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(Circulation. 1997;96:2914-2919.)
© 1997 American Heart Association, Inc.
Articles |
Association Between Serum Amyloid A Proteins and Coronary Artery Disease
Evidence From Two Distinct Arteriosclerotic Processes
From the Divisions of Cardiology (A.I.F., A.J.L.) and Medical Genetics (L.S.R.), Department of Medicine, Department of Microbiology and Molecular Genetics (A.J.L.), Molecular Biology Institute, UCLA, Los Angeles, Calif; the University of Kentucky College of Medicine (F.C.D.), Lexington, Ky; and the Division of Medical Genetics (R.M.C., J.I.R.), Departments of Medicine and Pediatrics, Cedars-Sinai Research Institute, Los Angeles, Calif.
Background Serum amyloid A (SAA) proteins are a family of inflammatory apolipoproteins that may modify high-density lipoprotein structure and function. Elevations of SAA have been reported in unstable coronary syndromes, but the levels and types of SAA protein in humans with spontaneous or transplant-associated coronary artery disease are not known.
Methods and Results SAA levels were analyzed using an ELISA in 76 sera from 36 patients after cardiac transplantation and in 346 other individuals, 85 patients with atherosclerotic coronary disease plus 261 of their relatives. The mean SAA level was 5-fold higher in transplant patients (203±181 µg/mL [23 to 934 µg/mL]) compared with normal subjects without coronary disease (36±16 µg/mL [2.8 to 193 µg/mL], P<.005). The mean SAA level was significantly elevated in patients with transplant coronary disease (206±160 µg/mL, n=23) compared with those without (140±104 µg/mL, n=12, P=.02). Elevated SAA levels were associated with increased mortality after transplantation. On multiple regression analysis, SAA levels were predicted by corticosteroid dose, pretransplant diagnosis of atherosclerotic coronary artery disease, and the presence of transplant coronary disease. SAA levels were elevated in patients with spontaneous atherosclerotic coronary disease (49±31 µg/mL) compared with unaffected relatives (39±36 µg/mL, mean±SD, P=.02). There was no evidence for a genetic contribution to SAA levels. All inducible human SAA protein types were documented by immunoblotting in both spontaneous and transplant coronary disease.
Conclusions Environmentally determined elevations in SAA levels in patients with both spontaneous and transplant coronary artery disease provide further evidence for a potential pathophysiological link between inflammation, lipoprotein metabolism, and the development of atherosclerosis.
Key Words: amyloid • coronary disease • atherosclerosis • transplantation • apolipoproteins • cholesterol
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