Send to

Choose Destination
ASAIO J. 2002 Sep-Oct;48(5):508-13.

A finite element model of left ventricular cellular transplantation in dilated cardiomyopathy.

Author information

San Francisco Veterans Affairs Medical Center, and Department of Surgery, School of Medicine of the University of California, San Francisco, 94121, USA.


Surgical therapies for heart failure that reduce left ventricular (LV) size have failed to improve LV function. Recent reports describe the direct injection of myocytes into the LV wall and suggest that myocyte transplantation improves regional contractile ability and improves LV function. Using a previously described finite element model, we simulated myocyte transplantation in the failing LV and tested the hypothesis that myocyte transplantation improves LV function (Starling relationship). An elastance model for active fiber stress was incorporated in an axisymmetric geometric model of the dilated, poorly contractile LV (dilated cardiomyopathy [DCM]). The nonlinear stress-strain relationship for the diastolic myocardium was anisotropic with respect to the local muscle fiber direction. Systolic material properties were depressed by assigning a peak intracellular calcium concentration (Ca2+) of 1.8 micromoL (normal value: 4.2 micromoL). Six different simulations of myocyte transplantation were performed in which transplanted areas were assigned a peak intracellular calcium concentration (Ca2+) of 4.2 micromoL. The pattern of myocyte engraftment was varied (transmural versus subepicardial; confluent versus heterogeneous), as was the amount of the LV free wall that was transplanted (17% vs 33%). Models were created and loaded with a range of physiologic LV pressures. Simulated myocyte transplantation increased the slope of the end-systolic elastance curve, improved the Starling relationship, and improved stroke volume and ejection fraction compared with DCM. This study demonstrated an improvement in LV function after myocyte transplantation.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wolters Kluwer
Loading ...
Support Center