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Plasma factor XI and XII activity in patients with slow coronary flow

Muhsin Türkmen1, Cüneyt Toprak, Göksel Açar

  • 1aDepartment of Cardiology, Faculty of Medicine, Medipol University bDepartment of Cardiology, Kartal Kosuyolu Yuksek İhtisas Education and Research Hospital, Istanbul, Turkey.

Blood Coagulation & Fibrinolysis : an International Journal in Haemostasis and Thrombosis
|February 11, 2014
PubMed

Insights

Patients with slow coronary flow (SCF) have higher levels of coagulation factors XI and XII. This suggests an enhanced procoagulant state may contribute to the pathophysiology of SCF.

Area of Science:

  • Cardiology
  • Hematology
  • Pathophysiology

Background:

  • Slow coronary flow (SCF) is a condition of delayed coronary artery opacification during angiography.
  • The exact pathophysiology of SCF remains unclear, though endothelial dysfunction, inflammation, and atherosclerosis are implicated.
  • Coagulation pathway abnormalities have not been extensively studied in relation to SCF.

Purpose of the Study:

  • To investigate potential coagulation pathway abnormalities in patients with SCF.
  • To measure plasma factor XI and XII activity in patients with SCF and compare them to individuals with normal coronary flow (NCF).

Main Methods:

  • The study included 55 patients with angiographically proven SCF and 40 individuals with NCF.
  • Plasma levels of factor XI and factor XII activity were measured in both groups.
  • Demographic and echocardiographic parameters were assessed and compared between groups.

Main Results:

  • Factor XI activity was significantly higher in the SCF group compared to the NCF group.
  • Factor XII activity was also significantly higher in the SCF group compared to the NCF group.
  • Baseline demographic and echocardiographic characteristics were similar between the two groups.

Conclusions:

  • The SCF phenomenon is associated with an enhanced procoagulant state.
  • Elevated levels of factor XI and XII activity may play a role in the pathogenesis of SCF.
  • These findings support the potential involvement of inflammation and atherosclerosis in SCF.

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