Circulation, Vol 90, 2679-2686, Copyright © 1994 by American Heart Association
T Herren, H Stricker, A Haeberli, DD Do and PW Straub
BACKGROUND: The blood coagulation cascade was reported to be activated in
patients with arteriosclerotic disease of the lower limbs (peripheral
arterial disease, PAD). There is more thrombin and fibrin formation
compared with healthy control subjects. In many studies, however, the
presence of arteriosclerotic disease had not been thoroughly ruled out in
the control group. Therefore, markers of the activation of the blood
coagulation cascade were measured in patients with PAD and in a carefully
defined control group, both groups being subjected to an exercise test.
METHODS AND RESULTS: Twenty-two patients with angiographically documented
PAD of grade II (Fontaine classification) and 13 control subjects in whom
the presence of arteriosclerotic lesions was ruled out by noninvasive means
in the carotid arteries, abdominal aorta, leg arteries, and coronary
arteries took part in the study. Before and immediately after a treadmill
stress test, the concentrations of prothrombin fragment F1 + 2 (F1 + 2),
thrombin-antithrombin III complexes (TAT), fibrinopeptide A (FPA; this
peptide was measured in spot urine also), and D-dimers were measured.
Before exercise, the concentrations of F1 + 2 (1.0 +/- 0.6 versus 0.7 +/-
0.3 nmol/L), TAT (2.9 +/- 2.1 versus 1.9 +/- 0.8 micrograms/L), and
D-dimers (318.2 +/- 270.1 versus 150.0 +/- 91.4 micrograms/L) were
significantly higher in the patients with PAD compared with the healthy
control subjects. FPA concentrations in plasma (1.9 +/- 1.0 versus 1.4 +/-
0.6 micrograms/L) and spot urine were not different, however. F1 + 2, FPA,
and D-dimer concentrations correlated with the severity of the PAD as
assessed by the ankle systolic blood pressure index (ABPI). The
symptom-limited stress test did not lead to further activation of the blood
coagulation cascade. However, concentrations of F1 + 2 (P < .001) and
TAT (P < .01) after exercise correlated with the presence of ischemic
changes in the stress-test ECG. CONCLUSIONS: There is evidence of enhanced
thrombin formation in patients with PAD compared with an age- and
sex-matched control group without clinical and sonographic evidence of
arteriosclerosis. The thrombin formed, however, appears to be almost
completely neutralized by antithrombin III. No direct evidence of fibrin
formation was obtained, since the FPA concentrations were not different. In
the patients with PAD, the higher concentrations of D-dimers are indicative
of in vivo fibrinolysis. Thus, some fibrin formation must be postulated to
occur in patients with arteriosclerosis.
ARTICLES
Fibrin formation and degradation in patients with arteriosclerotic disease
Laboratory for Thrombosis Research, University Hospital, Inselspital, Bern, Switzerland.
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