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Updated: Jun 23, 2026

Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms
08:46

Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms

Published on: December 9, 2015

Aspirin and clopidogrel resistance: an emerging clinical entity

Thomas H Wang1, Deepak L Bhatt, Eric J Topol

  • 1Department of Cardiovascular Medicine, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA.

European Heart Journal
|December 21, 2005
PubMed

Insights

Millions on antiplatelet therapy may be undertreated due to aspirin or clopidogrel resistance. Understanding resistance mechanisms and improving diagnosis can lead to personalized antiplatelet therapy for better cardiovascular care.

Area of Science:

  • Cardiovascular Medicine
  • Pharmacology
  • Clinical Diagnostics

Background:

  • Antiplatelet therapy, including aspirin and clopidogrel, is crucial for cardiovascular disease management.
  • Despite widespread use, a significant number of patients experience complications, with undertreatment or inappropriate medication potentially contributing.
  • Emerging clinical entities of aspirin and clopidogrel resistance pose severe risks, including recurrent myocardial infarction, stroke, and death.

Purpose of the Study:

  • To explore the mechanisms underlying aspirin and clopidogrel resistance.
  • To identify clinical, cellular, and genetic factors influencing therapeutic failure with antiplatelet agents.
  • To highlight the need for improved diagnostic methods for antiplatelet resistance.

Main Methods:

  • Review of existing literature on antiplatelet therapy, resistance mechanisms, and diagnostic challenges.
  • Analysis of factors contributing to therapeutic failure, including prescribing practices and genetic polymorphisms.
  • Discussion of emerging diagnostic technologies for assessing platelet activity.

Main Results:

  • Therapeutic failure in antiplatelet therapy is influenced by a complex interplay of factors.
  • Clinical, cellular, and genetic elements, such as physician prescribing habits and platelet glycoprotein polymorphisms, contribute to resistance.
  • Current diagnostic methods for antiplatelet resistance are still developing, posing challenges for timely and accurate assessment.

Conclusions:

  • Understanding the mechanisms of therapeutic failure is essential for advancing antiplatelet therapy.
  • Improved diagnosis of antiplatelet resistance is critical for clinical management.
  • Individualized antiplatelet therapy, guided by routine platelet activity monitoring, holds promise for improving patient outcomes in cardiovascular medicine.

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