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Effect of withdrawal of statin on C-reactive protein
Kun-Tai Lee1, Wen-Ter Lai, Chin-Sheng Chu
1Section of Cardiology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
Insights
Statin therapy lowers C-reactive protein, a risk factor for heart disease. Stopping statins caused C-reactive protein levels to rise, potentially increasing cardiac event risk.
Area of Science:
- Cardiology
- Biochemistry
Background:
- C-reactive protein (CRP) is a risk factor for coronary artery disease.
- Statins lower CRP levels and are used for hyperlipidemia.
- The effect of statin withdrawal on CRP levels is not well understood.
Purpose of the Study:
- To investigate the changes in C-reactive protein (CRP) levels after abrupt cessation of statin therapy.
- To assess the impact of statin withdrawal on lipid profiles.
Main Methods:
- Twenty hyperlipidemia patients received atorvastatin (10 mg/day) for 3 months.
- Lipid profiles and CRP levels were measured before, immediately after, and 3 days post-statin withdrawal.
Main Results:
- Statin therapy significantly reduced total cholesterol, LDL-cholesterol, and CRP levels.
- CRP levels increased significantly by the second day after statin withdrawal.
- Total cholesterol and LDL-cholesterol did not increase within 3 days of statin withdrawal.
Conclusions:
- Abruptly stopping statin therapy leads to an increase in C-reactive protein (CRP) levels.
- Elevated CRP following statin withdrawal may contribute to cardiac events in patients with atherosclerotic heart disease.
Background:
C-reactive protein is considered a risk factor for coronary artery disease. In addition to its lipid-lowering properties, statin decreases the level of C-reactive protein. Abrupt cessation of statin therapy during treatment could increase the incidence of cardiac events in patients with atherosclerotic heart disease. The changes of C-reactive protein after withdrawal of statin therapy are still unknown.
Methods:
Twenty patients with hyperlipidemia received statin (atorvastatin, 10 mg/day) therapy for 3 months. The levels of lipid profiles and C-reactive protein were assessed before receiving the statin therapy, immediately after 3 months of therapy, and on the 3 consecutive days after withdrawal of statin treatment.
Results:
After 3 months of statin therapy, the total cholesterol, low-density lipoprotein cholesterol (LDL-chol), and C-reactive protein were significantly reduced (264.94 +/- 16.23 vs. 183.44 +/- 16.34 mg/dl, 183.17 +/- 34.56 vs. 122.00 +/- 17.66 mg/dl, and 2,309.00 +/- 437.85 vs. 1,257.95 +/- 207.99 ng/ml, respectively). The level of C-reactive protein increased on the second day after withdrawal of statin therapy (2,590.14 +/- 1,045.05 vs. 1,257.95 +/- 207.99 ng/ml); however, the total cholesterol and LDL-chol did not increase during the 3-day period after withdrawal of statin therapy.
Conclusions:
The increase in the level of C-reactive protein after withdrawal of statin therapy may be a contributing factor to the increased incidence of cardiac events in patients who have abruptly stopped statin therapy.
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