Published online before print June 7, 2004, doi: 10.1161/01.CIR.0000130786.28008.56
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(Circulation. 2004;109:3158-3163.)
© 2004 American Heart Association, Inc.
Clinical Investigation and Reports |
Inflammation as a Possible Link Between Coronary and Carotid Plaque Instability
From the Cardiology Institute, Catholic University, Rome (A.L., L.M.B., G.A.L., S.C., P.S., G.L., F.B., F.C.), and Department of Cardiothoracic and Vascular Diseases, University Vita-Salute, San Raffaele Scientific Institute, Milan (D.C., A.M.), Italy.
Correspondence to Antonella Lombardo, MD, Cardiology Institute, Catholic University, L. go A. Gemelli, 8-00168 Rome, Italy. E-mail a.lombardo{at}rm.unicatt.it
Received September 12, 2003; de novo received January 13, 2004; revision received March 4, 2004; accepted March 27, 2004.
Background— Multiple complex stenoses, plaque fissures, and widespread coronary inflammation are common in acute coronary syndromes. A systemic cause of atherosclerotic plaque instability is also suggested by studies of ischemic cerebrovascular disease. We investigated the association between coronary and carotid plaque instability and the potential common causal role of inflammation.
Methods and Results— The ultrasound characteristics of carotid plaques were evaluated retrospectively in patients scheduled for coronary bypass surgery, 181 with unstable and 92 with stable angina, and prospectively in a similar group of patients, 67 with unstable and 25 with stable angina, in whom serum C-reactive protein levels were also measured. The prevalence of carotid plaques was similar in the retrospective and prospective studies and >64% in both unstable and stable coronary patients. The prevalence of complex, presumably unstable carotid plaques was 23.2% in unstable versus 3.2% in stable patients (P<0.001) in the retrospective study and 41.8% versus 8.0% (P=0.002) in the prospective study. C-reactive protein levels were higher in patients with complex (7.55 mg/L) than in those with simple (3.94 mg/L; P<0.05) plaques or without plaques (2.45 mg/L; P<0.05). On multivariate analysis, unstable angina and C-reactive protein levels >3 mg/L were independently associated with complex carotid plaques (OR, 6.09; 95% CI, 1.01 to 33.72; P=0.039, and OR, 5.80; 95% CI, 1.55 to 21.69; P=0.009, respectively).
Conclusions— In unstable angina, plaque instability may not be confined to coronary arteries, and inflammation may be the common link with carotid plaque instability. These observations may have relevant implications for understanding the mechanisms of acute widespread atherothrombotic plaque inflammation.
Key Words: angina • carotid arteries • inflammation • plaque
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