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The inhibitory effect of statins on urinary 11-dehydrothromboxane levels
S Alusik1, Z Paluch, M Lejsková
1Department of Medicine I, Thomayer University Hospital, Prague, Czech Republic. stefan.alusik@ftn.cz
Insights
Three-month statin therapy significantly reduces urinary 11-dehydrothromboxane levels, a marker for cardiovascular risk, even when combined with acetylsalicylic acid. This therapy also lowers LDL cholesterol and C-reactive protein.
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Biochemistry
Background:
- Elevated urinary 11-dehydrothromboxane indicates increased cardiovascular event risk.
- Statins are known to inhibit platelet activity.
- Acetylsalicylic acid is a common antiplatelet therapy.
Purpose of the Study:
- To evaluate the impact of 3-month statin therapy on 11-dehydrothromboxane elimination.
- To compare these effects in patients with and without concurrent acetylsalicylic acid therapy.
Main Methods:
- 58 patients received 3-month statin therapy (simvastatin, fluvastatin, or atorvastatin).
- Urinary 11-dehydrothromboxane levels were measured pre- and post-therapy.
- Plasma lipid profiles, C-reactive protein, and blood glucose were also assessed.
Main Results:
- Both patient groups (with and without acetylsalicylic acid) showed significant reductions in urinary 11-dehydrothromboxane.
- Significant decreases in LDL cholesterol, total cholesterol, and C-reactive protein were observed.
- No significant changes were noted in other measured parameters.
Conclusions:
- Three-month statin therapy effectively reduces 11-dehydrothromboxane elimination, irrespective of acetylsalicylic acid use.
- Statins offer additional benefits by lowering C-reactive protein levels.
- Combination therapy with statins and acetylsalicylic acid may enhance outcomes in patients with suboptimal thromboxane inhibition.
Aim:
Elevated urinary 11-dehydrothromboxane levels place patients at an increased risk for experiencing cardiovascular events. Statins exert an inhibitory effect on platelets. The aim of our study was to determine the effect of 3-month statin therapy on 11-dehydrothromboxane elimination in two groups of patients, one not receiving antiplatelet therapy with acetylsalicylic acid and the other receiving 100 mg acetylsalicylic acid per day.
Methods:
We examined the urinary levels of 11-dehydrothromboxane in a total of 58 patients before and after 3-month therapy with a statin at standard doses (simvastatin, fluvastatin, atorvastatin). We also examined the plasma levels of total cholesterol, triglycerides, LDL- and HDL-cholesterol, C-reactive protein, and blood glucose.
Results:
After 3-month statin therapy, both groups of patients (with and without antiplatelet therapy) showed a significant decrease in urinary 11-dehydrothromboxane levels. Significant decreases were also seen in LDL- and total cholesterol, and C-reactive protein. Changes in the other parameters were not significant.
Conclusion:
Three-month statin therapy significant reduces the rate of 11-dehydrothromboxane elimination, even in patients on acetylsalicylic acid. In addition to its usual lipid-lowering effect, it significantly decreases the plasma levels of C-reactive protein. Combination therapy with a statin plus acetylsalicylic acid may be effective even in patients with incomplete thromboxane inhibition on antiplatelet therapy with acetylsalicylic acid.
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