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Objective Although blood thrombogenicity seems to be one of the determinant factors for the development of acute myocardial infarction (MI), it has not been dealt with in-depth. This study aimed to investigate blood thrombogenicity and its change in acute MI patients. Methods and Results We designed a prospective, observational study that included 51 acute MI patients and 83 stable coronary artery disease (CAD) patients who underwent cardiac catheterization, comparing thrombogenicity of the whole blood between: (1) acute MI patients and stable CAD patients; and (2) acute and chronic phase in MI patients. Blood thrombogenicity was evaluated by the Total Thrombus-Formation Analysis System (T-TAS) using the area under the flow pressure curve (AUC30) for the AR-chip. Acute MI patients had significantly higher AUC30 than stable CAD patients (median [interquartile range], 1,771 [1,585–1,884] vs. 1,677 [1,527–1,756], p = 0.010). Multivariate regression analysis identified acute MI with initial TIMI flow grade 0/1 as an independent determinant of high AUC30 (β = 0.211, p = 0.013). In acute MI patients, AUC30 decreased significantly from acute to chronic phase (1,859 [1,550–2,008] to 1,521 [1,328–1,745], p = 0.001). Conclusion Blood thrombogenicity was significantly higher in acute MI patients than in stable CAD patients. Acute MI with initial TIMI flow grade 0/1 was significantly associated with high blood thrombogenicity by multivariate analysis. In acute MI patients, blood thrombogenicity was temporarily higher in acute phase than in chronic phase.

• Mechanism for the occurrence of acute myocardial infarction (MI) has not been clarified. • Many silent plaque disruptions are detected in the coronary artery. • Many vulnerable plaques may disrupt and heal without causing acute MI. • Blood thrombogenicity changes dynamically due to many factors. • Blood thrombogenicity increase may directly trigger the onset of acute MI. Although the mechanism for the occurrence of acute myocardial infarction (MI) has been investigated by many pathological and clinical studies, it has not been adequately clarified yet. Although the disruption of vulnerable plaque is a well-known cause of acute MI, there are many silent plaque disruptions detected in the coronary artery by intravascular imaging studies. Therefore, many vulnerable plaques may disrupt and heal without causing acute MI. Some additional mechanisms other than the disruption of vulnerable plaque would be essential for the onset of acute MI. On the other hand, blood thrombogenicity would change dynamically due to circadian rhythms and many other factors. The combination of plaque and blood thrombogenicity would play an important and determinant role for the onset of acute MI. [ABSTRACT FROM AUTHOR]

Background: An evolving strategy in the setting of percutaneous coronary intervention (PCI) involves withdrawal of acetylsalicylic acid (ASA), or aspirin, while maintaining P2Y12 inhibition. However, the pharmacodynamic effects of this approach on blood thrombogenicity and platelet reactivity remain unknown.Objectives: This study sought to compare the antithrombotic potency of ticagrelor alone versus ticagrelor plus ASA among high-risk patients undergoing PCI with drug-eluting stents.Methods: This was a mechanistic substudy within the TWILIGHT (Ticagrelor With Aspirin or Alone in High-Risk Patients After Coronary Intervention) trial, which randomized patients undergoing PCI to ticagrelor plus placebo versus ticagrelor plus ASA following 3 months of dual antiplatelet therapy. Substudy participants were enrolled after randomization, at which time ex vivo assays to quantify thrombus size under dynamic flow conditions and platelet reactivity were performed. Pharmacodynamic assessments were repeated 1 to 6 months thereafter. The primary endpoint was thrombus size at the post-randomization visit with platelet reactivity following stimuli to arachidonic acid, collagen, adenosine diphosphate, and thrombin as secondary endpoints. Results were analyzed using analysis of covariance.Results: A total of 51 patients were enrolled, among whom 42 underwent perfusion assays at baseline and follow-up with a median time between studies of 1.5 months. The adjusted mean difference in post-randomization thrombus area was similar between groups: -218.2 μm2 (95% confidence interval [CI]: -575.9 to 139.9 μm2; p = 0.22). Markers sensitive to cyclo-oxygenase-1 blockade, including platelet reactivity in response to arachidonic acid (mean difference: 10.9 U; 95% CI: 1.9 to 19.9 U) and collagen (mean difference: 9.8 U; 95% CI: 0.8 to 18.8 U) stimuli were higher among patients receiving placebo, whereas levels of platelet reactivity were similar with adenosine diphosphate and thrombin.Conclusions: Among high-risk patients receiving drug-eluting stents, the antithrombotic potency of ticagrelor monotherapy is similar to that of ticagrelor plus ASA with respect to ex vivo blood thrombogenicity, whereas markers sensitive to cyclo-oxygenase-1 blockade are increased in the absence of ASA. (Platelet Substudy of the TWILIGHT Trial; NCT04001374). [ABSTRACT FROM AUTHOR]

Background: Although extremely high blood thrombogenicity has been reported in patients with acute myocardial infarction, it has not been clarified if the increased blood thrombogenicity is a cause of acute myocardial infarction or a mere result induced by thrombus formation at the disrupted plaque. Therefore, we examined if blood thrombogenicity is extremely increased as in acute myocardial infarction patients when disrupted plaque is present in patients with stable coronary artery disease. Methods and results: Consecutive patients (n = 38) with stable coronary artery disease who received angioscopic examination were included. Patients were divided into two groups according to presence or absence of disrupted plaque that accompanied thrombus. Blood thrombogenicity was evaluated by blood vulnerability index and compared between the patients with and without disrupted plaque. Among 38 study patients, 16 had disrupted plaque and 22 did not. Blood vulnerability index was not different between the patients with and without disrupted plaque (2395±612 vs. 3013±1476, p = 0.12). Multi-variate analysis revealed no significant association between blood vulnerability index and the presence of disrupted plaque. Conclusion: The presence of disrupted plaque, in comparison with its absence, was not associated with higher blood thrombogenicity evaluated by blood vulnerability index. [ABSTRACT FROM AUTHOR]