Key result
A one-week daily infusion of iloprost significantly decreased urinary 11-dehydro-TXB2 (380 vs 499 pg/mg creatinine, p<0.0001) in aspirin-treated patients with critical limb ischaemia.
Why the study?
Does daily iloprost infusion reduce platelet activation and oxidative stress biomarkers in patients with critical limb ischaemia on low-dose aspirin?
Does daily iloprost infusion reduce platelet activation and oxidative stress biomarkers in patients with critical limb ischaemia on low-dose aspirin?
Absolute Event Rate: 380% vs 499%
p-value: p=< 0.0001
A short-term course of iloprost significantly reduces residual thromboxane biosynthesis, oxidative stress, and platelet-derived inflammation in aspirin-treated patients with critical limb ischemia.
Iloprost infusion was associated with reduced thromboxane in aspirin-treated CLI; hypothesis-generating, requires randomized confirmation before practice change.
Platelets critically contribute to atherothrombosis and worsening ischaemia in patients with peripheral arterial disease (PAD), eventually leading to critical limb ischaemia (CLI). Furthermore, persistent platelet activation despite antiplatelet therapy has been reported in this setting. The prostacyclin analogue iloprost is currently recommended in CLI patients for its effects in relieving symptoms by promoting local perfusion. In this study, we investigated the effects of iloprost infusion on urinary 11-dehydro-TXB₂ and 8-iso-PGF(₂α) excretion rate, as in vivo indexes of thromboxane-dependent platelet activation and lipid peroxidation, respectively, and on platelet-derived proinflammatory sCD40L and nitric oxide bioavailability in 44 patients with CLI while on chronic treatment with low-dose aspirin. Daily iloprost infusion for one-week significantly decreased urinary 11-dehydro-TXB₂ [499 (277-807) vs. 380 (189-560) pg/mg creatinine, p < 0.0001] and 8-iso-PGF(₂α) [533 (316-842) vs. 334 (196-540) pg/mg creatinine, p < 0.0001] as well as plasma sCD40L [1540 (1005-3015) vs. 948 (845-2030) pg/ml, p < 0.0001]. Furthermore, a significant increase in plasma nitrate plus nitrite levels has been observed [26.8 (18.8-35.9) vs. 43.7 (33.0-75.5) μM, p < 0.0001]. A significant direct correlation was also found between urinary 8-iso-PGF(₂α) and 11-dehydro-TXB2 before and after iloprost treatment (Rho = 0.695, p < 0.0001). In conclusion, we report that a short-term course of iloprost is able to significantly reduce residual thromboxane biosynthesis, oxidative stress, endothelial dysfunction and platelet-derived inflammation in low-dose aspirin treated patients with CLI.
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Cuccurullo et al. (2010) studied Critical limb ischaemia (n=44). Iloprost infusion vs. Baseline (before treatment) was evaluated on Urinary 11-dehydro-TXB2 excretion rate (p=< 0.0001). A one-week daily infusion of iloprost significantly decreased urinary 11-dehydro-TXB2 (380 vs 499 pg/mg creatinine, p<0.0001) in aspirin-treated patients with critical limb ischaemia.
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