Plaque burden, arterial remodeling and plaque vulnerability: Determined bysystemic factors?

Citation
A. Vink et al., Plaque burden, arterial remodeling and plaque vulnerability: Determined bysystemic factors?, J AM COL C, 38(3), 2001, pp. 718-723
Citations number
25
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
ISSN journal
07351097 → ACNP
Volume
38
Issue
3
Year of publication
2001
Pages
718 - 723
Database
ISI
SICI code
0735-1097(200109)38:3<718:PBARAP>2.0.ZU;2-I
Abstract
OBJECTIVES This study was designed to determine whether arterial remodeling and plaque vulnerability are influenced by systemic factors. BACKGROUND Atherosclerotic luminal narrowing is caused by gradual plaque gr owth and arterial remodeling. In the acute phase, luminal narrowing may be accelerated by acute thrombus formation, usually precipitated by rupture of a vulnerable plaque. METHODS Femoral arteries were obtained from elderly individuals at autopsy. Pairs of atherosclerotic femoral arteries from 42 individuals were examine d. The arteries were divided in 1-cm intervals. Plaque size, the mode of ar terial remodeling and histopathologic characteristics of plaque vulnerabili ty (lipid-rich core and plaque inflammation) were compared between right an d left femoral arteries obtained from the same individual. A role for syste mic factors was assumed if a phenomenon was equally present in both arterie s. RESULTS There was concordance in average plaque size (r(2) = 0.5, p < 0.001 ), expansive remodeling (kappa = 0.42, p = 0.007) and occurrence of plaques containing a large lipid-rich core (kappa = 0.60, p = 0.001), but no conco rdance in plaque inflammation (kappa = 0.067, p = 0.61) between right and l eft arteries. CONCLUSIONS These results suggest that not only the amount of atheroscleros is, but also arterial remodeling and lipid deposition in plaques, are influ enced by systemic factors. The nonhomogeneous distribution of inflammation in atherosclerotic arteries supports the hypothesis that plaque inflammatio n is locally affected. (C) 2001 by the American College of Cardiology.