Pa. Gurbel et al., Soluble P-selectin is not a surrogate marker for platelet P-selectin: Evidence from a Multicenter Chest Pain Study Group, J THROMB TH, 10(1), 2000, pp. 15-22
It has been reported that platelet expression and plasma levels of soluble
P-selectin are increased in patients with unstable coronary artery syndrome
s. However, the origin of soluble P-selectin remains unknown. We sought to
determine whether platelet expression of P-selectin correlates with plasma
levels in the population of patients presenting to the emergency department
with chest pain. In 338 patients presenting with chest pain to the emergen
cy departments of three different hospitals, simultaneous soluble and plate
let P-selection levels were determined using enzyme-linked immunosorbent as
say (ELISA) and whole blood flow cytometry, respectively. Using regression
analysis no correlation (R-2=0.055) was found between soluble and platelet-
bound P-selectin for the study population, including those patients with no
ncardiac chest pain (R-2=0.019), unstable angina (R-2=0.007), acute myocard
ial infraction (R-2=0.033), congestive heart failure (R-2=0.231), and gastr
ointestinal illness (R-2=0.020). The platelet expression of P-selectin is u
nrelated to the level found in plasma in patients with acute chest pain, ir
respective of the etiology of chest pain. Dissociation between platelet and
soluble P-selectin suggests that the soluble form cannot serve as a surrog
ate marker to indicate platelet activation in the chest pain population.