Investigating the mechanisms of hyporesponse to antiplatelet approaches.
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.
Duke Scholars
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Related Subject Headings
- Treatment Outcome
- Ticlopidine
- Risk Factors
- Risk Assessment
- Platelet Function Tests
- Platelet Aggregation Inhibitors
- Patient Selection
- Humans
- Genetic Predisposition to Disease
- Drug Therapy, Combination
Citation
Published In
DOI
ISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Treatment Outcome
- Ticlopidine
- Risk Factors
- Risk Assessment
- Platelet Function Tests
- Platelet Aggregation Inhibitors
- Patient Selection
- Humans
- Genetic Predisposition to Disease
- Drug Therapy, Combination