Impact of oxidative stress on arterial elasticity in patients with atherosclerosis.
BACKGROUND
Alterations in the elastic behavior of arteries is an early sign of vascular damage in atherogenesis and may be promoted by oxidative stress (OxS). However, studies designed for simultaneous assessment of arterial elasticity and OxS status in patients with peripheral arterial disease (PAD) are absent. The purpose of this study was to assess large (C1) and small artery elasticity (C2) and indices of OxS in patients with PAD as well as to investigate possible relationships between these parameters.


METHODS
Arterial elasticity was assessed noninvasively by pulse wave analysis (PWA) and biochemical measurements were taken from 38 patients with PAD and from 28 matched control subjects. The elasticity indices of the arteries were derived from PWA based on the modified Windkessel model and the OxS status was measured using urinary 8-iso-prostaglandin F2alpha (F2-IsoPs) and plasma baseline diene conjugates of low-density lipoproteins (LDL-BDC).


RESULTS
Patients with PAD showed significantly reduced C1 and C2 and increased values of F2-IsoPs and LDL-BDC. There was an inverse association between C1 and F2-IsoPs, as well as between C2 and F2-IsoPs (R=-.3, P=.04; R=-.49, P=.002, respectively) in the patient group, but not in the controls. After controlling for potential confounders in a multiple regression model, the associations between C2 and F2-IsoPs remained significant in the patient group (P<.001).


CONCLUSIONS
The possible link between arterial elasticity and F2-IsoPs in patients with PAD suggests that oxidative modifications may be involved in alterations of arterial elastic properties in atherosclerosis.
Kals
Jaak
J
Department of Biochemistry, Center of Molecular and Clinical Medicine, University of Tartu, Tartu, Estonia. Jaak.kals@kliinikum.ee
Kampus
Priit
P
Kals
Mart
M
Zilmer
Kersti
K
Kullisaar
Tiiu
T
Teesalu
Rein
R
Pulges
Andres
A
Zilmer
Mihkel
M
D000368:Aged; D001158:Arteries / Q000378:metabolism / Q000503:physiopathology; D001161:Arteriosclerosis / Q000097:blood / Q000378:metabolism* / Q000503:physiopathology* / Q000652:urine; D015415:Biomarkers / Q000097:blood / Q000652:urine; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D016022:Case-Control Studies; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003404:Creatinine / Q000652:urine; D015237:Dinoprost / Q000031:analogs & derivatives / Q000652:urine; D004548:Elasticity; D006339:Heart Rate; D006801:Humans; D007383:Intermittent Claudication / Q000378:metabolism / Q000503:physiopathology; D016014:Linear Models; D035002:Lower Extremity / Q000098:blood supply*; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D016491:Peripheral Vascular Diseases / Q000378:metabolism / Q000503:physiopathology; D012720:Severity of Illness Index; D014280:Triglycerides / Q000097:blood
D015415:Biomarkers; D001786:Blood Glucose; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D014280:Triglycerides; C075750:8-epi-prostaglandin F2alpha; D003404:Creatinine; D015237:Dinoprost