Dipyrone comedication in aspirin treated stroke patients impairs outcome

Dannenberg, Lisa; Erschoff, Vladimir; Gliem, Michael; Jander, Sebastian; Levkau, Bodo; Kelm, Malte; Hohlfeld, Thomas; Zeus, Tobias; Polzin, Amin

doi:10.1016/j.vph.2016.06.003

Cited by 20 publications

(9 citation statements)

References 11 publications

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“…In our investigations, incidence of HTPR to aspirin was between 4 and 62% in different patient cohorts [17][18][19][20][21]. Higher rates of MACCE and a worse clinical outcome have been described in patients with HTPR [21][22][23][24][25]. We recently reported impaired aspirin antiplatelet effects in dipyrone-treated patients [3,4,20].…”

Section: Discussionmentioning

confidence: 59%

“…enosine diphosphate receptor blockers, but recent data negated a correlation [27,28]. Further factors that are associated with HTPR to aspirin are enhanced platelet turnover, genetic polymorphisms, patient attributed incompliance and comorbidities like chronic kidney disease or diabetes [5,21,29]. Many tests are available to evaluate aspirin antiplatelet effects [6].…”

Section: Discussionmentioning

confidence: 99%

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Malondialdehyde Assay in the Evaluation of Aspirin Antiplatelet Effects

et al. 2018

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Aspirin is essential in secondary prevention of patients after myocardial infarction and with coronary artery disease. However, impaired pharmacodynamic response to aspirin is frequent (high on-treatment platelet reactivity [HTPR]). This leads to an enhanced prevalence of cardiovascular events and to an impaired clinical outcome. The current specific assays to evaluate aspirin antiplatelet effects are complex, time-consuming and demand for a high laboratory expertise. Therefore, we developed a potentially bedside assay based on the determination of malondialdehyde (MDA). MDA is a by-product of the thromboxane (TX) formation, which is synthesized in equimolar concentrations. In this study, we compared this MDA assay to the conventional assays in determination of pharmacodynamic aspirin response. For this, aspirin antiplatelet effects were measured in 22 healthy individuals and 63 aspirin treated patients using TX B2 formation enzyme-linked antibody assay, arachidonic acid induced light transmission aggregometry (LTA) and the new fluorometric MDA assay. In patients, MDA levels correlated well with TX formation (R = 0.81; 95% CI 0.69–0.88; p < 0.001) and LTA (R = 0.84; CI 0.74–0.91; p < 0.001). Receiver operating characteristic analyses revealed that the MDA assay does detect HTPR to aspirin sufficiently (area under the curve: 0.965; p < 0.001). The optimal cut-off was > 128 nmol/L (sensitivity of 100%, specificity of 91%). The new MDA assay is reliable in detecting HTPR. It is highly specific in the evaluation of antiplatelet effects by aspirin. This promising and potential bedside assay needs to be evaluated in clinical practice.

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Section: Discussionmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Malondialdehyde Assay in the Evaluation of Aspirin Antiplatelet Effects

et al. 2018

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“…A possible reason for transient postsurgical HTPR is a higher platelet turnover in this clinical setting or higher COX-2 expression in platelets after surgical interventions [18-21]. Although several reports have described resistance to antiplatelet therapy in patients undergoing a percutaneous intervention or coronary arterial bypass grafting or after stroke, limited data describing resistance to aspirin amongst patients with PAD are available [2, 5, 17-19, 22-24]. We have found only one study which examined the incidence and clinical significance of HTPR in patients with PAD [5].…”

Section: Discussionmentioning

confidence: 99%

Role of Dipyrone in the High On-Treatment Platelet Reactivity amongst Acetylsalicylic Acid-Treated Patients Undergoing Peripheral Artery Revascularisation

et al. 2018

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Objective: To evaluate the effects of dipyrone on sensitivity to aspirin (acetylsalicylic acid [ASA]) in patients who underwent peripheral artery vascular reconstruction. Subjects and Methods: Impedance aggregometry and light transmission aggregometry were used to determine the effects of dipyrone on ASA treatment in 21 patients. Blood samples were drawn in a 7-day period after the surgery. The cut-off value for high on-treatment platelet reactivity (HTPR) was set at < 65% of aggregation inhibition for impedance aggregometry. For light transmission aggregometry the cut-off value for arachidonic acid-induced aggregation was set at > 20% of aggregating platelets, and the cut-off value for epinephrine-induced aggregation was > 44% of aggregating platelets. The cut-off value for each method was derived from a large number of patients treated with a daily dose of 100 mg of ASA. Results: We found HTPR in 14 (67%) of the 21 patients. None had primary resistance to ASA, i.e., after the addition of ASA in vitro all samples showed antiplatelet efficacy. Regression analysis showed a possible correlation between lower efficacy of ASA treatment and higher daily doses of dipyrone (p = 0.005 for impedance aggregometry, p = 0.04 for light transmission aggregometry), higher platelet count (p = 0.005 for impedance aggregometry), and shorter time from surgery (p = 0.03 for impedance aggregometry). Conclusion: HTPR occurs in 67% of ASA-treated patients after lower limb vascular surgery. The occurrence of HTPR correlates with the daily dose of dipyrone. Therefore, dipyrone should not be used as a postoperative analgesic in ASA-treated patients after peripheral artery revascularisation due to its influence on the effectiveness of ASA.

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“…The reasons for aspirin failure are unclear, although insufficient platelet inhibition by aspirin is considered an important reason. Several factors are reported to be associated with insufficient platelet inhibition by aspirin, including chronic kidney disease 32 , body weight 33 , and drug-drug interactions 34 . However, our study was limited because we did not investigate the mechanisms of aspirin failure, such as aspirin resistance, on the platelet function test.…”

Section: Discussionmentioning

confidence: 99%

Risk of recurrent stroke and antiplatelet choice in breakthrough stroke while on aspirin

Kim

Park

et al. 2020

Sci Rep

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Uncertainty regarding an optimal antiplatelet regimen still exists in patients with breakthrough acute ischemic stroke (AIS) while on aspirin. This study provides an analysis of a prospective multicenter registry between April 2008 and April 2014. Eligible patients were on aspirin at the time of AIS and treated with antiplatelet regimens (aspirin, clopidogrel, or clopidogrel-aspirin). Potential factors associated with the choice of each antiplatelet regimen were explored and included a predictive risk score for future vascular events, the Essen Stroke Risk Score (ESRS). A total of 2348 patients (age, 69 ± 11 years; male, 57.7%) were analyzed, and 55.3%, 25.3% and 19.4% were treated with clopidogrel-aspirin, aspirin and clopidogrel, respectively. While the likelihood of choosing clopidogrel-aspirin increased as the ESRS increased, the likelihood of choosing aspirin decreased as the ESRS increased (Ptrend < 0.001). The ESRS category (0–1/2–3/ ≥ 4) modified the effect of antiplatelet regimens for 1-year vascular events (Pinteraction < 0.01). Among patients with ESRS ≥ 4, clopidogrel-aspirin (HR 0.47 [0.30–0.74]) and clopidogrel (HR 0.30 [0.15–0.60]) significantly reduced the risk of outcome events. Our study showed that more than half of the patients with aspirin failure were treated with clopidogrel-aspirin. In particular, a higher ESRS, which indicates an increased risk of recurrent stroke, was associated with the choice of clopidogrel-aspirin rather than aspirin.

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Dipyrone comedication in aspirin treated stroke patients impairs outcome

Cited by 20 publications

References 11 publications

Malondialdehyde Assay in the Evaluation of Aspirin Antiplatelet Effects

Malondialdehyde Assay in the Evaluation of Aspirin Antiplatelet Effects

Role of Dipyrone in the High On-Treatment Platelet Reactivity amongst Acetylsalicylic Acid-Treated Patients Undergoing Peripheral Artery Revascularisation

Risk of recurrent stroke and antiplatelet choice in breakthrough stroke while on aspirin

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