TY - JOUR
T1 - Investigating the mechanisms of hyporesponse to antiplatelet approaches
AU - Braunwald, Eugene
AU - Angiolillo, Dominick
AU - Bates, Eric
AU - Berger, Peter B.
AU - Bhatt, Deepak
AU - Cannon, Christopher P.
AU - Furman, Mark I.
AU - Gurbel, Paul
AU - Michelson, Alan D.
AU - Peterson, Eric
AU - Wiviott, Stephen
PY - 2008/3
Y1 - 2008/3
N2 - 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.
AB - 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.
KW - Acute coronary syndromes<ischemic heart disease
KW - Catheterization/diagnostic interventional<cardiac
KW - Myocardial infarction<ischemic heart disease
KW - Platelets
KW - Thrombosis/hypercoagulable states
UR - http://www.scopus.com/inward/record.url?scp=41149124824&partnerID=8YFLogxK
U2 - 10.1002/clc.20360
DO - 10.1002/clc.20360
M3 - Article
C2 - 18481819
AN - SCOPUS:41149124824
SN - 0160-9289
VL - 31
SP - I21-I27
JO - Clinical Cardiology
JF - Clinical Cardiology
IS - 3 SUUPL. 1
ER -