The effects of coronary artery disease severity on time-dependent changes in platelet activation indices in stored whole blood.
BACKGROUND
Platelets play a pivotal role in the pathogenesis of the thrombotic complications in cardiovascular disease (CVD). Abnormal platelet activation indices are evolving as potentially useful markers in CVD risk stratification. Whilst there has been some investigation into the effects of storage time on several of these indices, the effects of underlying disease severity on these temporal changes have not been previously studied.


METHODS
Using the ADVIA 120 haematology analyser, we assessed the effects of time-dependent storage of whole blood in EDTA, on a number of platelet activation indices: mean platelet volume (MPV), mean platelet component (MPC, measure of platelet density) and platelet component distribution width (PCDW, a marker of platelet shape change. We studied three age- and sex-matched patient groups: (i) healthy controls (n = 10), (ii) stable patients with coronary artery disease (CAD, n = 9); and (iii) patients with acute myocardial infarction (n = 8). Whole blood samples were processed at exactly 5 min following venesection and at 15, 30, 60 and 120 min later in storage in EDTA tubes at room temperature.


RESULTS
There was a significant and stepwise increase in MPV (P = 0.01) and decrease in PCDW (P = 0.03), with a non-significant trend to increasing MPM and decreasing MPC with increasing underlying disease (that is healthy, 'stable' and 'acute' artery disease). There was a significant time-dependent increase in MPV and decrease in MPC and PCDW (all P < 0.05), which were all significant on 'post-hoc' analyses by 30 min. There were no significant changes in platelet count or MPM with time. There was no interaction of underlying disease with whole-blood storage time for any of the platelet indices reported (P = NS).


CONCLUSIONS
There is a temporal increase in MPV and decrease in MPC and PCDW in venous blood stored over 2 h in EDTA. These changes are not influenced by the underlying CVD disease severity.
Boos
Christopher J
CJ
Haemostasis, Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, B18 7QH, UK.
Balakrishnan
Balu
B
Lip
Gregory Y H
GY
D000368:Aged; D001793:Blood Preservation; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000097:blood*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood*; D015539:Platelet Activation / Q000502:physiology*; D010976:Platelet Count; D013997:Time Factors