A serum amyloid A and LDL complex as a new prognostic marker in stable coronary artery disease

被引:78
作者
Ogasawara, K
Mashiba, S
Wada, Y
Sahara, M
Uchida, K
Aizawa, T
Kodama, T
机构
[1] Cardiovasc Inst, Minato Ku, Tokyo 1060032, Japan
[2] Ikagaku Co Ltd, Tokyo, Japan
[3] Univ Tokyo, Dept Mol Biol & Med 35, Adv Sci & Technol Res Ctr, Tokyo, Japan
关键词
atherosclerosis; coronary disease; inflammation; prognosis;
D O I
10.1016/j.atherosclerosis.2004.01.030
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Although some reports have indicated that acute phase proteins such as C-reactive protein (CRP) and serum amyloid A (SAA) can predict the prognosis in patients with acute coronary syndrome, the value of these markers in patients with stable coronary artery disease (CAD) still remains obscure. Therefore, our aim was to determine the prognostic value of inflammatory markers in patients with stable coronary artery disease. Methods and results: We conducted a prospective cohort study in 140 consecutive patients with stable coronary artery disease who had at least one coronary stenosis more than 50% in diameter seen on diagnostic coronary angiography (CAG). We determined serum levels of the SAA/LDL complex as a new marker in addition to CRP and SAA. Serum levels of the SAA/LDL complex were measured by a sandwich enzyme-linked immunosorbent assay (ELISA). End-points were defined as cardiac death, myocardial infarction, cerebral infarction, and coronary revascularization. End-point events occurred in 21 patients (2 death from myocardial infarction, 2 cerebral infarction, and 17 revascularization). Age (year) (OR = 1.14, CI: 1.05-1.25), diabetes mellitus (OR = 3.50, CI: 1.08-11.40), triglyceride (10 mg/dl) (OR = 1.12, CI: 1.01-1.23) and SAA/LDL complex (10 mug/ml) (OR = 2.32, CI: 1.05-4.70) were independently related to the events. A reconstitution experiment suggested that the SAA/LDL complex is derived by oxidative interaction between SAA and lipoproteins. Conclusions: The SAA/LDL complex reflects intravascular inflammation directly and can be a new marker more sensitive than CRP or SAA for prediction of prognosis in patients with stable coronary artery disease. (C) 2004 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:349 / 356
页数:8
相关论文
共 28 条
[1]   AMYLOID PROTEIN SAA IS AN APOPROTEIN OF MOUSE PLASMA HIGH-DENSITY LIPOPROTEIN [J].
BENDITT, EP ;
ERIKSEN, N ;
HANSON, RH .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1979, 76 (08) :4092-4096
[2]   AMYLOID PROTEIN SAA IS ASSOCIATED WITH HIGH-DENSITY LIPOPROTEIN FROM HUMAN-SERUM - (APOLIPOPROTEINS) [J].
BENDITT, EP ;
ERIKSEN, N .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1977, 74 (09) :4025-4028
[3]   ELEVATION OF C-REACTIVE PROTEIN IN ACTIVE CORONARY-ARTERY DISEASE [J].
BERK, BC ;
WEINTRAUB, WS ;
ALEXANDER, RW .
AMERICAN JOURNAL OF CARDIOLOGY, 1990, 65 (03) :168-172
[4]   Elevated levels of C-reactive protein at discharge in patients with unstable angina predict recurrent instability [J].
Biasucci, LM ;
Liuzzo, G ;
Grillo, RL ;
Caligiuri, G ;
Rebuzzi, AG ;
Buffon, A ;
Summaria, F ;
Ginnetti, F ;
Fadda, G ;
Maseri, A .
CIRCULATION, 1999, 99 (07) :855-860
[5]  
BURSTEIN M, 1970, J LIPID RES, V11, P583
[6]   Effect of prior exposure to Chlamydia pneumoniae, Helicobacter pylori, or cytomegalovirus on the degree of inflammation and one-year prognosis of patients with unstable angina pectoris or non-Q-wave acute myocardial infarction [J].
Choussat, R ;
Montalescot, G ;
Collet, JP ;
Jardel, C ;
Ankri, A ;
Fillet, AM ;
Thomas, D ;
Raymond, J ;
Bastard, JP ;
Drobinski, G ;
Orfila, J ;
Agut, H ;
Thomas, D .
AMERICAN JOURNAL OF CARDIOLOGY, 2000, 86 (04) :379-384
[7]   Low grade inflammation and coronary heart disease: prospective study and updated meta-analyses [J].
Danesh, J ;
Whincup, P ;
Walker, M ;
Lennon, L ;
Thomson, A ;
Appleby, P ;
Gallimore, JR ;
Pepys, MB .
BMJ-BRITISH MEDICAL JOURNAL, 2000, 321 (7255) :199-204
[8]  
GOLDSTEIN JL, 1983, METHOD ENZYMOL, V98, P241
[9]  
Hatch F T, 1968, Adv Lipid Res, V6, P1
[10]  
Haverkate F, 1997, LANCET, V349, P462, DOI 10.1016/S0140-6736(96)07591-5