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Influence of plaque calcifications on coronary stent fracture: A numerical fatigue life analysis including cardiac wall movement
Influence of plaque calcifications on coronary stent fracture: A numerical fatigue life analysis including cardiac wall movement
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Influence of plaque calcifications on coronary stent fracture: A numerical fatigue life analysis including cardiac wall movement
Influence of plaque calcifications on coronary stent fracture: A numerical fatigue life analysis including cardiac wall movement

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Influence of plaque calcifications on coronary stent fracture: A numerical fatigue life analysis including cardiac wall movement
Influence of plaque calcifications on coronary stent fracture: A numerical fatigue life analysis including cardiac wall movement
Journal Article

Influence of plaque calcifications on coronary stent fracture: A numerical fatigue life analysis including cardiac wall movement

2014
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Overview
Coronary stent fracture is still an unresolved issue in the field of minimally invasive cardiovascular interventions due to its high rate of incidence and uncertain clinical consequences. Recent studies, based on clinical data, proved that there are several factors which can be identified as independently responsible of coronary stent fracture. Among these, calcifications, which increase the local stiffness and heterogeneity of atherosclerotic plaques, seem to play a major role. From a mechanical point of view, stent fracture in coronary arteries is triggered by the cyclic loading of pulsatile blood pressure combined with the movement of cardiac wall. In this context, this study aims at simulating the stent expansion in a model of epicardial atherosclerotic coronary artery and correlating the effects of cyclic blood pressure and cardiac wall movement on the stent fatigue resistance. Two ideal cases of atherosclerotic plaques were modelled: the first one included a localised plaque calcification; the latter one did not include such calcification. Results of stress/strain and fatigue analyses confirmed the influence of the plaque calcification on potential fracture of the devices. In addition, the effects of cardiac wall movement were quantified as more dangerous causes of the stent fatigue fracture with respect to the internal blood pressure oscillations. In conclusion, this study demonstrates the increased risk of coronary stent fracture associated to the presence of localised plaque calcifications. This work also suggests the necessity of more realistic biomechanical models which takes into account the heterogeneity of atherosclerotic plaques in order to assess the mechanical performances of coronary stents.