Yi Liu

Reconstruction of myocardial tissue motion and strain fields from displacement-encoded MR imaging

A quantitative analysis of myocardial mechanics is fundamental to understanding cardiac function, diagnosis of heart disease, and assessment of therapeutic intervention. Displacement encoding with stimulated-echo (DENSE) magnetic resonance imaging (MRI) technique was developed to track the three-dimensional (3D) displacement vector of discrete material grid points in the myocardial tissue. Despite the wealth of information gained from DENSE images, the current software only provides two-dimensional in-plane deformation. The objective of this study is to introduce a postprocessing method to reconstruct and visualize continuous dynamic 3D displacement and strain fields in the ventricular wall from DENSE data. An anatomically accurate hexagonal finite-element model of the left ventricle (LV) is reconstructed by fitting a prolate spheroidal primitive to contour points of the epi- and endocardial surfaces. The continuous displacement field in the model is described mathematically based on the discrete DENSE vectors using a minimization method with smoothness regularization. Based on the displacement, heart motion and myocardial stretch (or strain) are analyzed. Illustratory computations were conducted with DENSE data of three infarcted and one normal sheep ventricles. The full 3D results show stronger overall axial shortening, wall thickening, and twisting of the normal LV compared with the infarcted hearts. Local myocardial stretches show a dyskinetic LV in the apical region, dilation of apex in systole, and a compensatory increase in strain in the healthy basal region as a compensatory mechanism. We conclude that the proposed postprocessing method significantly extends the utility of DENSE MRI, which may provide a patient-specific 3D model of cardiac mechanics.

Diameter-dependent axial prestretch of porcine coronary arteries and veins

The pressure-diameter relation (PDR) and the wall strain of coronary blood vessels have important implications for coronary blood flow and arthrosclerosis, respectively. Previous studies have shown that these mechanical quantities are significantly affected by the axial stretch of the vessels. The objective of this study was to measure the physiological axial stretch in the coronary vasculature; i.e., from left anterior descending (LAD) artery tree to coronary sinus vein and to determine its effect on the PDR and hence wall stiffness. Silicone elastomer was perfused through the LAD artery and coronary sinus trees to cast the vessels at the physiologic pressure. The results show that the physiological axial stretch exists for orders 4 to 11 (> 24 μm in diameter) arteries and orders -4 to -12 (>38 μm in diameter) veins but vanishes for the smaller vessels. Statistically, the axial stretch is higher for larger vessels and is higher for arteries than veins. The axial stretch λ(z) shows a linear variation with the order number (n) as: λ(z) = 0.062n + 0.75 (R(2) = 0.99) for artery and λ(z) = -0.029n + 0.89 (R(2) = 0.99) for vein. The mechanical analysis shows that the axial stretch significantly affects the PDR of the larger vessels. The circumferential stretch/strain was found to be significantly higher for the epicardial arteries (orders 9-11), which are free of myocardium constraint, than the intramyocardial arteries (orders 4-8). These findings have fundamental implications for coronary blood vessel mechanics.

Simulation of LV pacemaker lead in marginal vein: potential risk factors for acute dislodgement.

Although left ventricular (LV) coronary sinus lead dislodgement remains a problem, the risk factors for dislodgement have not been clearly defined. In order to identify potential risk factors for acute lead dislodgement, we conducted dynamic finite element simulations of pacemaker lead dislodgement in marginal LV vein. We considered factors such as mismatch in lead and vein diameters, velocity of myocardial motion, branch angle between the insertion vein and the coronary sinus, degree of slack, and depth of insertion. The results show that large lead-to-vein diameter mismatch, rapid myocardial motion, and superficial insertion are potential risk factors for lead dislodgement. In addition, the degree of slack presents either a positive or negative effect on dislodgement risk depending on the branch angle. The prevention of acute lead dislodgment can be enforced by inducing as much static friction force as possible at the lead-vein interface, while reducing the external force. If the latter exceeds the former, dislodgement will occur. The present findings underscore the major risk factors for lead dislodgment, which may improve implantation criterion and future lead design.

Simulation of Mechanical Environment in Active Lead Fixation: Effect of Fixation Helix Size

The risk of myocardial penetration due to active-fixation screw-in type pacing leads has been reported to increase as the helix electrodes become smaller. In order to understand the contributing factors for lead penetration, we conducted finite element analyses of acute myocardial micro-damage induced by a pacemaker lead screw-in helix electrode. We compared the propensity for myocardial micro-damage of seven lead designs including a baseline model, three modified designs with various helix wire cross-sectional diameters, and three modified designs with different helix diameters. The comparisons show that electrodes with a smaller helix wire diameter cause more severe micro-damage to the myocardium in the early stage. The damage severity, represented by the volume of failed elements, is roughly the same in the middle stage, whereas in the later stage the larger helix wire diameter generally causes more severe damage. The onset of myocardial damage is not significantly affected by the helix diameter. As the helix diameter increases, however, the extent of myocardial damage increases accordingly. The present findings identified several of the major risk factors for myocardial damage whose consideration for lead use and design might improve acute and chronic lead performance.