Published online before print September 20, 2004, doi: 10.1161/01.CIR.0000142664.18739.92
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(Circulation. 2004;110:1747-1753.)
© 2004 American Heart Association, Inc.
Coronary Heart Disease |
Markers of Inflammation and Rapid Coronary Artery Disease Progression in Patients With Stable Angina Pectoris
From the Coronary Artery Disease Research Unit, Department of Cardiological Sciences, St George’s Hospital Medical School, London, UK (E.Z., S.F., J.C.K.); Hospital General Universitario Gregorio Marañón, Madrid, Spain (P.A.); and Hospital General Universitario, Guadalajara, Spain (R.A.-E.).
Reprint requests to Professor Juan Carlos Kaski, Head, Cardiological Sciences, St. George’s Hospital Medical School, Cranmer Terrace, London SW17 0RE UK. E-mail jkaski{at}sghms.ac.uk
Received August 8, 2003; de novo received April 22, 2004; accepted May 21, 2004.
Background— Both endothelial cell activation and macrophage activation play a significant role in atherogenesis and atheromatous plaque vulnerability and may determine rapid coronary artery disease (CAD) progression. We sought to assess the association between serum inflammatory markers and rapid CAD progression in patients with chronic stable angina pectoris.
Methods and Results— We studied 124 chronic stable angina pectoris patients (84 men; mean age, 61±10 years) who were on a waiting list for coronary angioplasty for a mean time of 4.8±2.4 months. CAD progression was defined as 
10% diameter reduction of a pre-existing stenosis 50%, 30% diameter reduction of a stenosis <50%, development of a new stenosis 30% in a previously normal segment, or progression of any stenosis to total occlusion. CAD progression occurred in 35 patients (28%). After adjustment with binary logistic regression, neopterin (P<0.001), high-sensitivity C-reactive protein (P=0.017), matrix metalloproteinase-9 (P=0.002), soluble intercellular adhesion molecule 1 (P<0.001), and previous history of unstable angina (P=0.01) were independent predictors of rapid CAD progression. The association between rapid disease progression and inflammatory markers remained significant even when presence of complex lesions was introduced into the multivariate model.
Conclusions— Rapid CAD progression in patients with stable angina pectoris is associated with increased C-reactive protein levels and raised concentrations of biochemical markers of endothelial and macrophage activation.
Key Words: C-reactive protein • cell adhesion molecules • coronary disease • inflammation • neopterin
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