title: Plasma pentraxin 3 is a more potent predictor of endothelial dysfunction than high-sensitive C-reactive protein.
abstract: An inflammatory response is a key event for endothelial dysfunction. Pentraxin 3 (PTX3) is an inflammatory protein produced at inflammation sites such as leukocytes and vascular endothelial cells. Here, we compared the relationships between endothelial function assessed by flow-mediated dilation (FMD), and the levels of plasma PTX3 and high-sensitive C-reactive protein (hsCRP), another inflammatory protein of the pentraxin family. Levels of FMD, PTX3 and hsCRP were measured twice within 6 to 8 months and retrospectively analyzed in 36 patients with coronary artery disease. We examined the associations between the values of FMD and the levels of PTX3 and hsCRP at the first measurement, and between the change ratios (second value/first value) of these parameters. Univariate linear regression analysis showed significantly negative correlations between FMD values and PTX3 and hsCRP levels at the first measurement, and significant associations with taking statins or calcium antagonists. Multivariate linear stepwise regression analysis identified PTX3 levels and taking statins and calcium antagonists as independent factors for endothelial function. The change ratio of FMD correlated more closely with that of PTX3 than of hsCRP (r = -0.446, P = 0.006 versus r = -0.330, P = 0.050). Significantly more patients with decreased FMD values had increased levels of PTX3 than those of hsCRP at the second measurement compared with the fi rst measurement. Furthermore, the ratio of patients with increased PTX3, but not increased hsCRP, was significantly reduced among those with increased, rather than decreased, FMD values. Endothelial dysfunction might be more accurately predicted by plasma PTX3 levels than by serum hsCRP levels.
authors.affiliation: Department of Cardiovascular Medicine, Nagasaki University Graduate School of Biomedical Sciences.
authors.forename: Tomohiko
authors.initials: T
authors.lastname: Yasunaga
authors.forename: Satoshi
authors.initials: S
authors.lastname: Ikeda
authors.forename: Seiji
authors.initials: S
authors.lastname: Koga
authors.forename: Tomoo
authors.initials: T
authors.lastname: Nakata
authors.forename: Takeo
authors.initials: T
authors.lastname: Yoshida
authors.forename: Nobuhito
authors.initials: N
authors.lastname: Masuda
authors.forename: Shigeru
authors.initials: S
authors.lastname: Kohno
authors.forename: Koji
authors.initials: K
authors.lastname: Maemura
mesh_terms: D000368:Aged; D050197:Atherosclerosis / Q000097:blood* / Q000175:diagnosis / Q000503:physiopathology; D015415:Biomarkers / Q000097:blood; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000503:physiopathology*; D002097:C-Reactive Protein / Q000378:metabolism*; D003324:Coronary Artery Disease / Q000097:blood* / Q000175:diagnosis / Q000503:physiopathology; D018450:Disease Progression; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D011237:Predictive Value of Tests; D012039:Regional Blood Flow / Q000502:physiology; D012189:Retrospective Studies; D000683:Serum Amyloid P-Component / Q000378:metabolism*; D018617:Ultrasonography, Doppler, Pulsed; D014664:Vasodilation / Q000502:physiology*; D000099153:Pentraxins
chemical_list: D015415:Biomarkers; D002097:C-Reactive Protein; D000683:Serum Amyloid P-Component; D000099153:Pentraxins