Aspirin irreversibly acetylates serine 529 of cyclooxygenase (COX)-1, resulting in inhibition of thromboxane A2 generation by platelets and prostacyclin by endothelial cells. Because platelets lack the synthetic machinery to generate significant amounts of new COX, aspirin-induced COX-1 inhibition lasts for the lifetime of the platelet. In contrast, endothelial cells retain their capacity to generate new COX and recover normal function shortly after exposure to aspirin. Platelets have an increasingly well-defined, critical role in the acute thrombotic events associated with arterial diseases. Antiplatelet drugs have therefore assumed a major role in the therapy of these disorders. Aspirin reduces the odds of an arterial thrombotic event in high-risk patients by about 25%. However, 10%–20% of patients with an arterial thrombotic event who are treated with aspirin have a recurrent arterial thrombotic event during long-term followup. In some studies, the occurrence of an arterial thrombotic event despite aspirin therapy has been termed aspirin resistance_. However, because arterial thrombosis is multifactorial, an arterial thrombotic event in a patient may reflect treatment failure rather than _resistance_ to aspirin. Furthermore, patient non-compliance with aspirin administration is a confounding problem. There is a well-documented variability between patients (and normal volunteers) with regard to laboratory test responses to aspirin. This variability in laboratory test response has also been termed aspirin resistance. Possible mechanisms of aspirin _resistance several. There is evidence that major adverse clinical events (MACE) in the settings of acute coronary syndromes, stroke/transient ischemic attacks, and peripheral arterial disease can be predicted by some tests of aspirin resistance. However, in most of these studies the number of MACE was low, and additional studies are therefore needed. Conclusions The correct treatment, if any, of aspirin _resistance_ is unknown. No published studies address the clinical effectiveness of altering therapy based on a laboratory finding of aspirin resistance. Therefore, other than in research trials, it is not currently appropriate to test for aspirin resistance in patients or to change therapy based on such tests. A clinically meaningful definition of aspirin _resistance_ needs to be developed, based on data linking aspirin-dependent laboratory tests to clinical outcomes in patients.

Aspirin resistance: position paper of the Working Group on Aspirin Resistance / Michelson, Ad; Cattaneo, M; Eikelboom, Jw; Gurbel, P; KOTTKE MARCHANT, K; Kunicki, Tj; Pulcinelli, FABIO MARIA; Cerletti, C; Rao, Ak; PLATELET PHYSIOLOGY SUBCOMMITTEE OF THE SCIENTIFIC AND STANDARDIZATION COMMITTEE OF THE INTERNATIONAL SOCIETY ON THROMBOSIS AND, Haemostasis; WORKING GROUP ON ASPIRIN, Resistance. - In: JOURNAL OF THROMBOSIS AND HAEMOSTASIS. - ISSN 1538-7933. - STAMPA. - 3:(2005), pp. 1309-1311. [10.1111/j.1538-7836.2005.01351.x]

Aspirin resistance: position paper of the Working Group on Aspirin Resistance.

PULCINELLI, FABIO MARIA;
2005

Abstract

Aspirin irreversibly acetylates serine 529 of cyclooxygenase (COX)-1, resulting in inhibition of thromboxane A2 generation by platelets and prostacyclin by endothelial cells. Because platelets lack the synthetic machinery to generate significant amounts of new COX, aspirin-induced COX-1 inhibition lasts for the lifetime of the platelet. In contrast, endothelial cells retain their capacity to generate new COX and recover normal function shortly after exposure to aspirin. Platelets have an increasingly well-defined, critical role in the acute thrombotic events associated with arterial diseases. Antiplatelet drugs have therefore assumed a major role in the therapy of these disorders. Aspirin reduces the odds of an arterial thrombotic event in high-risk patients by about 25%. However, 10%–20% of patients with an arterial thrombotic event who are treated with aspirin have a recurrent arterial thrombotic event during long-term followup. In some studies, the occurrence of an arterial thrombotic event despite aspirin therapy has been termed aspirin resistance_. However, because arterial thrombosis is multifactorial, an arterial thrombotic event in a patient may reflect treatment failure rather than _resistance_ to aspirin. Furthermore, patient non-compliance with aspirin administration is a confounding problem. There is a well-documented variability between patients (and normal volunteers) with regard to laboratory test responses to aspirin. This variability in laboratory test response has also been termed aspirin resistance. Possible mechanisms of aspirin _resistance several. There is evidence that major adverse clinical events (MACE) in the settings of acute coronary syndromes, stroke/transient ischemic attacks, and peripheral arterial disease can be predicted by some tests of aspirin resistance. However, in most of these studies the number of MACE was low, and additional studies are therefore needed. Conclusions The correct treatment, if any, of aspirin _resistance_ is unknown. No published studies address the clinical effectiveness of altering therapy based on a laboratory finding of aspirin resistance. Therefore, other than in research trials, it is not currently appropriate to test for aspirin resistance in patients or to change therapy based on such tests. A clinically meaningful definition of aspirin _resistance_ needs to be developed, based on data linking aspirin-dependent laboratory tests to clinical outcomes in patients.
2005
Platelet; aspirin; thromboxane
01 Pubblicazione su rivista::01a Articolo in rivista
Aspirin resistance: position paper of the Working Group on Aspirin Resistance / Michelson, Ad; Cattaneo, M; Eikelboom, Jw; Gurbel, P; KOTTKE MARCHANT, K; Kunicki, Tj; Pulcinelli, FABIO MARIA; Cerletti, C; Rao, Ak; PLATELET PHYSIOLOGY SUBCOMMITTEE OF THE SCIENTIFIC AND STANDARDIZATION COMMITTEE OF THE INTERNATIONAL SOCIETY ON THROMBOSIS AND, Haemostasis; WORKING GROUP ON ASPIRIN, Resistance. - In: JOURNAL OF THROMBOSIS AND HAEMOSTASIS. - ISSN 1538-7933. - STAMPA. - 3:(2005), pp. 1309-1311. [10.1111/j.1538-7836.2005.01351.x]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/106041
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