BACKGROUND: Associations between hemostatic and inflammatory markers relative to the presence of peripheral arterial disease (PAD), are not fully understood. We determined whether higher levels of D-dimer, high-sensitive C-reactive protein (hsCRP), and fibrinogen are associated independently with extent of atherosclerosis in patients with PAD. METHODS: Participants were PAD patients (Group I, n=67, 69짹9 years) underwent percutaneous transluminal angioplasty (PTA) for claudication (Fontine II-IV) and matched stable angina pectoris patients (Group II, n=67, 62짹9 year) without PAD during same periods. Baseline, clinical characteristics, and hemostatic, inflammatory factors such as, D-dimer, hs-CRP, fibrinogen, and N-terminal-pro brain natriuretic peptide (NT-proBNP) were examinated. RESULTS: Mean age was higher (69 vs 62 years, p<0.01) in group I, and more male patients in group I (97 vs 78%, p<0.01). We observed that PAD patients (Group I) are more frequently diabetes (42 vs 23%, p=0.02), smokers (46 vs 34%), stroke history (17 vs 0%, p<0.01), and previous coronary intervention (45 vs 23%, p<0.01), but no significant difference between the two groups in hypercholesterolemia and hypertension. In hemostatic and inflammatory marker analysis, group I was higher in hs-CRP (3.6짹3.5 vs 2.1짹2.7 mg/dL, p=0.01), NT-pro BNP (327짹396 vs 180짹324 pg/mL, p=0.03), D-dimer (939짹614 vs 610짹529 ng/mL, p=0.01), and fibrinogen (336짹88 vs 283짹74 mg/dL, p<0.01). In multivariable regression analyses adjusting for all factors, D-dimer was associated independently with ankle-brachial index (ABI) in participants with/without a history of cardiac or cerebrovascular disease (respectively, p<0.01). CRP was associated independently with ABI among participants with a history of cardiac or cerebrovascular disease (p=0.02). CONCLUSION: We conclude that D-dimer and hs-CRP levels may be useful blood markers for measuring the extent of atherosclerosis in lower extremity arteries. Additional study is needed to determine whether D-dimer and CRP are involved in the pathophysiology of PAD or whether they are simply sensitive markers of the extent of systemic atherosclerosis.