Based thereon, this model can also be used to diagnose impaired LVs. Further, the value of the compression principal stress and its orientation can be adopted as a measure of LV contractility.