Aspirin antiplatelet effects are associated with body weight.


Journal

Vascular pharmacology
ISSN: 1879-3649
Titre abrégé: Vascul Pharmacol
Pays: United States
ID NLM: 101130615

Informations de publication

Date de publication:
Historique:
received: 02 11 2019
revised: 01 12 2019
accepted: 17 12 2019
pubmed: 22 12 2019
medline: 21 10 2020
entrez: 22 12 2019
Statut: ppublish

Résumé

Aspirin is indispensable in secondary prevention of ischemic events. Recently, it was reported that clinical aspirin effects are hampered in patients above 70 kg body weight. It is well known that a plethora of reasons beside obesity is associated with increased platelet reactivity and insufficient aspirin effects (HTPR). However, data regarding an association between pharmacodynamic response to aspirin and body weight are missing. In this pilot study, we included 59 patients from University Hospital Duesseldorf. Impedance aggregometry was used to assess pharmacodynamic response to aspirin. AA-induced platelet reactivity was significantly higher in patients above 70 kg (<70 kg: 28.27 ± 26.33 vs. >70 kg: 45.93 ± 27.1, p = .035) and correlated well with the bodyweight of patients in this study (r = 0.33, R Insufficient pharmacodynamic response to aspirin is associated with body weight. This finding may play a role in the impaired clinical efficacy of aspirin in patients >70 kg. An optimal aspirin regime in these patients needs to be evaluated in large scale trials.

Sections du résumé

BACKGROUND
Aspirin is indispensable in secondary prevention of ischemic events. Recently, it was reported that clinical aspirin effects are hampered in patients above 70 kg body weight. It is well known that a plethora of reasons beside obesity is associated with increased platelet reactivity and insufficient aspirin effects (HTPR). However, data regarding an association between pharmacodynamic response to aspirin and body weight are missing.
METHODS
In this pilot study, we included 59 patients from University Hospital Duesseldorf. Impedance aggregometry was used to assess pharmacodynamic response to aspirin.
RESULTS
AA-induced platelet reactivity was significantly higher in patients above 70 kg (<70 kg: 28.27 ± 26.33 vs. >70 kg: 45.93 ± 27.1, p = .035) and correlated well with the bodyweight of patients in this study (r = 0.33, R
CONCLUSION
Insufficient pharmacodynamic response to aspirin is associated with body weight. This finding may play a role in the impaired clinical efficacy of aspirin in patients >70 kg. An optimal aspirin regime in these patients needs to be evaluated in large scale trials.

Identifiants

pubmed: 31862488
pii: S1537-1891(19)30337-4
doi: 10.1016/j.vph.2019.106635
pii:
doi:

Substances chimiques

Platelet Aggregation Inhibitors 0
Aspirin R16CO5Y76E

Types de publication

Comparative Study Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

106635

Informations de copyright

Copyright © 2019 Elsevier Inc. All rights reserved.

Auteurs

Philipp Mourikis (P)

Division of Cardiology, Pulmonology, and Vascular Medicine, Heinrich Heine University Medical Center Düsseldorf, Düsseldorf, Germany; Cardiovascular Research Institute Düsseldorf (CARID), Germany.

Saif Zako (S)

Division of Cardiology, Pulmonology, and Vascular Medicine, Heinrich Heine University Medical Center Düsseldorf, Düsseldorf, Germany; Cardiovascular Research Institute Düsseldorf (CARID), Germany.

Lisa Dannenberg (L)

Division of Cardiology, Pulmonology, and Vascular Medicine, Heinrich Heine University Medical Center Düsseldorf, Düsseldorf, Germany; Cardiovascular Research Institute Düsseldorf (CARID), Germany.

Carolin Helten (C)

Division of Cardiology, Pulmonology, and Vascular Medicine, Heinrich Heine University Medical Center Düsseldorf, Düsseldorf, Germany; Cardiovascular Research Institute Düsseldorf (CARID), Germany.

David Naguib (D)

Division of Cardiology, Pulmonology, and Vascular Medicine, Heinrich Heine University Medical Center Düsseldorf, Düsseldorf, Germany; Cardiovascular Research Institute Düsseldorf (CARID), Germany.

Thomas Hohlfeld (T)

Institute for Pharmacology and Clinical Pharmacology, Heinrich Heine University, Dusseldorf, Germany.

Tobias Petzold (T)

Medizinische Klinik und Poliklinik I, Klinikum der Universität München, Ludwig-Maximilians- University Munich, Germany.

Bodo Levkau (B)

Institute of Pathophysiology, West German Heart and Vascular Center, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.

Tobias Zeus (T)

Division of Cardiology, Pulmonology, and Vascular Medicine, Heinrich Heine University Medical Center Düsseldorf, Düsseldorf, Germany; Cardiovascular Research Institute Düsseldorf (CARID), Germany.

Malte Kelm (M)

Division of Cardiology, Pulmonology, and Vascular Medicine, Heinrich Heine University Medical Center Düsseldorf, Düsseldorf, Germany; Cardiovascular Research Institute Düsseldorf (CARID), Germany.

Amin Polzin (A)

Division of Cardiology, Pulmonology, and Vascular Medicine, Heinrich Heine University Medical Center Düsseldorf, Düsseldorf, Germany; Cardiovascular Research Institute Düsseldorf (CARID), Germany. Electronic address: amin.polzin@med.uni-duesseldorf.de.

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Classifications MeSH