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Published on: November 10, 2017
Comparison of atorvastatin, pitavastatin and rosuvastatin for residual cardiovascular risk using non-fasting blood
Hirokazu Kakuda1, Munetoshi Matoba, Hideaki Nakatoh
1Kakuda Clinic , Ishikawa , Japan.
Insights
Pitavastatin effectively increased high-density lipoprotein cholesterol (HDL-C), apolipoprotein A-I (Apo A-I), and lipoprotein lipase (LPL) mass, suggesting it may be a superior statin for improving these cardiovascular risk factors beyond low-density lipoprotein cholesterol (LDL-C).
Area of Science:
- Cardiology
- Pharmacology
- Biochemistry
Background:
- Low-density lipoprotein cholesterol (LDL-C) is a primary risk factor for cardiovascular disease.
- Some patients with coronary heart disease (CHD) have controlled LDL-C, highlighting the need to address other risk factors.
- Dyslipidemia management requires comprehensive assessment beyond LDL-C levels.
Purpose of the Study:
- To compare the effects of switching between atorvastatin (ATO), pitavastatin (PIT), and rosuvastatin (ROS) on lipid profiles and lipoprotein fractions in dyslipidemic patients.
- To evaluate the impact of different statin treatments on high-density lipoprotein cholesterol (HDL-C), apolipoprotein A-I (Apo A-I), and lipoprotein lipase (LPL) mass.
- To determine if pitavastatin demonstrates superior efficacy in improving HDL-C and related markers compared to atorvastatin and rosuvastatin.
Main Methods:
- 129 outpatients with dyslipidemia were enrolled and switched between ATO (10 mg/day), PIT (2 mg/day), or ROS (2.5 mg/day).
- Lipid profiles and lipoprotein fractions were analyzed using polyacrylamide gel electrophoresis (PAGE) before and after 3 months of treatment.
- Non-fasting blood samples were used for all analyses.
Main Results:
- LDL-C levels remained stable around 2.59 mmol/L across all statin groups after switching.
- HDL-C significantly increased with PIT treatment (ATO→PIT and ROS→PIT) but decreased with PIT→ATO.
- Changes in HDL-C correlated positively with Apo A-I and LPL mass, and negatively with Lp(a) and intermediate-density lipoprotein (IDL).
Conclusions:
- Atorvastatin, pitavastatin, and rosuvastatin exhibit comparable efficacy in lowering LDL-C.
- Pitavastatin demonstrated the greatest effectiveness in increasing HDL-C, Apo A-I, and LPL mass.
- Statin-induced changes in HDL-C are closely associated with alterations in Apo A-I and LPL mass, indicating their importance in cardiovascular risk management.
Background:
Low-density lipoprotein cholesterol (LDL-C) is a major cardiovascular risk. However, some patients show symptoms of coronary heart disease (CHD) even though their LDL-C is strictly controlled. Therefore, it is important to treat other risk factors.
Methods:
Some 129 outpatients with dyslipidemia who were treated with either atorvastatin 10 mg/day (ATO), pitavastatin 2 mg/day (PIT), or rosuvastatin 2.5 mg/day (ROS) were enrolled. After informed consent was obtained, these patients were switched to another statin. Lipid profiles and lipoprotein fraction by polyacrylamide gel electrophoresis (PAGE) were compared between before and after 3 months of treatment with non-fasting blood sample.
Results:
LDL-C did not show any significant changes after switching and was maintained around 2.59 mmol/L in all groups. High-density lipoprotein cholesterol (HDL-C) was significantly increased in group ATO→PIT (1.43→1.54 mmol/L, p = 0.0010) and ROS→PIT (1.46→1.57 mmol/L, p = 0.0004), and was significantly decreased in group PIT→ATO (1.44→1.36 mmol/L, p = 0.0290). Apolipoprotein A-I (Apo A-I) and preheparin lipoprotein lipase (LPL) mass showed similar changes in HDL-C. Changes in HDL-C showed a significant positive correlation with those in Apo A-I and preheparin LPL mass, and a little but significant negative correlation with changes in Lp(a) and intermediate density lipoprotein (IDL) fraction.
Conclusions:
ATO, PIT, and ROS have comparable effect on LDL-C lowering. Changes in HDL-C were similar to those in Apo A-I and preheparin LPL mass, and PIT was the most effective treatment in increasing HDL-C, Apo A-I, and preheparin LPL mass.
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