Association between LDL-cholesterol, statin therapy, physical activity and inflammatory markers in patients with stable coronary heart disease

Abstract

Evidence suggests that inflammatory parameters such as high sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), serum amyloid-A (SAA) and fibrinogen (Fib) are associated with cardiovascular morbidity and mortality. In this study we investigated the association between LDL-cholesterol (LDL-C), lipid lowering drug therapy (LLD) and inflammatory markers in 436 subjects (age 64,2 +/- 4.1 yr, BMI 27,6 +/- 3,9 kg/m2) with coronary heart disease, participating in outpatient exercise groups for cardiac rehabilitation. In a subgroup analysis (n=229), we looked at the respective effects of physical activity (PA) alone and in combination with LLD. For the whole group the levels of inflammatory markers were: hs-CRP 0,31 +/- 0,4 mg/dl; IL-6 2,04 +/- 1,6 pg/ml; SAA 6,26 +/- 14 mg/l; Fib 381 +/- 97 mg/dl. Compared to patients without LLD, those with LLD showed modestly lower concentrations for CRP (-7%) and IL-6 (-12%), (p<0.05, respectively). In patients with an LDL-C < 100 mg/dl, CRP (-12%) and Fib (-8%) were significantly lower (p<0.05, respectively) than in patients with LDL-C > 100 mg/dl. Patients with a high level of PA (PA >= 3 times/week) exhibited significantly lower values for CRP (-18%), Fib (-11%) and SAA (-37 %) (p<0.01, respectively) than patients with a low level of PA (<= 1 time/week). The combination of a high level of PA, and intake of LLD further reduced CRP (-37 %) and SAA (-45 %, with no additional decrease in Fib (-10 %) (p<0.01, respectively) compared to patients with a low level of PA and taking LLD. The data from this cross-sectional study suggest that factors such as LLD, LDL-C (< 100 mg/dl), and a high level of physical activity are associated with lower levels of inflammatory markers in patients with coronary heart disease. Particularly with respect to CRP and SAA values, a high level of PA in combination with LLD, showed the most pronounced effects. The proof of causality of these findings should further be investigated in randomized controlled trials.