Key result
ASA-resistant patients with acute coronary syndrome exhibited increased spontaneous and ADP-induced platelet aggregation and altered platelet enzyme activity compared to ASA-sensitive patients.
Why the study?
Do hemostasis and platelet enzyme activities differ between acetylsalicylic acid-sensitive and resistant patients with acute coronary syndrome?
Observational (n=103)
Do hemostasis and platelet enzyme activities differ between acetylsalicylic acid-sensitive and resistant patients with acute coronary syndrome?
Answers are grounded in this paper and cite their sources.
ASA-resistant patients with ACS exhibit distinct platelet metabolic changes and persistent aggregation activity despite dual antiplatelet therapy, suggesting a continued high risk of thrombotic events.
Aim. To study the features of the state of hemostasis and platelet enzymes activity in acetylsalicylic acid (ASA) sensitive and resistant patients with acute coronary syndrome (ACS). Material and methods. The study included 53 patients (25 men and 28 women) with ACS during the first 24 hours and after 10 days. The control group included 50 healthy volunteers. Before treatment the patients were tested on the sensitivity and resistance to ASA. The indicators of vascularplatelet and plasma hemostasis were evaluated as well as the NAD(P)- dependent dehydrogenases activity in platelets was assessed by the bioluminescent method in the first day of ACS before antiplatelet therapy and on day 10. Results. Increase in spontaneous [1.72 U (1.28-2.72 U) and 1.60 U (1.49-2.78 U), respectively] and ADP-induced [24.4% (21.1-29.8%) and 19.2% (16.1-22.9%), respectively] platelet aggregation, von Willebrand factor activity [159.0% (108.0-190.0%) and 155.0% (149.0-185.1%), respectively] was found in ASA-resistant patients with ACS in 1 and 10 day. Besides the ASA-resistant patients with ACS had very low pentose phosphate cycle and lactate dehydrogenase aerobic activity. They also demonstrated, compared with ASA-sensitive patients, higher intensity of aerobic respiration and the level of NADP-dependent substrate exchange between the tricarboxylic acid cycle and reactions of amino acid metabolism. Conclusion. Despite the dual antiplatelet therapy with ASA and clopidogrel, risk of thrombotic events is saved in ASA resistant patients with ACS. The metabolic changes in platelet influence their aggregation activity and cause an inadequate response to the antiplatelet therapy in ACS patients.
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Grinshtein et al. (2016) conducted an observational in Acute coronary syndrome (n=103). Acetylsalicylic acid (ASA) resistance vs. ASA-sensitive patients and healthy volunteers was evaluated on Spontaneous and ADP-induced platelet aggregation, von Willebrand factor activity, and platelet enzyme activity. ASA-resistant patients with acute coronary syndrome exhibited increased spontaneous and ADP-induced platelet aggregation and altered platelet enzyme activity compared to ASA-sensitive patients.
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