» Articles » PMID: 18759978

Non-compliance is the Predominant Cause of Aspirin Resistance in Chronic Coronary Arterial Disease Patients

Overview
Journal J Transl Med
Publisher Biomed Central
Date 2008 Sep 2
PMID 18759978
Citations 21
Authors
Affiliations
Soon will be listed here.
Abstract

Background: Our previous publication showed that 9% of patients with a history of myocardial infarction MI. could be labeled as aspirin resistant; all of these patients were aspirin resistant because of non-compliance. This report compares the relative frequency of aspirin resistance between known compliant and non-compliance subjects to demonstrate that non-compliance is the predominant cause of aspirin resistance.

Methods: The difference in the slopes of the platelet prostaglandin agonist (PPA) light aggregation curves off aspirin and 2 hours after observed aspirin ingestion was defined as net aspirin inhibition.

Results: After supposedly refraining from aspirin for 7 days, 46 subjects were judged non-compliant with the protocol. Of the remaining 184 compliant subjects 39 were normals and 145 had a past history of MI. In known compliant subjects there was no difference in net aspirin inhibition between normal and MI subjects. Net aspirin inhibition in known compliant patients was statistically normally distributed. Only 3% of compliant subjects (2 normals and 5 MI) had a net aspirin inhibitory response of less than one standard deviation which could qualify as a conservative designation of aspirin resistance. A maximum of 35% of the 191 post MI subjects could be classified as aspirin resistant and/or non-compliant: 9% aspirin resistant because of non-compliance, 23% non-compliant with the protocol and possibly 3% because of a decreased net aspirin inhibitory response in known compliant patients.

Conclusion: Our data supports the thesis that the predominant cause of aspirin resistance is noncompliance.

Citing Articles

Personalized Dual Antiplatelet Therapy in Acute Coronary Syndromes: Striking a Balance Between Bleeding and Thrombosis.

Shpigelman J, Proshkina A, Daly M, Cox D Curr Cardiol Rep. 2023; 25(7):693-710.

PMID: 37261665 PMC: 10307718. DOI: 10.1007/s11886-023-01892-9.


Antiplatelet Use in Ischemic Stroke.

Kamarova M, Baig S, Patel H, Monks K, Wasay M, Ali A Ann Pharmacother. 2022; 56(10):1159-1173.

PMID: 35094598 PMC: 9393649. DOI: 10.1177/10600280211073009.


Perioperative changes of response to antiplatelet medication in vascular surgery patients.

Hummel T, Meves S, Breuer-Kaiser A, Dusterwald J, Muhlberger D, Mumme A PLoS One. 2020; 15(12):e0244330.

PMID: 33373378 PMC: 7771706. DOI: 10.1371/journal.pone.0244330.


[Evaluation of treatment adaptation for low response to ASA in vascular surgery].

Hummel T, Meves S, Breuer-Kaiser A, Dusterwald J, Muhlberger D, Mumme A Chirurg. 2020; 92(7):640-646.

PMID: 32945920 PMC: 8484201. DOI: 10.1007/s00104-020-01280-x.


Prevalence rate of laboratory defined aspirin resistance in cardiovascular disease patients: A systematic review and meta-analysis.

Ebrahimi P, Farhadi Z, Behzadifar M, Shabaninejad H, Abolghasem Gorji H, Taheri Mirghaed M Caspian J Intern Med. 2020; 11(2):124-134.

PMID: 32509239 PMC: 7265510. DOI: 10.22088/cjim.11.2.124.


References
1.
Grotemeyer K, Scharafinski H, Husstedt I . Two-year follow-up of aspirin responder and aspirin non responder. A pilot-study including 180 post-stroke patients. Thromb Res. 1993; 71(5):397-403. DOI: 10.1016/0049-3848(93)90164-j. View

2.
von Pape K, Strupp G, Bonzel T, Bohner J . Effect of compliance and dosage adaptation of long term aspirin on platelet function with PFA-100 in patients after myocardial infarction. Thromb Haemost. 2005; 94(4):889-91. DOI: 10.1160/TH05-04-0889. View

3.
Schwartz K, Schwartz D, Ghosheh K, Reeves M, Barber K, DeFranco A . Compliance as a critical consideration in patients who appear to be resistant to aspirin after healing of myocardial infarction. Am J Cardiol. 2005; 95(8):973-5. DOI: 10.1016/j.amjcard.2004.12.038. View

4.
Frelinger 3rd A, Furman M, Linden M, Li Y, Fox M, Barnard M . Residual arachidonic acid-induced platelet activation via an adenosine diphosphate-dependent but cyclooxygenase-1- and cyclooxygenase-2-independent pathway: a 700-patient study of aspirin resistance. Circulation. 2006; 113(25):2888-96. DOI: 10.1161/CIRCULATIONAHA.105.596627. View

5.
Ho P, Spertus J, Masoudi F, Reid K, Peterson E, Magid D . Impact of medication therapy discontinuation on mortality after myocardial infarction. Arch Intern Med. 2006; 166(17):1842-7. DOI: 10.1001/archinte.166.17.1842. View