Thromb Haemost 2010; 104(01): 71-77
DOI: 10.1160/TH09-11-0772
Blood Coagulation, Fibrinolysis and Cellular Haemostasis
Schattauer GmbH

Thrombophilic risk factors and peripheral arterial disease severity

Michelangelo Sartori
1   Angiology and Haemostasis Unit “Marino Golinelli”, University Hospital S. Orsola-Malpighi, Bologna, Italy
,
Elisabetta Favaretto
1   Angiology and Haemostasis Unit “Marino Golinelli”, University Hospital S. Orsola-Malpighi, Bologna, Italy
,
Cristina Legnani
1   Angiology and Haemostasis Unit “Marino Golinelli”, University Hospital S. Orsola-Malpighi, Bologna, Italy
,
Michela Cini
1   Angiology and Haemostasis Unit “Marino Golinelli”, University Hospital S. Orsola-Malpighi, Bologna, Italy
,
Eleonora Conti
1   Angiology and Haemostasis Unit “Marino Golinelli”, University Hospital S. Orsola-Malpighi, Bologna, Italy
,
Alfio Amato
1   Angiology and Haemostasis Unit “Marino Golinelli”, University Hospital S. Orsola-Malpighi, Bologna, Italy
,
Gualtiero Palareti
1   Angiology and Haemostasis Unit “Marino Golinelli”, University Hospital S. Orsola-Malpighi, Bologna, Italy
› Author Affiliations
Further Information

Publication History

Received: 14 November 2009

Accepted after major revision: 12 February 2010

Publication Date:
23 November 2017 (online)

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Summary

Few data are available on thrombophilic risk factors and progression of atherosclerotic peripheral arterial disease (PAD). Thrombophilic alterations can be an aggravating factor when arterial stenoses are present. In a cross-sectional study, we evaluated the presence of the thrombophilic factors fibrinogen, homocysteine, factor (F)VIII, lupus anticoagulant (LAC), FII G20210A, and FV R506Q mutations in 181 patients with PAD at Fontaine’s stage II (claudication), in 110 patients with critical limb ischaemia (CLI), and in 210 controls. Fibrinogen was higher in patients with CLI vs. those with claudication and controls (427.9 ± 10.5 vs. 373.1 ± 5.2 vs. 348.9 ± 7.0 p=0.001, respectively). Homocysteine and FVIII were higher in patients with PAD than in controls, but were similar in patients with CLI and claudication. The prevalence of LAC increased in patients with CLI vs. those with claudication and controls (21.4% vs. 7.8% vs. 5.2% p<0.001, respectively). The prevalence of FII 20210A allele was higher in patients with CLI vs. those with claudication and controls. Using a logistic model, FII G20210A mutation (odds ratio [OR] 19.8, confidence interval [CI] 4.5–87.1, p=0.001), LAC (OR 2.7, CI1.1–6.5, p=0.032), and fibrinogen (OR 1.01, CI 1.00–1.01, p=0.001) were associated with CLI, whereas homocysteine, FVIII, and FV R506Q mutation were not. CLI risk increased according to the number of thrombophilic alterations. In conclusion, altered levels of some important thrombophilic risk factors are independently associated with PAD severity. These data suggest that the presence of two or more thrombophilic risk factors raise the likelihood of PAD being more severe, justifying the need for larger longitudinal studies.