Serum amyloid A is independently related to apolipoprotein A-I but not to HDL-cholesterol in patients with angina pectoris |
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| Authors: | Irena Korita Anyla Bulo Michel R Langlois Eline Verhoye Victor Blaton |
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| Institution: | 1. Laboratory Department, Faculty of Medicine, University Hospital Center “Mother Teresa”, Tirana, Albania;2. Department of Laboratory Medicine AZ St Jan Av Brugge, UGent and KU, Leuven, Belgium;1. Department of Cardiothoracic Surgery, Affiliated People''s Hospital of Jiangsu University, Zhenjiang 212002, China;2. Department of Cardiovascular Medicine, Cardiovascular Clinical College of Tianjin Medical University & TEDA International Cardiovascular Hospital, Tianjin 300457, China;3. Department of Cardiology, Wuxi People''s Hospital Affiliated to Nanjing Medical University, Wuxi 214002, China;1. Dept. of Medical Sciences, Cardiology, Uppsala University, 75237 Uppsala, Sweden;2. Dept. of Medical Sciences, Clinical Chemistry, Uppsala University, 75237 Uppsala, Sweden;3. Uppsala Clinical Research Center, Uppsala University, 75237 Uppsala, Sweden;4. Dept. of Medicine, Division of Cardiology, University of Alberta, Edmonton, AB T6G2H7, Canada;5. Duke Translational Medicine Institute, Duke University School of Medicine, 2301 Erwin Road, Durham, NC 27710, USA;6. Thoraxcenter, Dept. of Cardiology, Erasmus Medical Center, ''s Grafendijkwal 230, 3000 CA Rotterdam, The Netherlands;1. Department of Cardiac Surgery, Hospital Universitari Germans Trias i Pujol, Badalona, Barcelona, Spain;2. Department of Cardiac, Thoracic and Vascular Sciences, University of Padua, Italy;3. Department of Cardiovascular and Thoracic Surgery, University of Rennes, France;4. Department of Cardiothoracic Surgery, St. Antonius Hospital, Nieuwegein, The Netherlands;5. Department of Cardiothoracic Surgery, School of Medicine, University of Coimbra, Portugal;1. Department of Pathology and Laboratory Medicine, Landseed Hospital, Taoyuan, Taiwan;2. Department of Cardiology, Landseed Hospital, Taoyuan, Taiwan;3. Department of Microbiology and Immunology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan;4. Center for Reproductive Medicine and Sciences, Taipei Medical University, Taipei, Taiwan;1. Department of Cardiology, Sichuan Province Hospital of CAPF, Leshan, China;2. Department of Obstetrics and Gynecology, Molecular and Genetic Unit, Peking University People''s Hospital, Beijing, China |
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| Abstract: | BackgroundInflammation processes are considered important links between classical lipid risk factors and the progression of atherosclerosis. The interrelationship of high density lipoproteins (HDL) and apolipoprotein apoA-1 with acute phase proteins and cytokines was examined in a clinical setting of patients with angina pectoris.MethodsOn exclusion criteria (myocardial infarction, heart failure, CHD > 2 years, anticoagulant therapy), 198 patients were recruited and were subdivided according to angiographically documented stenosis, no stenosis vs. = 50% stenosis, in accordance with CASS guidelines. Lipids, apoA-1 and apoB, C-reactive protein (hs-CRP), fibrinogen, serum amyloid A (SAA) and cytokines (IL-6, IL-8, IL-10, IL2R, TNFα) were measured.ResultsLow HDL-C (and apoA-I) is associated with advanced coronary stenosis (= 50%) and with the number of diseased vessels, independent of age, gender, diabetes, smoking and lipid-lowering therapy. In contrast to hs-CRP and fibrinogen, SAA as well as cytokine levels were not significantly associated with stenosis. SAA (P = 0.0003) and diabetes (P = 0.0002) were strong predictors of apoA-I concentration independent of age, gender, BMI, smoking, CRP, as well as IL-6 in a multiple regression model. High SAA (P = 0.0067) and TG (P = 0.0123) were significant predictors of apoA-I/HDL-C ratio. However, SAA was not independently related to HDL-C.ConclusionsSAA is independently and inversely related to apoA-I but not to HDL-C in patients with angina pectoris, reflecting the effect of SAA on the quality of HDL particles. However, HDL-c but not SAA is inversely related to the degree of coronary artery stenosis. |
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