In acute coronary events, plaque rupture and the subsequent formation of th
e catalytic tissue factor-factor VIIa complex is considered to initiate coa
gulation. It is unknown whether clotting factors XI and IX are activated in
acute coronary events. Therefore, we prospectively investigated the activa
tion of clotting factors XI and IX as well as activation of the contact sys
tem and the common pathway in 50 patients with acute myocardial infarction
(AMI), in 50 patients with unstable angina pectoris (UAP), and in 50 patien
ts with stable angina pectoris (SAP). Factor XIa-C1 inhibitor complexes, wh
ich reflect acute activation of factor XI, were detected in 24% of the pati
ents with AMI, 8% of the patients with UAP, and 4% of the patients with SAP
(P<0.05), whereas factor XIa-<alpha>(1)-antitrypsin complexes, which refle
ct chronic activation, were observed equally in all 3 study groups. Factor
IX peptide levels were significantly higher in the patients with AMI and UA
P compared with the patients with SAP (P<0.01). No differences regarding ma
rkers of the common pathway were demonstrated. Fibrinopeptide A levels were
elevated in patients with AMI compared with patients with UAP and those wi
th SAP (P<0.01). Factor XIIa- or kallikrein-C1 inhibitor complexes were not
increased. In conclusion, this is the first demonstration of the activatio
n of clotting factors XI and IX in patients with acute coronary syndromes.
Because these clotting factors are considered to be important for continuou
s thrombin generation and clot stability, their activation might have clini
cal and therapeutic consequences.