Platelet hyperfunction is decreased by additional aspirin loading in patients presenting with myocardial infarction on daily aspirin therapy

Fuchs, Ingrid; Spiel, Alexander; Frossard, Martin; Derhaschnig, Ulla; Riedmüller, Eva; Jilma, Bernd

doi:10.1097/ccm.0b013e3181de8b1e

Cited by 18 publications

(17 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It also produces greater inhibition of TX-dependent platelet reactions such as serotonin release, arachidonic-acidinduced aggregation, and thrombus formation under high shear rate conditions, as evaluated with the PFA-100 system ( Figure 2B and D). These results are in agreement with a previous report demonstrating that an intravenous loading dose of aspirin (250 mg) prolonged the CEPI closure time with the PFA-100 system in 44 patients presenting with AMI while on daily aspirin therapy, and a reduced serum TX in the 22 patients in whom measurements were possible after the loading dose of aspirin [16].…”

Section: Discussionsupporting

confidence: 95%

“…The system determines the time of occlusion of an orifice in a membrane coated with collagen and epinephrine (CEPI) or with collagen and ADP (CADP). The CEPI analysis is aspirin sensitive, whereas the CADP analysis is considered to be largely aspirin insensitive [16,23], reflecting the platelet activity independent of TX.…”

Section: Platelet Function Under High Shear Conditionsmentioning

confidence: 99%

“…Data on platelet TX synthesis in aspirin-treated patients with AMI are particularly scarce. Our previous data [13][14][15] and those of others [16] indicated that platelet TX suppression is incomplete after aspirin treatment in a significant proportion of patients with AMI, and that this is associated with an increase in myocardial necrosis [13].…”

Section: Introductionmentioning

confidence: 95%

See 2 more Smart Citations

The administration of a loading dose of aspirin to patients presenting with acute myocardial infarction while receiving chronic aspirin treatment reduces thromboxane A₂-dependent platelet reactivity

Santos¹,

Madrid

Moscardó³

et al. 2013

Platelets

View full text Add to dashboard Cite

The optimal dose of aspirin for patients presenting with acute myocardial infarction (AMI) while receiving chronic aspirin therapy has not been clearly established. We evaluated whether continued treatment with 100 mg of aspirin or a loading dose (200-500 mg) influences thromboxane A2 (TX) suppression or platelet reactivity. Sixty-four consecutive patients with AMI and 98 healthy subjects (82 aspirin-free and 16 receiving 100 mg daily for a week) were evaluated. Treatment was at the discretion of the attending physician. Collagen (1 µg/ml)-induced TX synthesis, (14)C-serotonin-release, platelet aggregation, and the PFA-100 assay were evaluated. The platelet TX synthesis of patients receiving a loading dose of aspirin was sixfold lower than that of patients receiving 100 mg of aspirin (p<0.005). This was associated with marked reductions in (14)C-serotonin-release and arachidonic-acid-induced aggregation and an increase in the PFA-100 closure time (p<0.01). Categorization of patients according to their TX synthesis (<95% or ≥ 95% inhibition vs. healthy aspirin-free subjects) revealed that 8% of the patients treated with loading doses had a poor response (<95% inhibition) vs. 53% of those treated with 100 mg (p<0.001). Patients with lower TX inhibition had higher serum NT-Pro-BNP (p<0.005), a marker of poor left ventricular systolic function. Administration of a loading dose of aspirin to patients with AMI during existing chronic aspirin treatment induced greater reductions in platelet TX synthesis and TX-dependent platelet reactivity than the continued treatment alone.

show abstract

Section: Discussionsupporting

confidence: 95%

Section: Platelet Function Under High Shear Conditionsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 95%

See 1 more Smart Citation

The administration of a loading dose of aspirin to patients presenting with acute myocardial infarction while receiving chronic aspirin treatment reduces thromboxane A₂-dependent platelet reactivity

Santos¹,

Madrid

Moscardó³

et al. 2013

Platelets

View full text Add to dashboard Cite

show abstract

“…This corresponds well to the observed T max of acetylsalicylic acid (27 min) but occurs earlier than the T max of salicylic acid (69 min). A strength of the current trial is the rather large sample size, which allowed us to detect two outliers in terms of delayed absorption, who showed maximal inhibition of aggregation only after 2-3 h. Such a delayed platelet inhibition could be avoided by infusion of aspirin, which completely inhibited platelet function in less than 5 min in patients with acute coronary syndromes [27]. Figure 1 indicates that concentrations of~1Á8 mg/L acetylsalicylic acid and 6 mg/L salicylic acid are sufficient to fully inhibit platelet aggregation, whereas further increases in concentrations not further increased the effect.…”

Section: Discussionmentioning

confidence: 98%

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

Hobl

Schmid

Stimpfl

et al. 2014

Eur J Clin Investigation

Self Cite

View full text Add to dashboard Cite

Background This study describes the implications of the pharmacokinetics of low-dose chewable aspirin for acute coronary syndromes. Current guidelines recommend the administration of 162-325 mg aspirin chewing tablets for the treatment of acute myocardial infarction. Although aspirin is widely used and a cornerstone in myocardial infarction, there is no information available on the pharmacokinetics of low doses of chewable aspirin.

show abstract

“…In patients with acute myocardial infarction with chronic ASA therapy, TXB2 levels were 0·09 ng/mL (quartiles: 0·03–0·43) . Additional infusion of 250 mg ASA decreased TXB2 levels to 0·04 ng/mL (0·01–0·04 ng/mL) and significantly lowered HTPR . This indicates that thromboxane levels < 0·43 ng/mL are still relevant.…”

Section: Discussionmentioning

confidence: 99%

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

Schoergenhofer

Hobl

Schwameis

et al. 2017

Eur J Clin Investigation

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Platelet hyperfunction is decreased by additional aspirin loading in patients presenting with myocardial infarction on daily aspirin therapy

Abstract: Aspirin loading in the emergency room further reduced thromboxane B(2) levels and further inhibited platelet function in many patients with acute coronary syndrome already on 100 mg aspirin.

Cited by 18 publications

References 40 publications

The administration of a loading dose of aspirin to patients presenting with acute myocardial infarction while receiving chronic aspirin treatment reduces thromboxane A₂-dependent platelet reactivity

The administration of a loading dose of aspirin to patients presenting with acute myocardial infarction while receiving chronic aspirin treatment reduces thromboxane A₂-dependent platelet reactivity

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

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

Contact Info

Product

Resources

About

Platelet hyperfunction is decreased by additional aspirin loading in patients presenting with myocardial infarction on daily aspirin therapy

Abstract: Aspirin loading in the emergency room further reduced thromboxane B(2) levels and further inhibited platelet function in many patients with acute coronary syndrome already on 100 mg aspirin.

Cited by 18 publications

References 40 publications

The administration of a loading dose of aspirin to patients presenting with acute myocardial infarction while receiving chronic aspirin treatment reduces thromboxane A2-dependent platelet reactivity

The administration of a loading dose of aspirin to patients presenting with acute myocardial infarction while receiving chronic aspirin treatment reduces thromboxane A2-dependent platelet reactivity

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

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

Contact Info

Product

Resources

About

The administration of a loading dose of aspirin to patients presenting with acute myocardial infarction while receiving chronic aspirin treatment reduces thromboxane A₂-dependent platelet reactivity

The administration of a loading dose of aspirin to patients presenting with acute myocardial infarction while receiving chronic aspirin treatment reduces thromboxane A₂-dependent platelet reactivity