Antithrombin III (AT-III) deficiency has been associated with increased risk of venous and arterial thromboses and arterial graft failure. Deficiency of this circulating glycoprotein may be congenital; however, acquired deficiencies may develop in protein-losing or protein-wasting states. In the present study, AT-III levels of 108 patients undergoing vascular surgical procedures were determined preoperatively and at intervals (third, fifth, and seventh days) postoperatively. The mean AT-III level was then compared to the patient's protein status. The effect of reduced AT-III activity on early graft failure was also noted. A low preoperative AT-III level (<80%) was found in 16.3% of the patients studied. Among 83 patients with serum albumin levels >3.0 gm/dl or transferrin levels >180 mg/dl, reduced AT-III activity was present in only 10 (12%). In contrast, when serum albumin levels were <3.0 gm/dl, AT-III deficiency was found in 12 of 25 patients (48%) (p < 0.01). Early thrombosis of a femorodistal graft occurred in 5 of 15 patients (33%) with reduced AT-III levels. When AT-III levels were normal, early bypass failure occurred in only 9 of 67 grafts (13.4%). However, this difference was not statistically significant. An additional 15 patients had sequential pre- and postoperative measurements (up to 3 weeks) of serum protein and AT-III levels to illustrate the relationship between the dynamics of protein metabolism and AT-III levels. There was a clear temporal relationship between albumin, transferrin, and AT-III levels. Following nutritional support, an increase in albumin was followed by a corresponding normalization of the AT-III level. The development of AT-III deficiency from sustained protein catabolism may result in a hypercoagulable state similar to that in the nephrotic syndrome. Recognition and reversal of this deficiency may reduce the likelihood of early graft failure in some patients.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine