Computational methods for parametric evaluation of the biventricular mechanics of direct cardiac compression.

Despite the increasing incidence of heart failure, advancements in mechanical circulatory support have become minimal. A new type of mechanical circulatory support, direct cardiac compression, is a novel support paradigm that involves a soft deformable cup around the ventricles, compressing it during systole. No group has yet investigated the biomechanical consequences of such an approach. This article uses a multiscale cardiac simulation software to create a patient-specific beating heart dilated cardiomyopathy model. Left and right ventricle (LV and RV) forces are applied parametrically, to a maximum of 2.9 and 0.46 kPa on each ventricle, respectively. Compression increased the ejection fraction in the left and right ventricles from 15.3% and 27.4% to 24.8% and 38.7%, respectively. During applied compression, the LV freewall thickening increased while the RV decreased; this was found to be due to a change in the balance of the preload and afterload in the freewalls. Principal strain renderings demonstrated strain concentrations on the anterior and posterior LV freewall. Strains in these regions were found to exponentially increase after 0.75 normalized LV force was applied. Component analysis of these strains illuminated a shift in the dominating strain from transmural to cross fiber once 0.75 normalized LV force is exceeded. An optimization plot was created by nondimensionalizing the stroke volume and maximum principal strain for each compression profile, selecting five potential compression schemes. This work demonstrates not only the importance of a computational approach to direct cardiac compression but a framework for tailoring compression profiles to patients.

Cardiac assist with a twist: apical torsion as a means to improve failing heart function.

Changes in muscle fiber orientation across the wall of the left ventricle (LV) cause the apex of the heart to turn 10-15 deg in opposition to its base during systole and are believed to increase stroke volume and lower wall stress in healthy hearts. Studies show that cardiac torsion is sensitive to various disease states, which suggests that it may be an important aspect of cardiac function. Modern imaging techniques have sparked renewed interest in cardiac torsion dynamics, but no work has been done to determine whether mechanically augmented apical torsion can be used to restore function to failing hearts. In this report, we discuss the potential advantages of this approach and present evidence that turning the cardiac apex by mechanical means can displace a clinically significant volume of blood from failing hearts. Computational models of normal and reduced-function LVs were created to predict the effects of applied apical torsion on ventricular stroke work and wall stress. These same conditions were reproduced in anesthetized pigs with drug-induced heart failure using a custom apical torsion device programmed to rotate over various angles during cardiac systole. Simulations of applied 90 deg torsion in a prolate spheroidal computational model of a reduced-function pig heart produced significant increases in stroke work (25%) and stroke volume with reduced fiber stress in the epicardial region. These calculations were in substantial agreement with corresponding in vivo measurements. Specifically, the computer model predicted torsion-induced stroke volume increases from 13.1 to 14.4 mL (9.9%) while actual stroke volume in a pig heart of similar size and degree of dysfunction increased from 11.1 to 13.0 mL (17.1%). Likewise, peak LV pressures in the computer model rose from 85 to 95 mm Hg (11.7%) with torsion while maximum ventricular pressures in vivo increased in similar proportion, from 55 to 61 mm Hg (10.9%). These data suggest that: (a) the computer model of apical torsion developed for this work is a fair and accurate predictor of experimental outcomes, and (b) supra-physiologic apical torsion may be a viable means to boost cardiac output while avoiding blood contact that occurs with other assist methods.

Computational Studies on the Effects of Applied Apical Torsion for Cardiac Assist on Regional Wall Mechanics.

OBJECTIVE: Here we report the results of parametric computational simulations evaluating the biomechanical effects of applied apical torsion (AAT) on a patient-specific bi-ventricular failing heart model. METHODS: We examined the resulting effects on cardiac biomechanics with varying device coverage areas and applied rotation angles to determine the practical working limits of AAT on a dilated cardiomyopathy heart model. RESULTS: The largest maximum principal stresses and strains observed in the heart failure model were 80.21 kPa (at the basal node of the left ventricular epicardium) and 0.56 (at the node of the device base of the left ventricular free wall). Results show that increasing levels of AAT beyond 45 degrees produce supra-physiologic levels of stress and strain in the myocardium. CONCLUSION: Maximum principal stresses greater than 100 kPa were observed at multiple nodes along the epicardium and endocardium of the ventricular base and in the endocardium at the device base. Maximum principal strains greater than 0.60 were observed at multiple nodes along the epicardium and endocardium of the ventricular base. SIGNIFICANCE: This suggests that while AAT has the potential to provide meaningful returns to hemodynamic function in failing hearts, the large deformations produced by this approach with the upper bounds of applied rotation angle realistically excludes supra-physiological rotations as a means for cardiac support. However, lower AAT angles - closer to that of the native left-ventricular torsion - coupled with another means of external cardiac compression may prove to be a viable method of cardiac assist.

Left ventricular simulation of cardiac compression: Hemodynamics and regional mechanics.

Heart failure is a global epidemic. Left ventricular assist devices provide added cardiac output for severe cases but cause infection and thromboembolism. Proposed direct cardiac compression devices eliminate blood contacting surfaces, but no group has optimized the balance between hemodynamic benefit and excessive ventricular wall strains and stresses. Here, we use left ventricular simulations to apply compressions and analyze hemodynamics as well as regional wall mechanics. This axisymmetric model corresponds with current symmetric bench prototypes. At nominal pressures of 3.1 kPa applied over the epicardial compression zone, hemodynamics improved substantially. Ejection fraction changed from 17.6% at baseline to 30.3% with compression and stroke work nearly doubled. Parametric studies were conducted by increasing and decreasing applied pressures; ejection fraction, peak pressure, and stroke work increased linearly with changes in applied compression. End-systolic volume decreased substantially. Regional mechanics analysis showed principal stress increases at the endocardium, in the middle of the compression region. Principal strains remained unchanged or increased moderately with nominal compression. However, at maximum applied compression, stresses and strains increased substantially providing potential constraints on allowable compressions. These results demonstrate a framework for analysis and optimization of cardiac compression as a prelude to biventricular simulations and subsequent animal experiments.

Computational Parametric Studies Investigating the Global Hemodynamic Effects of Applied Apical Torsion for Cardiac Assist.

Healthy hearts have an inherent twisting motion that is caused by large changes in muscle fiber orientation across the myocardial wall and is believed to help lower wall stress and increase cardiac output. It was demonstrated that applied apical torsion (AAT) of the heart could potentially treat congestive heart failure (CHF) by improving hemodynamic function. We report the results of parametric computational experiments where the effects of using a torsional ventricular assist device (tVAD) to treat CHF were examined using a patient-specific bi-ventricular computational model. We examined the effects on global hemodynamics as the device coverage area (CA) and applied rotation angle (ARA) were varied to determine ideal tVAD design parameters. When compared to a baseline, pretreatment CHF model, increases in ARA resulted in moderate to substantial increases in ejection fraction (EF), peak systolic pressures (PSP) and stroke work (SW) with concomitant decreases in end-systolic volumes (ESV). Increases in device CA resulted in increased hemodynamic function. The simulation representing the most aggressive level of cardiac assist yielded significant increases in left ventricular EF and SW, 49 and 72% respectively. Results with this more realistic computational model reinforce previous studies that have demonstrated the potential of AAT for cardiac assist.