ArticleJournal of cardiovascular translational research2017
Disaggregation Following Agonist-Induced Platelet Activation in Patients on Dual Antiplatelet Therapy.
Article in Journal of cardiovascular translational research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Integrating Network Pharmacology and Metabolomics to Elucidate the Mechanism of Cryptotanshinone Against Platelet Aggregation.Current issues in molecular biology · 2025Article
- Predictive Value of Platelet Aggregation Tests in Recurrent Cerebral Ischemia and Major Bleeding.Medical science monitor : international medical journal of experimental and clinical research · 2025Article
- Review
- Micro- and Macrovascular Effects of Inflammation in Peripheral Artery Disease-Pathophysiology and Translational Therapeutic Approaches.Biomedicines · 2023Review
- Review
- The association between platelet reactivity and lipoprotein levels in Framingham Heart Study participants.Thrombosis research · 2023Article
- Microvascular Thrombosis as a Critical Factor in Severe COVID-19.International journal of molecular sciences · 2023Article
- Platelet, Fibrinolytic and Other Coagulation Abnormalities in Newly-Diagnosed Patients with Chronic Thromboembolic Pulmonary Hypertension.Diagnostics (Basel, Switzerland) · 2022Article
- A comparative study between light transmission aggregometry and flow cytometric platelet aggregation test for the identification of platelet function defects in patients with bleeding.Blood research · 2021Article
- Comparison of Light Transmission Aggregometry With Impedance Aggregometry in Patients on Potent P2Y12 Inhibitors.Journal of cardiovascular pharmacology and therapeutics · 2021Article
- Platelet reactivity in response to aspirin and ticagrelor in African-Americans and European-Americans.Journal of thrombosis and thrombolysis · 2021Article
- Ticagrelor Inhibits Toll-Like and Protease-Activated Receptor Mediated Platelet Activation in Acute Coronary Syndromes.Cardiovascular drugs and therapy · 2020Observational
- Potentiation of thrombus instability: a contributory mechanism to the effectiveness of antithrombotic medications.Journal of thrombosis and thrombolysis · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Disaggregation as the difference between maximal and final platelet aggregation by light transmission aggregometry indicates the stability of platelet aggregates. We evaluated the extent of disaggregation after platelet stimulation with adenosine diphosphate (ADP), arachidonic acid (AA), collagen, epinephrine, and thrombin receptor-activating peptide (TRAP)-6 in 323 patients on dual antiplatelet therapy with daily aspirin and clopidogrel (group 1), prasugrel (group 2), or ticagrelor (group 3) therapy. All patients in group 1 underwent elective angioplasty and stenting, whereas all patients included in groups 2 and 3 suffered from acute coronary syndromes (STEMI or NSTEMI) and underwent urgent PCI. Significant differences between maximal and final platelet aggregation were observed with all agonists throughout the groups (all p<0.001). Disaggregation was highest using AA (clopidogrel 36.5%; prasugrel/ticagrelor 100%) and ADP (clopidogrel 21.7%; prasugrel/ticagrelor 100%). In contrast, low disaggregation was observed after platelet stimulation with collagen and TRAP-6 in clopidogrel-treated patients, and after platelet stimulation with collagen and epinephrine in prasugrel- and ticagrelor-treated patients. In conclusion, pathways of platelet activation that are not inhibited by standard antiplatelet therapy allow persisting platelet aggregation and may at least in part be responsible for adverse ischemic events.
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Registered trials
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