Aspirin ‘Resistance': Impact on No-Reflow, Platelet and Inflammatory Biomarkers in Diabetics after ST-Segment Elevation Myocardial Infarction

Abstract

Background: The no-reflow (NR) phenomenon exists despite percutaneous coronary intervention (PCI), and is especially prevalent in diabetics. The causes(s) of NR are not fully elucidated, but may be associated with impaired residual platelet and inflammatory reactivity during dual-antiplatelet therapy. Objective: To assess the relationship between dual-antiplatelet therapy, NR and conventional biomarkers suggestive of platelet and inflammatory response in diabetics following ST-segment elevation myocardial infarction (STEMI) treated with PCI. Methods: Sixty diabetics with (n = 27) and without NR (n = 33) were prospectively enrolled. All patients were treated with clopidogrel and aspirin. Platelet and inflammatory biomarkers were assessed serially in the peripheral blood and right atrium before and after PCI and then at 24 h, 7 days and 30 days. Results: Arachidonic acid (AA)-induced platelet aggregation and the serum thromboxane B₂ level before and after PCI (in the peripheral and right atrium blood) were significantly higher in the NR patients than in those with no NR. AA-induced aggregation >100 (AUC*min) before PCI predicted NR in diabetic patients with 96.2% sensitivity and 38.5% specificity (AUC 0.66; 95% CI 0.52-0.71; p = 0.029). There were no other correlations between NR and platelet reactivity (collagen, adenosine diphosphate, thrombin receptor agonist peptide-induced aggregation, vasodilator-stimulated phosphoprotein platelet reactivity index, soluble P-selectin, soluble CD40 ligand, platelet-derived growth factor AB and the level of platelet-monocyte aggregates) or between NR and inflammatory indices (i.e. high-sensitivity C-reactive protein, interleukin 6 and interleukin 10). Conclusion: An inadequate response to aspirin, but not to clopidogrel, may be associated with the occurrence of the NR phenomenon in diabetics with STEMI who have been treated with primary PCI.

Aspirin ‘Resistance', Diabetes Mellitus and No-Reflow: The Elusive Role of Individual Susceptibility in Myocardial Reperfusion

“…In agreement with these data, in the paper entitled ‘Aspirin ‘‘resistance'': impact on no-reflow, platelet and inflammatory biomarkers in diabetics after ST-segment elevation myocardial infarction', published in this issue of Cardiology [8], the authors made the effort to detect the mechanism behind the no-reflow, assessing the relationship between dual-antiplatelet therapy, platelet and inflammatory responses and no-reflow in a cohort of 60 diabetic patients with STEMI who were treated with primary PCI. Myocardial perfusion following angioplasty was principally evaluated by means of the TIMI myocardial perfusion (TMP) scale [9].…”

No-reflow and platelet reactivity in diabetic patients with ST-segment elevation myocardial infarction: is there a link?

“…The impact of platelets on MVO presence was investigated previously by our group and others [ 7 , 8 , 11 – 13 ]. Interestingly, there are few studies comparing platelet reactivity in STEMI with MVO diagnosed with CMR, which seems to be a “gold standard” of MVO assessment [ 3 ].…”

“…This is a sub-study of a larger series of patients included in the previously reported data [ 8 ]. In brief the previous study included patients with STEMI treated with PCI and diagnosed with diabetes before hospital admission.…”

Application of Mouse Embryonic Stem Cell Test to Detect Gender-Specific Effect of Chemicals: A Supplementary Tool for Embryotoxicity Prediction

“…Difference in sensitivity of Na + -K + -ATPase resulted in different responses to GE and DG in males and females. Large amount of studies indicated that, compared to males, females tolerated AS better and therefore were subject to aspirin resistance, although the conclusion is controversial and the mechanism has not been fully elucidated. − Even though no systemic study on female susceptibility has been performed, a great number of clinical cases revealed a higher incidence of some adverse drug reactions in female cardiovascular system, which provided an evidence of potential female susceptibility.…”