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European Heart Journal 2001 22(17):1572-1577; doi:10.1053/euhj.2000.2554
Copyright © 2001 by the European Society of Cardiology.
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Autoantibodies against oxidized low density lipoproteins in patients with stable angina, unstable angina or peripheral vascular disease; pathophysiological implications

C. Monacoa, F. Creaa,f1, G. Niccolia, F. Summariaa, D. Cianflonea, R. Bordoneb, G. Bellomob and A. Maseria

a Istituto di Cardiologia, Università Cattolica del Sacro Cuore, Rome, Italy
b Dipartimento di Scienze Mediche, Università di Torino, Novara, Italy

revised November 27, 2000; accepted November 29, 2000

Abstract

Background Antibody antioxidized low density lipoproteins (oxLDL) might play a role both in atherogenesis and in the pathogenesis of acute coronary syndromes.

Methods and Results Antibody titres to oxLDL and levels of C-reactive protein were compared in unstable angina, stable angina or peripheral artery disease. Antibody titres to LDL oxidated by CuSO4for 2, 4 and 18h (Cu-oxLDL-Ab2-4-18) or by peroxidase (HRP-oxLDL-Ab) were assessed by ELISA. Cu-oxLDL-Ab2-4-18were consistently higher in peripheral artery disease than in unstable angina (P<0·001, P<0·001, P=0·01, respectively) or in stable angina (P<0·001, P=0·01, P=ns) but similar in unstable and stable angina. Accordingly, HRP-oxLDL-Ab were higher in peripheral artery disease than in unstable angina (P<0·001) or stable angina (P=0·04) but similar in unstable and stable angina. The number of arterial stenoses was higher in peripheral artery disease than unstable and stable angina (P<0·01). Cu-oxLDL-Ab and HRP-oxLDL-Ab correlated with the severity of atherosclerosis (P<0·01, R=0·4;P=0·02, R=0·3 respectively). Conversely, C-reactive protein levels were higher in unstable than in stable angina (P<0·001) or in peripheral artery disease (P<0·03) but similar in stable angina and peripheral artery disease and did not correlate with the severity of atherosclerosis.

Conclusion The autoimmune response to oxLDL is likely to play an important role in atherogenesis but not in precipitating acute coronary syndromes.

Key Words: Lipoproteins, antibodies, inflammation, coronary artery disease, peripheral artery disease

f1 Correspondence: Prof. Filippo Crea, Istituto di Cardiologia, Università Cattolica del Sacro Cuore, L.go A. Gemelli, 8, 00168 Rome, Italy.

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