Key result
Statin omission linked to ~3-fold higher odds of elevated urinary thromboxane in suspected CAD.
Why the study?
The relation between statin therapy, in vivo thromboxane generation, and blood thrombogenicity in patients with coronary artery disease treated with high-dose aspirin had never been explored.
Does statin therapy reduce thromboxane generation in patients with suspected coronary artery disease treated with high-dose aspirin?
Observational (n=281)
Does statin therapy reduce thromboxane generation in patients with suspected coronary artery disease treated with high-dose aspirin?
Odds Ratio: 2.95 (95% CI 1.57–5.5)
p-value: p=0.0007
In aspirin-treated patients with suspected CAD, statin therapy is associated with a dose-dependent reduction in thromboxane generation and inflammation, suggesting a potential role for urinary 11-dh TxB2 measurement in optimizing statin dosing.
May support statin addition to reduce thromboxane in aspirin-treated CAD suspects; observational data leave open causal benefit and practice change.
Aspirin and statin therapy are mainstay treatments in patients with coronary artery disease (CAD). The relation between statin therapy, in vivo thromboxane (Tx) generation; a marker of inflammation, and blood thrombogenicity has never been explored. Urinary 11-dehydro (dh) TxB2 was determined in patients with suspected CAD on 325 mg daily aspirin therapy prior to undergoing cardiac catheterisation (n=281). Thrombogenicity was estimated by thrombelastographic measurement of thrombin-induced platelet-fibrin clot strength (TIP-FCS) and lipids/lipoproteins were determined by vertical density gradient ultracentrifugation/ELISA. The influence of statin therapy and dose was analysed by the atorvastatin equivalent dose (5-10 mg, 20-40 mg, or 80 mg daily). Statin therapy (n=186) was associated with a dose-dependent reduction in urinary 11-dh TxB2 (p=0.046) that was independent of LDL and apo B100 levels but was strongly related to TIP-FCS (p=0.006). By multivariate analysis, no statin therapy (n=95) and female gender were independently associated with high urinary 11-dh TxB2 [OR=2.95 (0.1.57-5.50, p=0.0007); OR=2.25 (1.24-4.05, p=0.007)], respectively. In aspirin-treated patients, statin therapy was independently and inversely associated with inflammation in a dose-dependent manner. Elevated 11-dh TxB2 was associated with a prothrombotic state indicated by high TIP-FCS. Our data suggest that measurement of urinary 11-dTxB2 may be a useful method to optimise statin dosing in order to reduce thrombotic risk.
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Bliden et al. (2014) conducted an observational in suspected coronary artery disease (CAD) (n=281). Statin therapy vs. No statin therapy was evaluated on high urinary 11-dh TxB2 (OR 2.95, 95% CI 1.57-5.50, p=0.0007). In patients with suspected CAD on high-dose aspirin, lack of statin therapy was independently associated with high urinary 11-dh TxB2 (OR 2.95; 95% CI 1.57-5.50; p=0.0007).
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