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Relationship between atorvastatin dose and the harm caused by torcetrapib
Philip J Barter1, Kerry-Anne Rye, Mohan S Beltangady
1The Heart Research Institute, Sydney, Australia. barterp@hri.org.au
Insights
The cholesteryl ester transfer protein (CETP) inhibitor torcetrapib caused harm, specifically increased mortality and cardiovascular events, but only in patients taking a low dose (10 mg) of atorvastatin. Higher atorvastatin doses appeared to mitigate these risks.
Area of Science:
- Cardiovascular Pharmacology
- Clinical Trial Analysis
- Drug Safety Evaluation
Background:
- Development of cholesteryl ester transfer protein (CETP) inhibitor torcetrapib was halted due to safety concerns.
- The ILLUMINATE trial indicated increased all-cause mortality (ACM) and major cardiovascular events (MCVEs) with torcetrapib use.
Purpose of the Study:
- To investigate the specific patient subgroup experiencing harm from torcetrapib.
- To determine if the dose of atorvastatin influenced torcetrapib-associated risks.
Main Methods:
- Subgroup analysis of the ILLUMINATE trial data.
- Statistical analysis of ACM and MCVEs in relation to torcetrapib and atorvastatin dosage.
- Multivariable regression to adjust for clinical risk factors.
Main Results:
- Torcetrapib-associated harm (ACM and MCVEs) was confined to the 10 mg atorvastatin subgroup.
- No increased risk was observed when torcetrapib was coadministered with higher doses of atorvastatin.
- Adjusting for baseline risk factors did not alter the observed harm in the 10 mg atorvastatin subgroup.
Conclusions:
- The adverse effects of torcetrapib were specifically linked to coadministration with low-dose atorvastatin (10 mg).
- Higher doses of atorvastatin may offer a protective effect against torcetrapib-induced harm.
- The mechanism of harm is independent of lipid changes, blood pressure, or electrolytes.
Abstract:
Development of the cholesteryl ester transfer protein (CETP) inhibitor, torcetrapib, was halted after the ILLUMINATE trial revealed an increase in both all-cause mortality (ACM) and major cardiovascular events (MCVEs) associated with its use. We now report that the harm caused by torcetrapib was confined to those in the 10 mg atorvastatin subgroup for both ACM [hazard ratio (HR) = 2.68, 95% CI (1.58, 4.54), P < 0.0001] and MCVEs [HR = 1.41, 95% CI (1.14, 1.74), P = 0.002], with no evidence of harm when torcetrapib was coadministered with higher doses of atorvastatin. In the atorvastatin 10 mg subgroup, age, prior heart failure and stroke were significantly associated with ACM, independent of torcetrapib treatment, whereas low apoA-I, smoking, hypertension, heart failure, myocardial infarction, and stroke were independently associated with MCVEs. After adjusting for these factors, the HR associated with torcetrapib treatment in the 10 mg atorvastatin subgroup remained elevated for both ACM [HR = 2.67, 95% CI (1.57, 4.54), P < 0.001] and MCVE [HR = 1.36, 95% CI (1.10, 1.69), P = 0.005]. Thus, the harm caused by torcetrapib was confined to individuals taking atorvastatin 10 mg. The harm could not be explained by torcetrapib-induced changes in lipid levels, blood pressure, or electrolytes. It is conceivable that higher doses of atorvastatin protected against the harm caused by torcetrapib.
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