CLINICAL STUDY: ATHEROSCLEROSIS
Plaque burden, arterial remodeling and plaque vulnerability: determined by systemic factors?
Aryan Vink, MD*  ,
Arjan H. Schoneveld, BSc* ,
Wietske Richard, MD*,
Dominique P. V. de Kleijn, PhD* ,
Erling Falk, MD, PhD, FACC ,
Cornelius Borst, MD, PhD, FACC* and
Gerard Pasterkamp, MD, PhD*
* Department of Cardiology, University Medical Center, Utrecht, The Netherlands
Interuniversity Cardiology Institute of the Netherlands, Utrecht, The Netherlands
Department of Cardiology, Aarhus University Hospital (Skejby), Aarhus, Denmark
Manuscript received January 29, 2001;
revised manuscript received May 11, 2001,
accepted May 23, 2001.
Reprint requests and correspondence: Dr. Gerard Pasterkamp, Experimental Cardiology Laboratory, University Medical Center Utrecht, Heidelberglaan 100, Room G02-523, 3584 CX Utrecht, the Netherlands
g.pasterkamp{at}hli.azu.nl
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 growth 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 examined. The arteries were divided in 1-cm intervals. Plaque size, the mode of arterial remodeling and histopathologic characteristics of plaque vulnerability (lipid-rich core and plaque inflammation) were compared between right and left femoral arteries obtained from the same individual. A role for systemic factors was assumed if a phenomenon was equally present in both arteries.
RESULTS
There was concordance in average plaque size (r2 = 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 concordance in plaque inflammation (kappa = 0.067, p = 0.61) between right and left arteries.
CONCLUSIONS
These results suggest that not only the amount of atherosclerosis, but also arterial remodeling and lipid deposition in plaques, are influenced by systemic factors. The nonhomogeneous distribution of inflammation in atherosclerotic arteries supports the hypothesis that plaque inflammation is locally affected.
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Abbreviations and Acronyms
| | CRP | = C-reactive protein | | IEL | = internal elastic lamina |
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