A brief review on high on-aspirin residual platelet reactivity
Although aspirin is effective in secondary prevention in coronary heart disease, new thromboembolic events in patients on aspirin are frequently seen. In trials on aspirin-treated patients, platelet function tests have revealed large variability in platelet aggregation. This phenomenon has been name...
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Published in | Vascular pharmacology Vol. 67-69; pp. 6 - 9 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
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United States
Elsevier Inc
01.04.2015
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ISSN | 1537-1891 1879-3649 |
DOI | 10.1016/j.vph.2015.03.018 |
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Abstract | Although aspirin is effective in secondary prevention in coronary heart disease, new thromboembolic events in patients on aspirin are frequently seen. In trials on aspirin-treated patients, platelet function tests have revealed large variability in platelet aggregation. This phenomenon has been named aspirin resistance, aspirin non-responsiveness or high-on-aspirin residual platelet reactivity.
The mechanism of aspirin antiplatelet effect is due to the inhibition of cyclooxygenase-1 enzyme in platelets. In some trials, almost all patients on aspirin have a very low level of serum thromboxane B2, indicating that the measured platelet reactivity in aspirin-treated patients might be due to platelet activation via other pathways, such as ADP or thrombin. The prevalence of real aspirin resistance seems to be very low, and probably the term “high-on-aspirin residual platelet reactivity” should be preferred to describe this phenomenon.
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AbstractList | Although aspirin is effective in secondary prevention in coronary heart disease, new thromboembolic events in patients on aspirin are frequently seen. In trials on aspirin-treated patients, platelet function tests have revealed large variability in platelet aggregation. This phenomenon has been named aspirin resistance, aspirin non-responsiveness or high-on-aspirin residual platelet reactivity.
The mechanism of aspirin antiplatelet effect is due to the inhibition of cyclooxygenase-1 enzyme in platelets. In some trials, almost all patients on aspirin have a very low level of serum thromboxane B2, indicating that the measured platelet reactivity in aspirin-treated patients might be due to platelet activation via other pathways, such as ADP or thrombin. The prevalence of real aspirin resistance seems to be very low, and probably the term “high-on-aspirin residual platelet reactivity” should be preferred to describe this phenomenon.
[Display omitted] Although aspirin is effective in secondary prevention in coronary heart disease, new thromboembolic events in patients on aspirin are frequently seen. In trials on aspirin-treated patients, platelet function tests have revealed large variability in platelet aggregation. This phenomenon has been named aspirin resistance, aspirin non-responsiveness or high-on-aspirin residual platelet reactivity. The mechanism of aspirin antiplatelet effect is due to the inhibition of cyclooxygenase-1 enzyme in platelets. In some trials, almost all patients on aspirin have a very low level of serum thromboxane B2, indicating that the measured platelet reactivity in aspirin-treated patients might be due to platelet activation via other pathways, such as ADP or thrombin. The prevalence of real aspirin resistance seems to be very low, and probably the term "high-on-aspirin residual platelet reactivity" should be preferred to describe this phenomenon. Abstract Although aspirin is effective in secondary prevention in coronary heart disease, new thromboembolic events in patients on aspirin are frequently seen. In trials on aspirin-treated patients, platelet function tests have revealed large variability in platelet aggregation. This phenomenon has been named aspirin resistance, aspirin non-responsiveness or high-on-aspirin residual platelet reactivity. The mechanism of aspirin antiplatelet effect is due to the inhibition of cyclooxygenase-1 enzyme in platelets. In some trials, almost all patients on aspirin have a very low level of serum thromboxane B2 , indicating that the measured platelet reactivity in aspirin-treated patients might be due to platelet activation via other pathways, such as ADP or thrombin. The prevalence of real aspirin resistance seems to be very low, and probably the term “high-on-aspirin residual platelet reactivity” should be preferred to describe this phenomenon. |
Author | Arnesen, H. Seljeflot, I. Pettersen, A.A. |
Author_xml | – sequence: 1 givenname: A.A. orcidid: 0000-0001-7543-475X surname: Pettersen fullname: Pettersen, A.A. email: alfaage@online.no organization: Center for Clinical Heart Research, Department of Cardiology, Oslo University Hospital, Ullevaal, Norway – sequence: 2 givenname: H. surname: Arnesen fullname: Arnesen, H. organization: Center for Clinical Heart Research, Department of Cardiology, Oslo University Hospital, Ullevaal, Norway – sequence: 3 givenname: I. surname: Seljeflot fullname: Seljeflot, I. organization: Center for Clinical Heart Research, Department of Cardiology, Oslo University Hospital, Ullevaal, Norway |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25869498$$D View this record in MEDLINE/PubMed |
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Keywords | Aspirin Cyclooxygenase Thromboxane Platelet reactivity Coronary artery disease |
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Snippet | Although aspirin is effective in secondary prevention in coronary heart disease, new thromboembolic events in patients on aspirin are frequently seen. In... Abstract Although aspirin is effective in secondary prevention in coronary heart disease, new thromboembolic events in patients on aspirin are frequently seen.... |
SourceID | pubmed crossref elsevier |
SourceType | Index Database Enrichment Source Publisher |
StartPage | 6 |
SubjectTerms | Animals Aspirin Aspirin - adverse effects Aspirin - pharmacology Blood Platelets - drug effects Blood Platelets - metabolism Cardiovascular Cardiovascular Diseases - blood Cardiovascular Diseases - chemically induced Cardiovascular Diseases - prevention & control Coronary artery disease Cyclooxygenase Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Humans Platelet Activation - drug effects Platelet Activation - physiology Platelet Aggregation - drug effects Platelet Aggregation - physiology Platelet Aggregation Inhibitors - adverse effects Platelet Aggregation Inhibitors - pharmacology Platelet Function Tests - methods Platelet reactivity Thromboxane |
Title | A brief review on high on-aspirin residual platelet reactivity |
URI | https://www.clinicalkey.com/#!/content/1-s2.0-S1537189115000683 https://www.clinicalkey.es/playcontent/1-s2.0-S1537189115000683 https://dx.doi.org/10.1016/j.vph.2015.03.018 https://www.ncbi.nlm.nih.gov/pubmed/25869498 |
Volume | 67-69 |
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