ABSTRACT
Our understanding of the central role of platelet function in the genesis of thrombotic events has stimulated the development of novel antiplatelet agents targeting specific pathways involved in adhesion, activation, and aggregation (1). The results of recent clinical trials evaluating aIIbb3 (GPIIb/IIIa) blockers and P2Y12 receptor inhibitors have supported the concept that improved platelet inhibition significantly attenuates ischemic event occurrence. However, the prevalence of recurrent thrombotic events still remains high (2,3) Moreover, the “one size fits all” approach employed in these clinical trials has also demonstrated that agents associated with superior platelet inhibition are also linked to increased bleeding. Recent translational research studies have strongly supported the relation of high on-treatment platelet reactivity to the occurrence of ischemic events including stent thrombosis, and a potential threshold level associated with event occurrence has been reported (4,5). The present strategy of treating all patients with the same dose of antiplatelet agents may be flawed. At one end of the spectrum, selected patients with excessively low platelet reactivity may bleed, while other patients with high platelet reactivity may have ischemic events. These concerns will be addressed by future strategies based on the measurement of platelet function and thrombotic potential in the individual patient. Platelet reactivity is a quantifiable and modifiable risk factor (5). The determination of a therapeutic target of platelet reactivity associated with reduced thrombotic risk and bleeding events remains an elusive and overall understudied goal at this time. Thus, the measurement of platelet function that optimally correlates with patient outcomes has assumed increased importance in cardiovascular medicine.
