Lisa Dannenberg1, Vladimir Erschoff2, Florian Bönner1, Michael Gliem3, Sebastian Jander3, Bodo Levkau4, Malte Kelm1, Thomas Hohlfeld2, Tobias Zeus1, Amin Polzin5. 1. Division of Cardiology, Pulmonology, and Vascular Medicine, Heinrich Heine University Medical Center Dusseldorf, Dusseldorf, Germany. 2. Institute for Pharmacology and Clinical Pharmacology, Heinrich Heine University, Dusseldorf, Germany. 3. Department of Neurology, Heinrich Heine University, Dusseldorf, Germany. 4. Institute of Pathophysiology, West German Heart and Vascular Center, University Hospital Essen, University of Duisburg-Essen, Essen, Germany. 5. Division of Cardiology, Pulmonology, and Vascular Medicine, Heinrich Heine University Medical Center Dusseldorf, Dusseldorf, Germany. Electronic address: Amin.polzin@med.uni-duesseldorf.de.
Abstract
BACKGROUND: >50% of stroke patients rely on analgesic medication to control pain. Aspirin is the mainstay of medical treatment of stroke patients; however analgesic medication with dipyrone impairs aspirin antiplatelet effects ex-vivo. The clinical impact of this impairment is unknown. Therefore, we aimed to determine aspirin antiplatelet effects and neurological outcome in stroke patients with aspirin and dipyrone comedication. METHODS: We conducted a prospective cohort study in 41 patients with stroke. Primary outcome was pharmacodynamic response to aspirin in dipyrone treated stroke patients. Secondary outcome was neurological recovery after stroke. Pharmacodynamic response to aspirin was measured using arachidonic acid induced aggregation in light-transmission aggregometry. Neurological outcome was determined three months after stroke onset by telephone interview. RESULTS: Patient's characteristics were similar in the aspirin-alone group and the aspirin+dipyrone group. Impaired pharmacodynamic response to aspirin occurred in 62% (14/21) of patients with aspirin and dipyrone co-medication. Only 10% (2/20) of aspirin treated patients without analgesic comedication displayed residual platelet reactivity (P=0.001; odds ratio [OR], 18 [95% CI, 3.2-100]). Excellent neurological recovery (measured by three months follow-up modified Rankin Scale<2) was observed in 80% (16/20) of patients in the aspirin-alone group and 48% (10/21) of patients in the aspirin+dipyrone group (P=0.037; OR, 4.4 [95% CI, 1.1-17.7]). CONCLUSIONS: Dipyrone comedication in patients with stroke impairs pharmacodynamic response to aspirin. This is associated with worse clinical outcome. Therefore dipyrone should be used with caution in aspirin treated stroke patients. CLINICAL TRIAL REGISTRATION: https://clinicaltrials.gov/show/NCT02148939; Identifier: NCT02148939.
BACKGROUND: >50% of strokepatients rely on analgesic medication to control pain. Aspirin is the mainstay of medical treatment of strokepatients; however analgesic medication with dipyrone impairs aspirin antiplatelet effects ex-vivo. The clinical impact of this impairment is unknown. Therefore, we aimed to determine aspirin antiplatelet effects and neurological outcome in strokepatients with aspirin and dipyrone comedication. METHODS: We conducted a prospective cohort study in 41 patients with stroke. Primary outcome was pharmacodynamic response to aspirin in dipyrone treated strokepatients. Secondary outcome was neurological recovery after stroke. Pharmacodynamic response to aspirin was measured using arachidonic acid induced aggregation in light-transmission aggregometry. Neurological outcome was determined three months after stroke onset by telephone interview. RESULTS:Patient's characteristics were similar in the aspirin-alone group and the aspirin+dipyrone group. Impaired pharmacodynamic response to aspirin occurred in 62% (14/21) of patients with aspirin and dipyrone co-medication. Only 10% (2/20) of aspirin treated patients without analgesic comedication displayed residual platelet reactivity (P=0.001; odds ratio [OR], 18 [95% CI, 3.2-100]). Excellent neurological recovery (measured by three months follow-up modified Rankin Scale<2) was observed in 80% (16/20) of patients in the aspirin-alone group and 48% (10/21) of patients in the aspirin+dipyrone group (P=0.037; OR, 4.4 [95% CI, 1.1-17.7]). CONCLUSIONS:Dipyrone comedication in patients with stroke impairs pharmacodynamic response to aspirin. This is associated with worse clinical outcome. Therefore dipyrone should be used with caution in aspirin treated strokepatients. CLINICAL TRIAL REGISTRATION: https://clinicaltrials.gov/show/NCT02148939; Identifier: NCT02148939.
Authors: Jan Hartinger; Robert Novotny; Jana Bilkova; Tomas Kvasnicka; Petr Mitas; Martin Sima; Jaroslav Hlubocky; Jan Kvasnicka; Ondrej Slanar; Jaroslav Lindner Journal: Med Princ Pract Date: 2018-05-13 Impact factor: 1.927