Related Experiment Video
Updated: Jun 14, 2026

Preparation of Washed Human Platelets for Quantitative Metabolic Flux Studies
Published on: January 10, 2025
Effect of obesity on platelet reactivity and response to low-dose aspirin
Bryan C Bordeaux1, Rehan Qayyum, Lisa R Yanek
1Department of Population Medicine, Harvard Medical School, Boston, MA, USA.
Insights
Obese individuals exhibit higher platelet reactivity, even after aspirin therapy. This suggests obesity may lead to reduced aspirin effectiveness in preventing cardiovascular events.
Area of Science:
- Cardiology
- Hematology
- Metabolic Disorders
Background:
- Aspirin is a cornerstone in preventing cardiovascular events.
- Insufficient platelet function suppression by aspirin is linked to adverse outcomes.
- Obesity is a growing public health concern with known cardiovascular risks.
Purpose of the Study:
- To investigate the impact of obesity on platelet responsiveness to aspirin.
- To determine if obesity influences aspirin resistance in high-risk patients.
Main Methods:
- Prospective study involving 2014 participants.
- Assessment of platelet reactivity via aggregometry and urinary thromboxane metabolite excretion.
- Measurements taken before and after a 2-week course of low-dose aspirin (81 mg/d).
Main Results:
- Obese individuals demonstrated significantly higher baseline platelet reactivity compared to nonobese individuals.
- After aspirin therapy, obese individuals showed greater residual platelet aggregation in response to arachidonic acid (AA) and higher urinary 11-dehydro-thromboxane B2 (Tx-M) excretion.
- Aspirin resistance was also significantly higher in the obese group (26.5% vs. 20.5%).
Conclusions:
- Obesity is associated with increased native platelet reactivity.
- Obese individuals retain greater platelet reactivity even after standard aspirin treatment, suggesting potential aspirin resistance.
- These findings highlight a potential mechanism linking obesity to increased cardiovascular event risk in patients treated with aspirin.
Abstract:
Insufficient platelet function suppression by aspirin is a predictor of cardiovascular events in high-risk patients. The authors assessed the impact of obesity on platelet responsiveness before and after 2 weeks of aspirin 81 mg/d in 2014 people. Obese individuals had greater baseline platelet reactivity. Comparing obese and nonobese individuals after aspirin therapy, results for aggregometry to collagen were 6.7 vs 6.1 ohms, P=.008; aggregometry to adenosine diphosphate were 13.1 vs 11.8 ohms,P<.0001; aggregometry to arachidonic acid (AA) were 4.9% vs 8.3% nonzero aggregation, P=.002; urinary excretion of 11-dehydro-thromboxane B2 (Tx-M) were 4.9% vs 8.3% nonzero aggregation, P=.002; and aspirin resistance were 26.% vs 20.5%, P=.002; respectively. These remained significantly different for AA aggregation and Tx-M excretion after adjustment for covariates. Obese individuals have greater native platelet reactivity and retain greater reactivity after suppression by aspirin.
Related Concept Videos
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Drug Dosing: Obese Patients
Pharmacokinetics in Obese Patients: Drug Absorption and Distribution
Pharmacokinetics in Obese Patients: Drug Metabolism and Excretion
Formation of the Platelet Plug
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Anticoagulant Drugs: Low-Molecular-Weight Heparins

