Elevated levels of shed membrane microparticles with procoagulant potential in the peripheral circulating blood of patients with acute coronary syndromes
Z. Mallat et al., Elevated levels of shed membrane microparticles with procoagulant potential in the peripheral circulating blood of patients with acute coronary syndromes, CIRCULATION, 101(8), 2000, pp. 841-843
Citations number
17
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Background-Apoptotic microparticles are responsible for almost all tissue f
actor activity of the plaque lipid core. We hypothesized that elevated leve
ls of procoagulant microparticles could also circulate in the peripheral bl
ood of patients with recent clinical signs of plaque disruption and thrombo
sis;
Methods and Results-We studied 39 patients with coronary heart disease, inc
luding 12 patients with stable angina and 27 patients with acute coronary s
yndromes (ACS), and 12 patients with noncoronary heart disease. We isolated
the circulating microparticles by capture with annexin V and determined th
eir procoagulant potential with a prothrombinase assay. The cell origins of
microparticles were determined in an additional 22 patients by antigenic c
apture with specific antibodies. The level of procoagulant microparticles d
id not differ between stable angina patients and noncoronary patients (10.1
+/- 1.6 nmol/L phosphatidylserine [PS] equivalent versus 9.9 +/- 1.6 nmol/
L PS equivalent, respectively). However, procoagulant microparticles were s
ignificantly elevated in patients with ACS (22.2 +/- 2.7 nmol/L PS equivale
nt) compared with other coronary (P<0.01) or noncoronary (P<0.01) patients.
Microparticles of endothelial origin were significantly elevated in patien
ts with ACS (P<0.01), which suggests an important role for endothelial inju
ry in inducing the procoagulant potential.
Conclusions-Hihh levels of procoagulant endothelial microparticles are pres
ent in the circulating blood of patients with ACS and may contribute to the
generation and perpetuation of intracoronary thrombi.