Investigating the mechanisms of hyporesponse to antiplatelet approaches.

Journal Article (Journal Article;Review)

Hyporesponsiveness, or resistance, to antiplatelet therapy may be a major contributor to poorer outcomes among cardiac patients and may be attributed to an array of mechanisms--both modifiable and unmodifiable. Recent evidence has uncovered clinical, cellular, and genetic factors associated with hyporesponsiveness. Patients with severe acute coronary syndromes (ACS), type 2 diabetes, and increased body mass index appear to be the most at risk for hyporesponsiveness. Addressing modifiable mechanisms may offset hyporesponsiveness, while recognizing unmodifiable mechanisms, such as genetic polymorphisms and diseases that affect response to antiplatelet therapy, may help identify patients who are more likely to be hyporesponsive. Hyporesponsive patients might benefit from different dosing strategies or additional antiplatelet therapies. Trials correlating platelet function test results to clinical outcomes are required. Results from these studies could cause a paradigm shift toward individualized antiplatelet therapy, improving predictability of platelet inhibition, and diminishing the likelihood for hyporesponsiveness.

Full Text

Duke Authors

Cited Authors

  • Braunwald, E; Angiolillo, D; Bates, E; Berger, PB; Bhatt, D; Cannon, CP; Furman, MI; Gurbel, P; Michelson, AD; Peterson, E; Wiviott, S

Published Date

  • March 2008

Published In

Volume / Issue

  • 31 / 3 Suppl 1

Start / End Page

  • I21 - I27

PubMed ID

  • 18481819

Pubmed Central ID

  • PMC6653508

International Standard Serial Number (ISSN)

  • 0160-9289

Digital Object Identifier (DOI)

  • 10.1002/clc.20360


  • eng

Conference Location

  • United States