Thromb Haemost 2015; 114(05): 876-882
DOI: 10.1160/TH15-03-0202
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Schattauer GmbH

Aspirin for primary prevention in diabetes mellitus: from the calculation of cardiovascular risk and risk/benefit profile to personalised treatment

Francesca Santilli
1   Department of Medicine and Aging, Center of Excellence on Aging, University of Chieti, Chieti, Italy
,
Pasquale Pignatelli
2   I Clinica Medica, Sapienza University, Rome, Italy
,
Francesco Violi
2   I Clinica Medica, Sapienza University, Rome, Italy
,
Giovanni Davì
1   Department of Medicine and Aging, Center of Excellence on Aging, University of Chieti, Chieti, Italy
› Author Affiliations
Further Information

Publication History

Received: 05 March 2015

Accepted after major revision: 29 May 2015

Publication Date:
06 December 2017 (online)

Summary

Type 2 diabetes mellitus is characterised by persistent thromboxane (TX)-dependent platelet activation, regardless of disease duration. Low-dose aspirin, that induces a permanent inactivation of platelet cyclooxygenase (COX)-1, thus inhibiting TXA2 biosynthesis, should be theoretically considered the drug of choice. The most up-to-date meta-analysis of aspirin prophylaxis in this setting, which includes three trials conducted in patients with diabetes and six other trials in which such patients represent a subgroup within a broader population, reported that aspirin is associated with a non-significant decrease in the risk of vascular events, although the limited amount of available data precludes a precise estimate of the effect size. An increasing body of evidence supports the concept that less-than-expected response to aspirin may underlie mechanisms related to residual platelet hyper-reactivity despite anti-platelet treatment, at least in a fraction of patients. Among the proposed mechanisms, the variable turnover rate of the drug target (platelet COX-1) appears to represent the most convincing determinant of the inter-individual variability in aspirin response. This review intends to develop the idea that the understanding of the determinants of less-than-adequate response to aspirin in certain individuals, although not changing the paradigm of the indication to low-dose aspirin prescription in primary prevention, may help identifying, in terms of easily detectable clinical or biochemical characteristics, individuals who would attain inadequate protection from aspirin, and for whom different strategies should be challenged.

 
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