Multiple anti‐atherosclerotic treatments impair aspirin compliance: effects on aspirin resistance

@article{Pignatelli2008MultipleAT,
  title={Multiple anti‐atherosclerotic treatments impair aspirin compliance: effects on aspirin resistance},
  author={Pasquale Pignatelli and Serena di Santo and Francesco Barill{\`a} and Carlo Gaudio and Francesco Violi},
  journal={Journal of Thrombosis and Haemostasis},
  year={2008},
  volume={6}
}
Funato M, Tamai H, Konno M, Kamide K, Kawano Y, Miyata T, Fujimura Y. Mutations and common polymorphisms in ADAMTS13 gene responsible for von Willebrand factor-cleaving protease activity. Proc Natl Acad Sci U S A 2002; 99: 11902– 7. 7 Jang MJ, Kim NK, Chong SY, Kim HJ, Lee SJ, Kang MS, Oh D. Frequency of Pro475Ser polymorphism of ADAMTS13 gene and its association with ADAMTS-13 activity in the Korean population. Yonsei Med J 2008; 49: 405–8. 8 Gao W, Dai L, Su J, Wang Z, Ruan C. The frequency… 
ADAMTS13 P475S polymorphism causes a lowered enzymatic activity and urea lability in vitro
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TLDR
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Incomplete inhibition of platelet function as assessed by the platelet function analyzer (PFA-100) identifies a subset of cardiovascular patients with high residual platelet response while on aspirin
Sixty-six patients with a history of ischemic events (myocardial infarction, unstable angina, or stroke) on chronic aspirin therapy were studied by different platelet function tests: 37 patients had
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References

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TLDR
This work presents a meta-analysis of Platelet Function Studies and Hemostasis in relation to Thrombosis and Haemostasis that shows clear trends in prognosis and in particular in cases of high-risk individuals, where the prognosis for survival is poorer for those with high levels of Aspirin resistance.
Persistent production of platelet thromboxane A2 in patients chronically treated with aspirin
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In some patients chronically treated with aspirin platelet production of TxA2 may persist and account for enhanced platelet aggregation, and incomplete inhibition of COX‐1 seems to be implicated in persistent T xA2 production.
Laboratory detection of 'aspirin resistance': what test should we use (if any)?
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TLDR
It is incorrect to consider ‘resistant’ to aspirin all those patients who experience atherothrombotic events while on treatment, and this phenomenon has been named ‘clinical resistance’, but it should be more properly termed ‘treatment failure’.
Aspirin resistance: is this term meaningful?
TLDR
Recurrence of cardiovascular events in aspirin-treated patients does not necessarily suggest ‘drug failure’, and the existence of ‘clinical resistance’ to aspirin should be reconsidered.
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TLDR
It is shown that patients biochemically identified as having laboratory aspirin resistance are more likely to also have "clinical resistance" to aspirin because they exhibit significantly higher risks of recurrent cardiovascular events compared with patients who are identified as (laboratory) aspirin sensitive.
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TLDR
There is a residual arachidonic acid–induced platelet activation in aspirin-treated patients that is caused by underdosing and/or noncompliance in only ≈2% of patients and in the remaining patients, occurs via a cyclooxygenase-1 and cyclo oxygenase-2 independent pathway.
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