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Ticagrelor is Associated with Increased Rosuvastatin Blood Concentrations in Patients who have had a Myocardial
Tjaša Dermota1,2, Borut Jug3, Jurij Trontelj4
1University Medical Centre Ljubljana, Zaloška cesta 7, 1000, Ljubljana, Slovenia. tjasa.dermota@kclj.si.
Insights
Ticagrelor significantly increases rosuvastatin plasma concentrations approximately twofold in myocardial infarction patients. This pharmacokinetic interaction, independent of other factors, highlights potential clinical relevance for statin therapy management.
Area of Science:
- Pharmacology and Clinical Pharmacy
- Cardiovascular Medicine
- Drug Interactions
Background:
- High-dose rosuvastatin is crucial for post-myocardial infarction (MI) care.
- P2Y12 inhibitors like ticagrelor are standard therapy after MI.
- Potential drug interactions impacting statin efficacy require investigation.
Purpose of the Study:
- To evaluate the effect of ticagrelor on rosuvastatin plasma concentrations.
- To compare rosuvastatin levels in patients on ticagrelor versus other P2Y12 inhibitors (prasugrel, clopidogrel).
Main Methods:
- 93 post-MI patients on rosuvastatin 40 mg/day and a P2Y12 inhibitor were studied.
- Liquid chromatography-tandem mass spectrometry (LC-MS/MS) measured rosuvastatin concentrations.
- Concomitant use of ticagrelor, prasugrel, or clopidogrel was assessed.
Main Results:
- Rosuvastatin concentrations were ~2x higher with ticagrelor (9.7 ng/mL) vs. prasugrel (5.1 ng/mL) or clopidogrel (5.0 ng/mL).
- Ticagrelor was an independent factor influencing rosuvastatin levels (p<0.001).
- Elevated creatinine levels also correlated with higher rosuvastatin concentrations (p=0.039).
Conclusions:
- A significant pharmacokinetic interaction exists between ticagrelor and rosuvastatin.
- Concomitant ticagrelor use leads to approximately doubled rosuvastatin plasma concentrations.
- This interaction has potential clinical implications for statin therapy management in post-MI patients.
Aims:
The primary objective of this study was to determine whether concomitant therapy with ticagrelor and rosuvastatin affects rosuvastatin plasma concentrations in patients receiving rosuvastatin 40 mg/day after myocardial infarction.
Methods:
We included 93 patients who had experienced a myocardial infarction and were receiving high-dose rosuvastatin 40 mg/day and a P2Y12 receptor antagonist, either ticagrelor, prasugrel or clopidogrel. We used liquid chromatography with tandem mass spectrometry to measure rosuvastatin plasma concentrations after liquid-liquid extraction.
Results:
Rosuvastatin plasma concentrations (9.7 ng/mL) were approximately twice as high in patients receiving ticagrelor therapy as in those receiving prasugrel (5.1 ng/mL, p < 0.001) or clopidogrel (5.0 ng/mL, p = 0.009), and ticagrelor was an independent factor influencing rosuvastatin concentrations. In addition, creatinine levels were associated with increased rosuvastatin concentrations (p = 0.039).
Conclusion:
Our results suggest an important pharmacokinetic interaction between ticagrelor and rosuvastatin, leading to approximately two-fold higher rosuvastatin plasma concentrations in those receiving concomitant ticagrelor than in those receiving prasugrel or clopidogrel. The association is significant and independent of other potential factors influencing rosuvastatin levels, indicating its potential clinical relevance.
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