Absorption kinetics of low‐dose chewable aspirin – implications for acute coronary syndromes

Hobl, Eva‐Luise; Schmid, Rainer; Stimpfl, Thomas; Ebner, Janine; Jilma, Bernd

doi:10.1111/eci.12373

Cited by 12 publications

(11 citation statements)

References 27 publications

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“…In some patients, drug absorption seems to be delayed possibly due to reduced gastrointestinal motility. Compared to healthy volunteers, the salicylic acid concentrations after intake of ASA were markedly lower in our patients, regardless of the formulation . Thus, absorption of orally administered drugs is severely impaired in some critically ill patients.…”

Section: Discussionmentioning

confidence: 56%

“…We estimated a mean area under the curve (AUC) of 30 U in AA‐induced platelet aggregation in patients with HTPR . Thus, a sample of n = 10 per group allowed us to detect a significant reduction in platelet function from an AUC of 30 to 10 with a power of > 90% and a corrected alpha error of 1·6%.…”

Section: Methodsmentioning

confidence: 54%

“…AA‐ and ADP‐induced platelet aggregation were performed as explained previously (Appendix ). Based on other trials, we chose a cut‐off of > 30 U (arbitrary units) .…”

Section: Methodsmentioning

confidence: 99%

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Acetylsalicylic acid in critically ill patients: a cross‐sectional and a randomized trial

Schoergenhofer

Hobl

Schwameis

et al. 2017

Eur J Clin Investigation

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BackgroundDespite decades of clinical use, the pharmacokinetics and the effects of acetylsalicylic acid (ASA) in critically ill patients remain ill‐defined. We aimed to investigate the pharmacokinetics and the effects of different ASA formulations during critical illness.DesignA cross‐sectional study and a randomized, parallel‐group trial were performed. Critically ill patients under chronic oral ASA treatment (100 mg enteric‐coated) were screened for high ‘on‐treatment’ platelet reactivity (HTPR) according to arachidonic acid‐induced whole‐blood aggregometry. Thirty patients with HTPR were randomized to receive 100 mg ASA intravenously, 100 mg enteric‐coated ASA bid (bis in die) or 81 mg chewable ASA (n = 10 per group). Serum thromboxane B2 (TXB2) levels, ASA and salicylic acid levels were quantified.ResultsOf 66 patients, 85% (95% confidence intervals 74–93%) had HTPR. Compared to baseline infusion of 100 mg, ASA significantly reduced platelet aggregation after 24 h to median 80% (Quartiles: 66–84%). Intake of 81 mg chewable ASA significantly reduced platelet aggregation to 75% (54–86%) after four hours, but increased it to 117% after 24 h (81–163%). Treatment with 100 mg enteric‐coated ASA bid decreased platelet aggregation after 24 h to median 56% (52–113%). Baseline TXB2 levels were median 0·35 ng/mL (0·07–0·94). Infusion of ASA or intake of 100 mg ASA bid reduced TXB2 levels to 0·07–0·18 ng/mL after 24 h, respectively. Chewable ASA reduced TXB2 levels only transiently. Pharmacokinetic analysis revealed highly variable absorption patterns of oral ASA formulations.ConclusionThere is a very high prevalence of HTPR in critically ill patients on peroral ASA therapy, caused by an incomplete suppression of TXB2 and/or by impaired absorption of ASA.

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Section: Discussionmentioning

confidence: 56%

Section: Methodsmentioning

confidence: 54%

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Acetylsalicylic acid in critically ill patients: a cross‐sectional and a randomized trial

Schoergenhofer

Hobl

Schwameis

et al. 2017

Eur J Clin Investigation

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“…One tube containing ethylenediaminetetraacetic acid was drawn first in order to complete a baseline CBC and was used to fill the blood collection set's dead space (within the tubing) with blood, and 2 tubes containing 3.2% sodium citrate (to minimize deterioration of platelet function) were drawn for baseline platelet function testing. Regardless of prior 81‐mg aspirin treatment, each participant was provided an initial 14‐day supply of chewable 81‐mg aspirin in order to provide maximum aspirin absorption and reduce potential variability that can be seen with other formulations such as enteric coated aspirin . Each patient returned to the clinic in 10 to 14 days to allow for complete platelet turnover before platelet aggregation and in vitro testing (Figure ) …”

Section: Methodsmentioning

confidence: 99%

Prospective Determination of Aspirin Sensitivity in Patients Resistant to Low Dose Aspirin: A Proof of Concept Study

Westphal

Rainka

Amsler

et al. 2018

The Journal of Clinical Pharma

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This study tested the capability of an assay to predict aspirin response and reduce ischemic events, and healthcare costs, and delays to optimal treatment. Patients who needed aspirin in the course of normal medical care were included. Patients were excluded if they had disorders affecting platelet function, alcohol use within 24 hours of a test, or NSAID use. Dose escalation of chewable aspirin from 81 mg, to 162 mg, to 325 mg daily occurred based on the results of whole blood impedance aggregation testing to the agonists, collagen (1ug/mL, 5 ug/mL) and arachidonate (0.5 mM) after 10-14 days of treatment. The experimental in vitro test was conducted in triplicate by performing aggregometry on samples spiked to a concentration of 10 uM of aspirin in 0.05% dimethyl sulfoxide. Of the 36 patients who were compliant 16 were found to be resistant to the antiplatelet effects of 81 mg daily aspirin. Nine of these patients were predicted to stay resistant despite dose increase. Once tested at higher doses, ten remained resistant. Seven of the 16 patients were predicted to become sensitive to a higher dose while six actually did. Predicted response to increased doses of aspirin was in good agreement with actual response. Sensitivity of the assay was 83% and specificity was 80%. Results are promising and indicate that it is possible to predict, with reasonable accuracy, if a patient will have an adequate platelet response to aspirin or if the patient will never respond to aspirin necessitating an alternative antiplatelet regimen. Larger, multisite studies are inevitably needed.

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“…Inhibition of platelet aggregation, measured with impedance aggregometry, was similar to that of acetylsalicylic acid (and its metabolite salicylic acid) concentration: 90% of platelets was inactivated after 30 minutes. 20 Nordt et al compared 3 different aspirin formulations on healthy volunteers: (1) solid aspirin tablet swallowed whole; (2) solid aspirin tablet chewed then swallowed; and (3) chewable aspirin formulation chewed and swallowed. Serum salicylate measurements were obtained over a 180-minute period.…”

mentioning

confidence: 99%

Is Aspirin Still the Cornerstone of Antiplatelet Therapy in Patients With Coronary Artery Disease? An Historical and Practical Narrative Review

et al. 2017

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Absorption kinetics of low‐dose chewable aspirin – implications for acute coronary syndromes

Cited by 12 publications

References 27 publications

Acetylsalicylic acid in critically ill patients: a cross‐sectional and a randomized trial

Acetylsalicylic acid in critically ill patients: a cross‐sectional and a randomized trial

Prospective Determination of Aspirin Sensitivity in Patients Resistant to Low Dose Aspirin: A Proof of Concept Study

Is Aspirin Still the Cornerstone of Antiplatelet Therapy in Patients With Coronary Artery Disease? An Historical and Practical Narrative Review

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