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Articles in PresS, published online ahead of print October 31, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00360.2002
Submitted on May 8, 2002
Accepted on October 7, 2002
1 Department of Surgery and the Harrison Department of Surgical Research, Hospital of the University of Pennsylvania, Philadelphia, PA, USA
2 Philips Medical Systems, Andover, MA, USA
3 Division of Cardiology, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, PA, USA
* To whom correspondence should be addressed. E-mail: benjamin.jackson{at}uphs.upenn.edu.
After myocardial infarction (MI), the borderzone expands chronically, causing ventricular dilatation and congestive heart failure (CHF). In an ovine model (n=4) of anteroapical MI that results in CHF, contrast echocardiography was used to image short-axis LV cross sections and identify borderzone myocardium before and after coronary artery ligation. In the borderzone at end systole, the LV endocardial curvature (K) decreased from 0.86±0.33 cm-1at baseline to 0.35±0.19 cm-1 at 1 hr (p<0.05), corresponding to a mean decrease of 55%. Also in the borderzone, the wall thickness (h) decreased from 1.14±0.26 cm at baseline to 1.01±0.25 cm at 1 hr (p<0.05), corresponding to a mean decrease of 11%. By Laplace's law, wall stress is inversely proportional to the product K.h. Therefore, a 55% decrease in K results in a 122% increase in circumferential stress; a 11% decrease in h results in a 12% increase in circumferential stress. These findings indicate that after MI, geometric changes cause increased dynamic wall stress, which likely contributes to borderzone expansion and remodeling.
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