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The plasma kallikrein-kinin system and risk of cardiovascular disease in men

J W P Govers-Riemslag1, M Smid, J A Cooper

  • 1Laboratory for Clinical Thrombosis and Haemostasis, Department of Internal Medicine and Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands.

Journal of Thrombosis and Haemostasis : JTH
|August 29, 2007
PubMed

Insights

Lower levels of plasma kallikrein-kinin system (PKKS) inhibitory complexes, especially factor XIIa (FXIIa), increase the risk of coronary heart disease (CHD) and stroke in men. This suggests PKKS involvement in atherothrombosis.

Area of Science:

  • Cardiovascular Science
  • Hemostasis and Thrombosis
  • Biochemistry

Background:

  • The plasma kallikrein-kinin system (PKKS) is linked to cardiovascular disease.
  • PKKS activation has not been directly studied in individuals at risk for coronary heart disease (CHD) or stroke.

Purpose of the Study:

  • To investigate the role of the PKKS, including factor XI (FXI), in cardiovascular disease.
  • A nested case-control study was conducted using data from the Second Northwick Park Heart Study (NPHS-II).

Main Methods:

  • A nested case-control study design was employed.
  • Concentrations of factor XIIa-C1 esterase inhibitor (FXIIa-C1-inhibitor) and kallikrein-C1-inhibitor complexes were measured.
  • Statistical analysis included odds ratios (ORs) and 95% confidence intervals (CIs).

Main Results:

  • After a median 10.7-year follow-up, 287 cases of CHD and stroke were identified among 542 controls.
  • Lower tertiles of FXIIa-C1-inhibitor were associated with increased CHD risk (OR=0.52; 0.34-0.80).
  • Lower tertiles of kallikrein-C1-inhibitor complexes correlated with increased stroke risk (OR=0.29; 0.12-0.72).
  • FXIIa-C1-inhibitor and kallikrein-C1-inhibitor complexes showed negative correlations with smoking and fibrinogen.
  • FXIa-inhibitor complexes strongly correlated with FXIIa-inhibitor complexes.

Conclusions:

  • Reduced levels of PKKS inhibitory complexes, particularly FXIIa, are linked to higher CHD and stroke risk in middle-aged men.
  • These findings support the involvement of the PKKS in the development of atherothrombosis.
Abstract

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