Serum amyloid A is independently related to apolipoprotein A-I but not to HDL-cholesterol in patients with angina pectoris.

Background: Inflammation 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.

Methods: On 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.

Results: Low 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.

Conclusions: SAA 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.