Relation of levels of hemostatic factors and inflammatory markers to the ankle brachial index.
Associations between hemostatic and inflammatory markers relative to the ankle brachial index (ABI), an indicator of the presence and severity of peripheral arterial disease (PAD), are not fully understood. We studied relations among selected hemostatic factors, inflammatory markers, and the ankle brachial index (ABI) in patients with and without peripheral arterial disease (PAD). Participants were 370 men and women with ABI <0.90 and 231 patients with ABI 0.90 to 1.50 identified from noninvasive vascular laboratories and general medicine practice. Blood factors were D-dimer, prothrombin 1.2, tissue plasminogen activator (t-PA) antigen, plasminogen activator inhibitor-1 (PAI-1), and inflammatory markers (high-sensitivity C-reactive protein [CRP], fibrinogen, and serum amyloid A [SAA]). Among patients without a history of cardiac or cerebrovascular disease, the ABI was significantly inversely associated with log D-dimer (p <0.001), log prothrombin 1.2 (p = 0.001), log CRP (p <0.001), and log fibrinogen (p = 0.005) in unadjusted analyses. In multivariable regression analyses adjusting for all blood factors as well as potential confounders, D-dimer was associated independently with ABI in participants with a history of cardiac or cerebrovascular disease (p = 0.003) and in participants without a history of cardiac or cerebrovascular disease (p = 0.017). In these analyses, CRP was associated independently with ABI among participants with a history of cardiac or cerebrovascular disease (p = 0.026). CRP was not associated independently with ABI in participants without a history of cardiac or cerebrovascular disease. We conclude that D-dimer levels may be more sensitive than other blood markers for measuring the extent of atherosclerosis in lower extremity arteries.
McDermott
Mary M
MM
Feinberg School of Medicine, Northwestern University, 675 N. St. Clair, Chicago, IL 60611, USA. mdm608@northwestern.edu
Green
David
D
Greenland
Philip
P
Liu
Kiang
K
Criqui
Michael H
MH
Chan
Cheeling
C
Guralnik
Jack M
JM
Pearce
William H
WH
Ridker
Paul M
PM
Taylor
Lloyd
L
Rifai
Nader
N
Schneider
Joseph R
JR
D000368:Aged; D000369:Aged, 80 and over; D000933:Antifibrinolytic Agents / Q000097:blood; D001794:Blood Pressure / Q000502:physiology*; D001916:Brachial Artery / Q000503:physiopathology*; D002097:C-Reactive Protein / Q000032:analysis; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005340:Fibrinogen / Q000032:analysis; D006487:Hemostasis / Q000502:physiology*; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D008297:Male; D008875:Middle Aged; D016491:Peripheral Vascular Diseases / Q000097:blood* / Q000175:diagnosis / Q000503:physiopathology*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D010960:Plasminogen Activators / Q000097:blood; D011516:Prothrombin / Q000032:analysis; D015842:Serine Proteinase Inhibitors / Q000097:blood; D000685:Serum Amyloid A Protein / Q000032:analysis; D012720:Severity of Illness Index; D010959:Tissue Plasminogen Activator / Q000097:blood
D000933:Antifibrinolytic Agents; D005338:Fibrin Fibrinogen Degradation Products; D018836:Inflammation Mediators; D017395:Plasminogen Activator Inhibitor 1; D015842:Serine Proteinase Inhibitors; D000685:Serum Amyloid A Protein; C036309:fibrin fragment D; D011516:Prothrombin; D005340:Fibrinogen; D002097:C-Reactive Protein; D010960:Plasminogen Activators; D010959:Tissue Plasminogen Activator