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Ann Thorac Surg 2003;76:1171-1180
© 2003 The Society of Thoracic Surgeons


Original article: cardiovascular

Myosplint decreases wall stress without depressing function in the failing heart: a finite element model study

Julius M. Guccione, PhDa,b,d*, Ali Salahieh, BSa, Scott M. Moonly, BSb, Jeroen Kortsmit, BSe, Arthur W. Wallace, MD, PhDc, Mark B. Ratcliffe, MDa,b

a Department of Surgery, San Francisco, CA, USA
b Department of Bioengineering, San Francisco, CA, USA
c Department of Anesthesia, Division of Cardiothoracic Surgery, School of Medicine of the University of California, San Francisco, California, USA
d San Francisco Veterans Affairs Medical Center, San Francisco, California, USA
e Department of Biophysics, Maastricht University, Maastricht, the the Netherlands

Accepted for publication April 18, 2003.

* Address reprint requests to Dr Guccione, Division of Surgical Services (112D), San Francisco Veterans Affairs Medical Center, 4150 Clement St, San Francisco, CA 94121, USA
e-mail: julius.guccione{at}med.va.gov

BACKGROUND: The Myocor Myosplint is a transcavitary tensioning device designed to change left ventricular (LV) shape and reduce wall stress. Regional wall stress cannot be measured in the intact heart and LV function after surgical remodeling is often confounded by inotropic agents and mitral repair. We used a realistic mathematical (finite element) model of the dilated human LV to test the hypothesis that Myosplint decreased regional ventricular fiber stress and improved LV function.

METHODS: A finite element model was used to simulate the effects of Myosplint on the LV stroke volume/end-diastolic pressure (Starling) relationship and regional distributions of stress in the local muscle fiber direction (fiber stress) for a wide range of diastolic and end-systolic material properties. The nonlinear stress-strain relationship for the diastolic myocardium was anisotropic with respect to the local muscle fiber direction. An elastance model for active fiber stress was incorporated in an axisymmetric geometric model of the globally dilated LV wall.

RESULTS: Both diastolic compliance and end-systolic elastance shifted to the left on the pressure-volume diagram. LV end-diastolic volume and end-systolic volumes were reduced by 7.6% and 8.6%, respectively. Mean end-diastolic and end-systolic fiber stress was decreased by 24% and 16%, respectively. Although the effect of Myosplint on the Starling relationship was not significant, there were trends toward an improvement in this relationship at low diastolic stiffness, C, high peak intracellular calcium concentration, Ca0, and high arterial elastance, EA. Of note, the effect of C was twice that of Ca0 and EA. Diastolic function would, therefore, be expected to be the prime determinant of success with Myosplint.

CONCLUSIONS: Myosplint reduces fiber stress without a decrement in the Starling relationship. Myosplint should be much more effective than partial ventriculectomy as a surgical therapy for patients with dilated cardiomyopathy and end-stage congestive heart failure.




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