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Ann Thorac Surg 2001;71:654-662
© 2001 The Society of Thoracic Surgeons
a Departments of Surgery and Bioengineering, University of California, San Francisco, California, USA
b Department of Surgery, Washington University, St. Louis, Missouri, USA
c Department of Biomedical Engineering, Columbia University, New York, New York, USA
Accepted for publication August 24, 2000.
Address reprint requests to Dr Guccione, Division of Surgical Services (112D), Department of Veterans Affairs Medical Center, 4150 Clement St, San Francisco, CA 94121
e-mail: Julius.Guccione{at}med.va.gov
Background. The global left ventricular dysfunction characteristic of left ventricular aneurysm is associated with muscle fiber stretching in the adjacent noninfarcted (border zone) region during isovolumic systole. The mechanism of this regional dysfunction is poorly understood.
Methods. An anteroapical transmural myocardial infarct was created by coronary arterial ligation in an adult Dorset sheep and was allowed to mature into left ventricular aneurysm for 10 weeks. The animal was imaged subsequently using magnetic resonance imaging with simultaneous recording of intraventricular pressures. A realistic mathematical model of the three-dimensional ovine left ventricle with an anteroapical aneurysm was constructed from multiple short-axis and long-axis magnetic resonance imaging slices at the beginning of diastolic filling.
Results. Three model simulations are presented: (1) normal border zone contractility and normal aneurysmal material properties; (2) greatly reduced border zone contractility (by 50%) and normal aneurysmal material properties; and (3) greatly reduced border zone contractility (by 50%) and stiffened aneurysmal material properties (by 1000%). Only the latter two simulations were able to reproduce experimentally observed stretching of border zone fibers during isovolumic systole.
Conclusions. The mechanism underlying mechanical dysfunction in the border zone region of left ventricular aneurysm is primarily the result of myocardial contractile dysfunction rather than increased wall stress in this region.
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