• Advances in biomechanics and applications
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• 제1권1호
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• pp.41-55
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• 2014

Acellular intra-myocardial biomaterial injections have been shown to be therapeutically beneficial in inhibiting ventricular remodelling of myocardial infarction (MI). Based on a biventricular canine cardiac geometry, various finite element models were developed that comprised an ischemic (II) or scarred infarct (SDI) in left ventricular (LV) antero-apical region, without and with intra-myocardial biomaterial injectate in layered (L) and bulk (B) distribution. Changes in myocardial properties and LV geometry were implemented corresponding to infarct stage (tissue softening vs. stiffening, infarct thinning, and cavity dilation) and injectate (infarct thickening). The layered and bulk injectate increased ejection fraction of the infarcted LV by 77% (II+L) and 25% (II+B) at the ischemic stage and by 61% (SDI+L) and 63% (SDI+B) at the remodelling stage. The injectates decreased the mean end-systolic myofibre stress in the infarct by 99% (II+L), 97% (II+B), 70% (SDI+L) and 36% (SDI+B). The bulk injectate was slightly more effective in improving LV function at the remodelling stage whereas the layered injectate was superior in functional improvement at ischemic stage and in reduction of wall stress at ischemic and remodelling stage. These findings may stimulate and guide further research towards tailoring acellular biomaterial injectate therapies for MI.

• 대한기계학회:학술대회논문집
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• 대한기계학회 2001년도 추계학술대회논문집B
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• pp.529-532
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• 2001

The purposes of the present study are to investigate hemodynamic characteristics and to define shear-sensitive remodeling in the stenosed coronary models. Two models for the compensatory remodelling used for this research are a pre-stenotic dilation and a post-stenotic dilation models for the computer simulation. The peak wall shear stress on the post-stenotic model is higher than that of the pre-stenotic model. Two recirculation zones are generated in the pre-stenotic model, and the zones in the pre-stenotic model are smaller than those in the post-stenotic model. Variation of the wall shear stress in the pre-stenotic model is lower than that in the post-stenotic model. In computer simulation with the post-stenotic model, higher temporal and spatial shear fluctuation and stress suggested shear-sensitive remodeling. Shear-sensitive remodeling may be associated with the increased risk of plaque rupture, the underlying cause of acute coronary syndromes, and sudden cardiac death.