Prevalence of aspirin resistance measured by PFA-100

Coma-Canella, Isabel; Velasco, A.; Castaño, Sara

doi:10.1016/j.ijcard.2004.03.069

Cited by 50 publications

(29 citation statements)

References 32 publications

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“…Importantly, the PFA system is known to demonstrate a sensitivity of 95% and a specificity of 89% for the evaluation of platelet function status and ASA resistance detection, compared with classical aggregometry which demonstrated a sensitivity of 94% and a specificity of 88% [1]. The mean closure time for CEP ranged from 161 up to 193 s for ASA resistance in different studies [11, 12]. …”

Section: Discussionmentioning

confidence: 99%

“…Later it has been reported that hyperlipidemia may serve as an independent predictor of ASA resistance in poststroke cohorts [10]. A slight association of hyperlipidemia and the incidence of ASA resistance assessed by the PFA-100 analyzer has been reported [11]. However, how the blood lipid profile affects ASA resistance has not been studied yet.…”

Section: Introductionmentioning

confidence: 99%

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Plasma Triglycerides as Predictors of Platelet Responsiveness to Aspirin in Patients after First Ischemic Stroke

Karepov¹,

Tolpina²,

Kuliczkowski

et al. 2008

Cerebrovasc Dis

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Background: Although aspirin (ASA) remains the most popular and accepted agent for secondary stroke prevention, its efficacy does not exceed 25%. Platelet function monitoring in ASA users suggests that some individuals exhibit a reduced or even absent antiplatelet response after ASA. This phenomenon, also known as ‘resistance’, is prevalent in stroke survivors. We sought to evaluate the blood lipid profile in poststroke ASA users dependent on their antiplatelet response to ASA. Methods: Ninety-six consecutive ASA users after first-ever ischemic stroke confirmed by imaging were prospectively enrolled. The platelet function analyzer (PFA-100, Dade Behring, USA) was utilized to assess the response after ASA. The lipid profile (total cholesterol, high-density lipoprotein, low-density lipoprotein and triglycerides) was measured using the Cardiochek instrument (Polymer Technology, USA) from the autologuos blood samples. Results: The poststroke duration was 3–26 months, and all patients were treated with ASA for at least 3 months. The allowed daily ASA doses were from 75 up to 325 mg, with a mean of 158 mg. The mean age of the patients was 71 years, almost 60% were women, and over 85% of the patients were treated with statins. Thirty-seven patients were identified as low ASA responders, while 59 patients exhibited an adequate response. There were no differences between ASA responders and nonresponders with regard to demographics, clinical characteristics, risk factors and concomitant medications. The lipid profile biomarkers were similar between groups with the exception of triglycerides, which were significantly increased in the patients with ASA resistance, compared with ASA responders. Conclusion: The fact that hypertriglyceridemia affects platelet response to ASA has potential practical implications in light of growing evidence that ASA may exert antiplatelet properties beyond the cyclooxygenase pathway. The mechanism of such an association is unclear but may be related to the diminished platelet membrane fluidity and inability of ASA to downregulate such ‘strong’ protected platelets.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Plasma Triglycerides as Predictors of Platelet Responsiveness to Aspirin in Patients after First Ischemic Stroke

Karepov¹,

Tolpina²,

Kuliczkowski

et al. 2008

Cerebrovasc Dis

View full text Add to dashboard Cite

show abstract

“…This paradox situation was explained by the possible interaction between statins and aspirin, resulting in reduced antiaggregant effect of the latter, the antithrombotic effects of statins in hyperlipidemic patients that may occur once lipid levels normalize, and increased platelet aggregation due to hyperlipidemia. [23] Some non-steroidal analgesic antiinflammatory drugs (e.g., indomethacin, ibuprofen, naproxen, and metamizol) temporarily bind to COX-1 in platelets and prevent the irreversible inhibition of platelet thromboxane formation. [24,25] In particular, the globally common use of analgesics such as dipyrone (metamizole) in management of postoperative pain is important in terms of the drug interaction with aspirin in the early period after CABG.…”

Section: Discussionmentioning

confidence: 99%

Frequency of development of aspirin resistance in the early postoperative period and inadequate inhibition of thromboxane A2 production after coronary artery bypass surgery

Özkan¹,

Kiriş²,

Gülmen

et al. 2018

Turk Gogus Kalp Dama

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“…Not all individuals or members of groups appear to receive the benefits of aspirin administration (14 -17), but whether this phenomenon of "aspirin resistance" is a valid description or even identifiable given difficulties in clinical measurement of platelet function (17) is debated (14,15). Platelet resistance to aspirin inhibition is, however, present in ex vivo assays (42) in certain in vivo studies (15) and correlates with measures of type 2 diabetes (22,23).…”

Section: Discussionmentioning

confidence: 99%

Aspirin Hydrolysis in Plasma Is a Variable Function of Butyrylcholinesterase and Platelet-activating Factor Acetylhydrolase 1b2 (PAFAH1b2)

Zhou

Marathe

Hartiala

et al. 2013

Journal of Biological Chemistry

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Background: Aspirin use is extensive, but its short half-life limits bioavailability. Results: Butyrylcholinesterase (BChE) and PAFAH1b2 hydrolyze aspirin in plasma. Aspirin hydrolysis in plasma varies by up to 12-fold from non-genetic modulation of BChE activity. Conclusion: Two enzymes hydrolyze aspirin in plasma, and their contribution varies among individuals. Significance: Aspirin hydrolysis in plasma is variable, affecting platelet inhibition by aspirin.

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Prevalence of aspirin resistance measured by PFA-100

Cited by 50 publications

References 32 publications

Plasma Triglycerides as Predictors of Platelet Responsiveness to Aspirin in Patients after First Ischemic Stroke

Plasma Triglycerides as Predictors of Platelet Responsiveness to Aspirin in Patients after First Ischemic Stroke

Frequency of development of aspirin resistance in the early postoperative period and inadequate inhibition of thromboxane A2 production after coronary artery bypass surgery

Aspirin Hydrolysis in Plasma Is a Variable Function of Butyrylcholinesterase and Platelet-activating Factor Acetylhydrolase 1b2 (PAFAH1b2)

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