Related Experiment Video

Updated: Aug 25, 2026

Microfluidics in Assessing Platelet Function
06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

Inhibition of platelet aggregation by aspirin progressively decreases in long-term treated patients

Fabio M Pulcinelli1, Pasquale Pignatelli, Andrea Celestini

  • 1Department of Experimental Medicine and Pathology, University La Sapienza, Viale Regina Elena 324, 00161 Rome, Italy. fabio.pulcinelli@uniroma1.it

Journal of the American College of Cardiology
|March 19, 2004
PubMed

Insights

Long-term aspirin treatment leads to reduced platelet sensitivity, diminishing its antiplatelet effects over time. This study monitored platelet aggregation in patients over two years.

Area of Science:

  • Cardiovascular Medicine
  • Pharmacology
  • Hematology

Background:

  • Platelet sensitivity to aspirin may decrease with long-term use, but the extent is unclear.
  • Understanding long-term aspirin effects is crucial for managing atherothrombotic risks.

Purpose of the Study:

  • To investigate the long-term effects of aspirin on platelet aggregation over a two-year period.
  • To compare aspirin's effects with ticlopidine on platelet aggregation.

Main Methods:

  • Adenosine diphosphate (ADP) and collagen-induced platelet aggregation were monitored.
  • Patients received either aspirin (n=150) or ticlopidine (n=80) for 24 months.
  • Measurements were taken at baseline and after 2, 6, 12, and 24 months.

Main Results:

  • Aspirin initially inhibited platelet aggregation, but this effect decreased over time.
  • Collagen-induced platelet aggregation was significantly higher at 24 months compared to 2 months.
  • Ticlopidine consistently inhibited platelet aggregation throughout the study.

Conclusions:

  • Long-term aspirin treatment progressively reduces platelet sensitivity to the drug.
  • This diminished sensitivity may impact the long-term efficacy of aspirin therapy.
  • Ticlopidine demonstrated sustained antiplatelet effects.
Abstract

More Related Videos

Dynamic Multiparameter Platelet Function Assessment Using a Capacitive Biosensor06:32

Dynamic Multiparameter Platelet Function Assessment Using a Capacitive Biosensor

Published on: May 2, 2025

Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells10:10

Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells

Published on: October 27, 2009

Related Concept Videos

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
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...
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
Peripheral Artery Disease III: Interprofessional Care01:27

Peripheral Artery Disease III: Interprofessional Care

Peripheral Artery Disease (PAD) is characterized by narrowed arteries that diminish blood flow to the extremities. Effective management of PAD requires an interprofessional approach involving various healthcare professionals. The critical aspects of interprofessional care for PAD patients focus on risk factor modification, drug therapy, exercise therapy, nutrition therapy, critical limb ischemia care, and interventional radiology and surgical procedures.The primary treatment goal for PAD...
Time Course of Drug Effect01:14

Time Course of Drug Effect

The progression of a drug's impact can be analyzed by examining both the concentration-time course and the effect-time course. The concentration-time course is determined by the drug's half-life and is influenced by factors such as its pharmacokinetics, including absorption, distribution, metabolism, and elimination. The effect of the drug is often related to its concentration in the plasma and is calculated using the maximum drug effect and the plasma concentration that generates 50 percent of...