Morning increase in the occurrence of myocardial infarction, stroke and sudden cardiac death is a well-recognized
phenomenon, which is in line with a morning enhancement of platelet aggregation. We investigated whether platelet
inhibition during clopidogrel and aspirin therapy varies during the day. Fifty-nine consecutive patients (45 men and 14
women) with first ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary
interventions (pPCI) on dual antiplatelet therapy were prospectively enrolled into the study. Blood samples were collected
4 days after start of clopidogrel treatment at 6.00 a.m., 10.00 a.m., 2.00 p.m. and 7.00 p.m. Arachidonic acid and adenosine
diphosphate (ADP)-induced platelet aggregation were assessed by impedance aggregometry. Platelet inhibition by
clopidogrel was lowest in the midmorning: median ADP-induced platelet aggregation was 55%, 17% and 27% higher at
10.00 a.m. compared to 6.00 a.m., 2.00 p.m. and 7.00 p.m., respectively ( p<0.002). Nonresponsiveness to clopidogrel
defined according to the device manufacturer was 2.4-fold more frequent in the midmorning than in the early morning.
We observed a more pronounced midmorning increase in ADP-induced platelet aggregation in diabetic patients when
compared to non-diabetics. In contrast, no diurnal variation in the antiplatelet effect of aspirin was observed. In conclusion,
in patients presenting with STEMI undergoing pPCI, platelet inhibition by clopidogrel is less strong in the midmorning
hours. This periodicity in platelet aggregation in patients on dual antiplatelet therapy should be taken into consideration
when assessing platelet function in clinical studies
