PubMed · 15401535
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G SABATINI. 1949-12-08. [Peripheral arteritis].. https://pubmed.ncbi.nlm.nih.gov/15401535/
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OBJECTIVES: The aim of the study was to test the hypothesis that circulating markers of inflammation (high-sensitive C-reactive protein, hsCRP) and oxidative modification of lipids (oxidized low-density lipoprotein, oxLDL) were associated with the occurrence of echolucent rather than echogenic femoral artery plaques in a cross-sectional population based cohort of 513, 61-year-old men. BACKGROUND: The relationships between circulating oxLDL, hsCRP and the occurrence of echolucent plaques in the femoral artery have not previously been investigated. METHODS: The levels of circulating oxLDL and hsCRP were determined in plasma by ELISA. Plaque occurrence, size and echogenicity were measured by B-mode ultrasound in the right femoral artery. Assessment of plaque echogenicity was based on the classification (grades 1-4) proposed by Gray-Weale et al. RESULTS: A higher frequency of echolucent femoral plaques was observed in subjects with the metabolic syndrome and current smokers (p=0.01 and p<0.001, respectively) as well as with increasing levels of oxLDL and hsCRP (p=0.002 and p=0.005, respectively). In a multiple logistic regression analysis oxLDL and current smokers turned out to be independent associated with the presence of echolucent femoral artery plaques. CONCLUSIONS: The results of the present study support our hypothesis that circulating oxLDL is a marker of an unstable echolucent plaque phenotype in the femoral artery in man.
INTRODUCTION: Peripheral arterial disease is one aspect of atherosclerosis, a disease associated with both inflammation and hypercoagulability. Many recent studies have focused on the diversity of mechanisms by which inflammation can promote blood clotting. However, the relationship between plasma concentrations of inflammatory and hemostatic markers and the severity of atherosclerosis is not yet well studied. We want to determine the relations among selected D-dimer, C-reactive protein, fibrinogen, prothrombin time and serum amyloid A, and the ankle brachial index in patients with and without peripheral arterial disease. MATERIALS AND METHODS: In a prospective cohort study, 45 consecutive patients with peripheral arterial disease of ankle brachial index<0.90, and 44 patients without peripheral arterial disease of ankle brachial index 0.90 to 1.50 were included. D-dimer, fibrinogen, C-reactive protein, serum amyloid A, and prothrombin time were measured at the recruitment. RESULTS: Median values of serum amyloid A, D-dimer, and C-reactive protein were significantly higher in the peripheral arterial disease group than in those without peripheral arterial disease group (p<0.001). The patients with PAD had moderately higher fibrinogen levels than without PAD (p<0.01). Prothrombin time levels were normal in both groups. In multivariable regression analyses adjusting for all blood factors as well as potential confounders, patients with peripheral arterial disease, levels of serum amyloid A, and C-reactive protein showed a highly significant, inverse association with the ankle brachial index. D-dimer and fibrinogen level increase were also found to be related to lower ankle brachial index, while no association was observed between prothrombin time levels. CONCLUSIONS: Higher C-reactive protein, serum amyloid A, and D-dimer levels are showing positive association with the presence of peripheral arterial disease. C-reactive protein and serum amyloid A levels are direct relations between the ankle brachial index and the extent of vascular inflammation.
Prospective epidemiological studies have shown associations of circulating inflammatory markers with risk of CHD (coronary heart disease); however, these associations are modest after adjustment for confounding by established risk factors, and do not add significantly to the predictive value of current clinical risk scores. In contrast, experimental human studies of local arterial inflammation, such as the brachial artery infusion of TNF-alpha (tumour necrosis factor-alpha) model reported in this issue of Clinical Science by Robinson and co-workers, are of value in elucidating the pathophysiology of atherothrombosis.