ScholarWorks@중앙대학교

초록

Introduction: Lipoprotein (a) [Lp(a)] has been found to be an additional risk marker for atherosclerotic cardiovascular diseases in selected cases. Lp(a) level is mainly determined by genetic variation. Hypothesis: This study investigated variables associated with Lp(a) levels and their implications. Methods: This study enrolled 2541 dyslipidemic patients by life style modification, 1154 patients by statin, 395 patients by fenofibrate, and 128 patients by withdrawal of fenofibrate. Lp(a) and lipid profiles were measured before and after management for 1~6 months. Results: In 2541 patients, baseline Lp(a) levels were influenced by many independent variables such as triglyceride (TG, r=-0.31, p<0.001), non high density lipoprotein cholesterol (r=0.15, p<0.001), alanine aminotransferase (ALT, r=-0.21, p<0.001), and alcohol drinking (r=-0.18, p<0.001). When patients were divided into 10 groups according to the baseline level, Lp(a) level of hypertriglyceridemic patients was 1/2-1/3 of that of normotriglyceridemic patients (Fig). In follow-up results, change from normotriglyceridemia to hypertriglyceridemia decreased Lp(a) level by 20-50% according to TG levels. Change from hypertriglyceridemia to normotriglyceridemia increased Lp(a) level by 15-40%. ALT levels showed similar effect on Lp(a) levels with triglyceride levels to a slightly lesser degree (Fig). Change of ALT has minor but statistically significant effect on Lp(a) level in follow-up result. Acute inflammation with high sensitive C-reactive protein >10 mg/L elevated Lp(a) level by 60% (Fig). Statin did not change Lp(a) levels, however, a small significant reduction was observed in patients with TG ≤200mg/dL (p<0.01). Fenofibrate elevated Lp(a) levels by 50% (p<0.01). But, withdrawal of fenofibrate did not change Lp(a) levels. Conclusions: Hypertriglyceridemia and acute inflammation should be considered for evaluation of Lp(a) levels to assess cardiovascular disease risk. The variable of liver function showed minor effect.

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