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 hypo...
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| Veröffentlicht in: | Clinical cardiology (Mahwah, N.J.) N.J.), 2008-03, Vol.31 (S1), p.I21-I27 |
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| container_title | Clinical cardiology (Mahwah, N.J.) |
| container_volume | 31 |
| creator | Braunwald, Eugene Angiolillo, Dominick Bates, Eric Berger, Peter B. Bhatt, Deepak Cannon, Christopher P. Furman, Mark I. Gurbel, Paul Michelson, Alan D. Peterson, Eric Wiviott, Stephen |
| description | 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. |
| doi_str_mv | 10.1002/clc.20360 |
| format | Article |
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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. 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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | acute coronary syndromes<ischemic heart disease Aspirin - therapeutic use Blood Platelets - drug effects catheterization/diagnostic interventional<cardiac Clopidogrel Drug Resistance Drug Therapy, Combination Genetic Predisposition to Disease Humans myocardial infarction<ischemic heart disease Patient Selection Platelet Aggregation Inhibitors - therapeutic use Platelet Function Tests platelets Risk Assessment Risk Factors thrombosis/hypercoagulable states Ticlopidine - analogs & derivatives Ticlopidine - therapeutic use Treatment Outcome |
| title | Investigating the Mechanisms of Hyporesponse to Antiplatelet Approaches |
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