Niccoli G et al. (2008) Plasma levels of thromboxane A2 on admission are associated with no-reflow after primary percutaneous coronary intervention. Eur Heart J 29: 1843–1850

Platelet aggregation is thought to be involved in the pathogenesis of the 'no-reflow' phenomenon, in which tissue perfusion is not improved after restoration of arterial patency. Niccoli et al. hypothesized that a high plasma level of thromboxane A2—a mediator of platelet activation—could be associated with no-reflow after primary percutaneous coronary intervention (PCI).

Their single-center study included 47 patients with ST-segment elevation myocardial infarction who were scheduled to undergo primary PCI. After arterial recanaliation, angiographic no-reflow (defined as Thrombosis In Myocardial Infarction flow grade ≤2, or flow grade 3 with myocardial blush grade of <2) occurred in 46.8% of patients. Electrocardiographic no-reflow was defined as a reduction in the ST-segment elevation value of 50% or less from baseline, and occurred in 44.7% of patients. Plasma levels of thromboxane A2 were higher, on average, among patients with angiographic no-reflow, and electrocardiographic no-reflow, than in those with normal perfusion (17.74 pg/ml versus 3.91 pg/ml, P = 0.005, and 19.58 pg/ml versus 3.99 pg/ml, P = 0.001, respectively). Multivariate analysis revealed that plasma level of thromboxane A2 was an independent predictor of both angiographic no-reflow (P = 0.04) and electrocardiographic no-reflow (P = 0.013). The incidence of no-reflow under both criteria increased with rising tertiles of thromboxane A2 level (P <0.01 for trend). The authors concluded that thromboxane A2 could represent a novel therapeutic target in patients who undergo primary PCI.