Published online before print April 25, 2005, doi: 10.1161/01.CIR.0000163569.97918.C0
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(Circulation. 2005;111:2203-2209.)
© 2005 American Heart Association, Inc.
Vascular Medicine |
Inflammation and Carotid Artery—Risk for Atherosclerosis Study (ICARAS)
From the Departments of Angiology (M.S., W.M., S.S., J.A., R.N., E.T., B.K., C.M., M.P., E.M.), Medical and Chemical Laboratory Diagnostics (M.E., H.R., O.W.), Neurology (W.L.), and Cardiology (G.M.), University of Vienna, Medical School, Vienna, Austria.
Correspondence to Martin Schillinger, MD, Department of Internal Medicine II, Division of Angiology, University of Vienna, Medical School, Waehringer Guertel 18-20, A-1090 Vienna, Austria. E-mail martin.schillinger{at}meduniwien.ac.at
Received June 2, 2004; revision received January 12, 2005; accepted January 19, 2005.
Background— Compelling evidence suggests that inflammation is fundamentally involved in the pathogenesis of atherosclerosis; however, temporal correlation between inflammation and morphological features of atherosclerosis progression has not been demonstrated unequivocally.
Methods and Results— We prospectively studied 1268 consecutive patients who were initially asymptomatic with respect to carotid artery disease. Patients underwent serial carotid ultrasound investigations at baseline and after a follow-up interval of a median of 7.5 months (range 6 to 9 months), with measurement of carotid flow velocities and categorization of carotid arteries as 0% to 29%, 30% to 49%, 50% to 69%, 70% to 89%, or 90% to 99% stenosed or occluded. High-sensitivity C-reactive protein (hs-CRP) and serum amyloid A (SAA) were measured at baseline and follow-up. Progression of carotid atherosclerosis was found in 103 (8.1%) of 1268 patients. Hs-CRP and SAA, respectively, at baseline (P=0.004 and P=0.014) and follow-up (P<0.001 and P<0.001) and the change from baseline to follow-up (P<0.001 and P<0.001) were significantly associated with progressive atherosclerosis. Adjusted ORs (95% CI) for atherosclerosis progression with increasing quintiles of baseline hs-CRP were 1.65 (0.71 to 3.84), 1.87 (0.8 to 4.37), 3.32 (1.49 to 7.39), and 3.65 (1.65 to 8.08), and with increasing quintiles of baseline SAA, they were 0.86 (0.38 to 1.92), 0.99 (0.49 to 1.99), 1.72 (0.91 to 3.28), and 2.28 (1.24 to 4.20), respectively, compared with the lowest quintiles.
Conclusions— These findings supply evidence for a close temporal correlation between inflammation and morphological features of rapidly progressive carotid atherosclerosis, which suggests that elevation or increase of the inflammatory biomarkers hs-CRP and SAA identifies the presence of active atherosclerotic disease.
Key Words: inflammation • atherosclerosis • carotid arteries • plaque • amyloid
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