Endothelium plays a pivotal role in the regulation of vascular relaxation.
Inflammation may in turn induce endothelial dysfunction and thus increase t
he risk of atherothrombosis. We investigated 31 men with angiographically v
erified coronary heart disease, aged 57.7 +/- 5.3 years, in regard to endot
helium-dependent, acetylcholine-induced, and to endothelium-independent, so
dium nitroprusside-induced vasodilatation in the forearm vasculature by str
ain-gauge plethysmography. Logistic regression analysis served to determine
the relation between forearm vascular function and the inflammatory factor
s measured, concentration of C-reactive protein, subtypes of peripheral blo
od T-lymphocytes, and other factors potentially affecting endothelial funct
ion (lipoprotein and glucose levels). Concentration of C-reactive protein w
as an independent determinant of endothelium-dependent vascular function (P
< 0.001 for low dose acetylcholine, P = 0.01 for high dose acetylcholine).
Other determinants of endothelium-dependent vascular dysfunction were CD8-
lymphocytes expressing ICAM-1 (P=0.001), antibodies to oxidized low-density
lipoprotein (P < 0.001), and body weight (P = 0.007). The present data sho
wed an association between inflammatory risk factors linked to atherothromb
osis and endothelial dysfunction in coronary heart disease patients. It is
possible that endothelial dysfunction in coronary heart disease patients is
related to the chronic inflammation or infection coexisting with atheroscl
erosis. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.