Open AccessInvestigating the Mechanisms of Hyporesponse to Antiplatelet Approaches
Author(s) -
Braunwald Eugene,
Angiolillo Dominick,
Bates Eric,
Berger Peter B.,
Bhatt Deepak,
Can Christopher P.,
Furman Mark I.,
Gurbel Paul,
Michelson Alan D.,
Peterson Eric,
Wiviott Stephen
Publication year - 2008
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.20360
Subject(s) - medicine , dosing , diabetes mellitus , intensive care medicine , mechanism (biology) , platelet activation , disease , clinical trial , type 2 diabetes , bioinformatics , platelet , immunology , endocrinology , philosophy , epistemology , biology
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. Copyright © 2008 Wiley Periodicals, Inc.