The Effects of Long Term Use of HMG-CoA Reductase Inhibitor on the Level of Lp (a).
10.4070/kcj.1999.29.12.1350
- Author:
Jin Won KIM
;
Hong Seog SEO
;
Sung Hee SIN
;
Yung Jae OH
;
Jung Chun AHN
;
Eun Mi LEE
;
Woo Hyuk SONG
;
Young Hoon KIM
;
Wan Joo SHIM
;
Dong Joo OH
;
Young Moo RO
- Publication Type:Original Article
- Keywords:
Lipoprotein(a);
HMG-CoA reductase inhibitor;
Hyperlipidemia;
Atherosclerosis;
Plaque stability
- MeSH:
Atherosclerosis;
Cholesterol;
Genotype;
Hyperlipidemias;
Inflammation;
Lipoprotein(a);
Lipoproteins;
Metabolism;
Oxidoreductases*;
Phenotype;
Plaque, Atherosclerotic;
Prospective Studies;
Vascular Diseases
- From:Korean Circulation Journal
1999;29(12):1350-1356
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Lipoprotein (a) concentration is mainly determined by apo (a) genotype, but elevated in the atherosclerotic vascular disease more than in normal group with the same apo (a) phenotype. It has been known that Lp (a) has independent metabolism in contrast with other lipoproteins and that the use of cholesterol lowering agent such as HMG-CoA reductase inhibitor for 6 months does not change the level of Lp (a). The results of several studies suggests that Lp (a) may be related to inflammation of atherosclerotic plaque and therefore, long term use of cholesterol lowering agents make plaque stable by reduction of inflammation at plaque. We hypothesized that there is a relationship between long term use of HMG-CoA reductase inhibitor and change of Lp (a) level. We prospectively measured Lp (a), lipids and inflammatory markers before and after long term use of HMG-CoA reductase inhibitor to examine our hypothesis. METHODS: Forty-nine subjects (M:F=28:21, age=59.1+/-12.0) with hyperlipidemia were administered HMG-CoA reductase inhibitor for 15 months (minimum 6 months, maximun 44 months), and Lp (a), lipids and inflammatory markers were measured before and after use of the HMG-CoA reductase inhibitor. In control group (ninty-nine subjects, M:F=60:39, age=61.2+/-9.2), these parameters were measured more than 6 months. RESULTS: In the hyperlipidemia group who were given HMG-CoA reductase inhibitor, baseline levels of total cholesterol, TG, LDL were significantly elevated more than those of the control group, but Lp (a) and inflammatory markers were not significantly different. After use of HMG-CoA reductase inhibitor, the level of Lp (a) was reduced significantly (before 28.9+/-29.3 mg/dl, after 20.0+/-19.0 mg/dl, p=0.009), but not significantly in the control group. There was a minimal relation between baseline Lp (a) levels and percent changes of Lp (a) levels. Total cholesterol and LDL levels reduced significantly after use of the drug, but inflammatory markers did not. CONCLUSION: These data showed that Lp (a) level in the hyperlipidemia group after the long term use of HMG-CoA reductase inhibitor decreased significantly. We suggest that these changes of Lp (a) level may be one of reliable markers for plaque stability in atherosclerotic vascular disease.
