Coagulation factor V (Arg506-->Gln) mutation and early saphenous vein graft occlusion after coronary artery bypass

E Moor1, A Silveira, F van't Hooft

  • 1Department of Cardiology, Karolinska Institute, Karolinska Hospital, Stockholm, Sweden.

Insights

The factor V Leiden mutation may increase the risk of early saphenous vein graft occlusion after coronary artery bypass grafting (CABG). This finding suggests a link between this genetic factor and vascular complications beyond deep vein thrombosis.

Area of Science:

  • Cardiovascular Surgery
  • Genetics
  • Thrombosis

Background:

  • The factor V (Arg506-->Gln) mutation is a known risk factor for deep vein thrombosis.
  • Its association with saphenous vein graft closure following coronary artery bypass grafting (CABG) is not well-established.

Purpose of the Study:

  • To investigate the role of the factor V Leiden mutation in early saphenous vein graft occlusion after CABG.
  • To examine the anticoagulant response to activated protein C (APC ratio) and its relation to surgical trauma.
  • To assess the impact of the mutation on postoperative thrombin generation and fibrin formation.

Main Methods:

  • A cohort of 108 men undergoing elective CABG for exertional angina pectoris was studied.
  • Saphenous vein graft patency was assessed via angiography three months post-CABG.
  • Factor V Leiden mutation status, APC ratios, prothrombin fragment 1+2, thrombin-antithrombin complexes, and soluble fibrin levels were analyzed.

Main Results:

  • Of 100 patients with reangiography, 23 experienced early vein graft occlusion.
  • Heterozygosity for the factor V Leiden mutation showed a trend towards association with early graft occlusion (p=0.06).
  • Pre- and postoperative APC ratios, and markers of thrombin generation and fibrin formation, did not differ significantly between carriers and non-carriers.

Conclusions:

  • Early saphenous vein graft occlusion after CABG may be tentatively linked to the factor V (Arg506-->Gln) mutation.
  • This vascular complication could potentially be added to deep vein thrombosis as a condition associated with the factor V Leiden mutation.

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