Activation of clotting factors XI and IX in patients with acute myocardialinfarction

Citation
Mc. Minnema et al., Activation of clotting factors XI and IX in patients with acute myocardialinfarction, ART THROM V, 20(11), 2000, pp. 2489-2493
Citations number
39
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
ISSN journal
10795642 → ACNP
Volume
20
Issue
11
Year of publication
2000
Pages
2489 - 2493
Database
ISI
SICI code
1079-5642(200011)20:11<2489:AOCFXA>2.0.ZU;2-S
Abstract
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.