title: Influence of residual stress/strain on the biomechanical stability of vulnerable coronary plaques: potential impact for evaluating the risk of plaque rupture.
abstract: In a vulnerable plaque (VP), rupture often occurs at a site of high stress within the cap. It is also known that vessels do not become free of stress when all external loads are removed. Previous studies have shown that such residual stress/strain (RS/S) tends to make the stress distribution more uniform throughout the media of a normal artery. However, the influence of RS/S on the wall stress distribution in pathological coronaries remains unclear. The aim of this study was to investigate the effects of RS/S on the biomechanical stability of VPs. RS/S patterns were studied ex vivo in six human vulnerable coronary plaque samples. Because the existence of RS/S can only be assessed by releasing it, the opening angle technique was the experimental approach used to study the geometrical opening configurations of the diseased arteries, producing an arterial wall in a near-zero stress state. Reciprocally, these opening geometries were used in finite element simulations to reconstruct the RS/S distributions in closed arteries. It was found that the RS/S 1) is not negligible, 2) dramatically affects the physiological peak stress amplitude in the thin fibrous cap, 3) spotlights some new high stress areas, and 4) could be a landmark of the lipid core's developmental process within a VP. This study demonstrates that plaque rupture is not to be viewed as a consequence of intravascular pressure alone, but rather of a subtle combination of external loading and intraplaque RS/S.
authors.affiliation: National Heart, Blood and Lung Institute, NIH, Pettigrew's Laboratory, Bldg. 10, 10 Center Drive, Bethesda, MD 20892, USA. ohayonj2@mail.nih.gov
authors.forename: Jacques
authors.initials: J
authors.lastname: Ohayon
authors.forename: Olivier
authors.initials: O
authors.lastname: Dubreuil
authors.forename: Philippe
authors.initials: P
authors.lastname: Tracqui
authors.forename: Simon
authors.initials: S
authors.lastname: Le Floc'h
authors.forename: Gilles
authors.initials: G
authors.lastname: Rioufol
authors.forename: Lara
authors.initials: L
authors.lastname: Chalabreysse
authors.forename: Françoise
authors.initials: F
authors.lastname: Thivolet
authors.forename: Roderic I
authors.initials: RI
authors.lastname: Pettigrew
authors.forename: Gérard
authors.initials: G
authors.lastname: Finet
mesh_terms: D003324:Coronary Artery Disease / Q000150:complications* / Q000473:pathology / Q000503:physiopathology*; D003331:Coronary Vessels / Q000473:pathology* / Q000503:physiopathology*; D020342:Finite Element Analysis; D006801:Humans; D008264:Macrophages / Q000473:pathology; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D012307:Risk Factors; D012421:Rupture / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D013314:Stress, Mechanical