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Obesity and Inflammation and Altered Clopidogrel Pharmacokinetics and Pharmacodynamics

Nicholas B Norgard1, Scott V Monte2

  • 1Department of Internal Medicine University of Missouri Kansas City School of Medicine, 2411 Holmes St, Kansas City, MO. United States.

Drug Metabolism Letters
|March 7, 2017
PubMed

Insights

Obesity reduces the effectiveness of clopidogrel, an antiplatelet medication, increasing cardiovascular event risk. Understanding these effects is crucial for optimizing antithrombotic therapy in obese patients.

Area of Science:

  • Pharmacology
  • Cardiovascular Medicine
  • Metabolic Disorders

Background:

  • Clopidogrel, a vital antiplatelet drug, exhibits significant variability in patient response.
  • Reduced platelet inhibition from clopidogrel is linked to higher cardiovascular event risk.
  • Obesity is an independent risk factor for cardiovascular disease, necessitating optimized antithrombotic strategies.

Purpose of the Study:

  • To investigate the impact of obesity on clopidogrel's pharmacodynamic response.
  • To elucidate the mechanisms behind obesity-related reduced clopidogrel efficacy.
  • To inform optimized antithrombotic therapy for obese individuals.

Main Methods:

  • Review of existing literature on clopidogrel response in obesity.
  • Analysis of obesity-associated pro-thrombotic states (insulin resistance, inflammation, oxidative stress, endothelial dysfunction).
  • Examination of inflammatory mechanisms, including metabolic endotoxemia, affecting platelet reactivity and drug metabolism.

Main Results:

  • Multiple studies indicate obesity is associated with a diminished clopidogrel pharmacodynamic response.
  • Obesity-related inflammation, particularly metabolic endotoxemia, contributes to increased platelet reactivity.
  • Factors like suppressed cytochrome P450 activity and increased platelet turnover further impair clopidogrel effectiveness.

Conclusions:

  • Obesity-related high on-clopidogrel platelet reactivity is a significant clinical concern.
  • Understanding these mechanisms is key to improving antithrombotic treatment for obese patients.
  • Optimized therapeutic strategies are needed to mitigate cardiovascular risks in this population.
Abstract

Keywords:
Obesityclopidogrelendotoxininflammationplatelet function.thienopyridine metabolism

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