Aspirin is indispensable in
secondary prevention of ischemic events in patients with
coronary artery disease (CAD). However, insufficient platelet inhibition despite
aspirin medication is frequent. This is referred to as high on-treatment platelet reactivity (HTPR). Nevertheless, if this is associated with clinical outcome instead of only laboratory phenomenon remains unclear so far. In this study, we test whether patients with ischemic events have higher platelet reactivity despite
aspirin medication than patients without ischemic events. In this prospective study of 72 CAD patients, we determined pharmacodynamic response to
aspirin by
arachidonic acid induced aggregation via light-transmission aggregometry and expressed as maximum of aggregation (MoA). During a mean follow-up duration of 3.2 years, major adverse cardiac and cerebrovascular events (MACCE), mortality,
non-ST-elevation myocardial infarction (
NSTEMI), and
stroke were assessed as endpoints via yearly telephone interviews with the treating physician of the patients. Patients who suffered from MACCE, death, and
NSTEMI had a significantly higher MoA than those without (MACCE: 5.4 vs. 16.4%, p < 0.05; death: 5.6 vs. 16.8%, p < 0.05;
NSTEMI: 1.8 vs. 21%, p < 0.001). MoA did not differ with regard to the occurrence of
stroke (10.1 vs. 14.9%, p = 0.59). Patients with MACCE, death, and
NSTEMI show enhanced platelet reactivity despite
aspirin medication as compared to patients without ischemic events. Hence, insufficient response to
aspirin medication should be regarded as risk factor for ischemic events in CAD patients. Further trials are needed to assess options to overcome HTPR to
aspirin.