title: Indexes of hypercoagulability measured in peripheral blood reflect levels in intracardiac blood in patients with atrial fibrillation secondary to mitral stenosis.
abstract: Systemic thromboembolism is a major complication in patients with mitral stenosis, especially in those who have atrial fibrillation (AF). It has been suggested that there may be increased regional left atrial coagulation activity in such patients, despite normal systemic coagulation activity on peripheral blood sampling. Our aim was to investigate whether there were significant differences between intracardiac versus peripheral indexes of hypercoagulability in 25 patients (5 men; mean age 60 years) with mitral stenosis who were undergoing percutaneous balloon mitral valvuloplasty and who were all in chronic AF. Two days after halting warfarin therapy, intracardiac (right and left atria) and peripheral (venous and arterial) blood samples from patients were obtained and compared with levels in matched healthy controls in sinus rhythm. Thrombogenicity was assessed by levels of fibrin D-dimer, fibrinogen, indexes of platelet activation (soluble P-selectin and beta thromboglobulin [betaTG]) and indexes of endothelial dysfunction (soluble thrombomodulin [sTM] and von Willebrand factor [vWF]). There were no statistically significant differences in the various markers between the femoral vein and artery, left and right atria, and between the femoral vein and both atria (all p = NS). Plasma fibrinogen, vWf (both p <0.005), and D-dimer (p = 0.011) were significantly higher and levels of sP-selectin and sTM were lower (both p <0.005) in patients when compared with controls. There was no significant difference in plasma betaTG levels. Our results suggest that there is no significant variation in indexes of thrombogenesis, platelet activation, and endothelial dysfunction between left atrium, right atrium, and the peripheral artery or vein. Peripheral samples therefore do reflect atrial coagulation, platelet, and endothelial activities.
authors.affiliation: Haemostasis Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, United Kingdom.
authors.forename: F L
authors.initials: FL
authors.lastname: Li-Saw-Hee
authors.forename: A D
authors.initials: AD
authors.lastname: Blann
authors.forename: I
authors.initials: I
authors.lastname: Goldsmith
authors.forename: G Y
authors.initials: GY
authors.lastname: Lip
mesh_terms: D001281:Atrial Fibrillation / Q000097:blood* / Q000209:etiology; D015415:Biomarkers / Q000097:blood; D001779:Blood Coagulation Factors / Q000378:metabolism*; D001808:Blood Vessels; D002404:Catheterization; D005260:Female; D005337:Fibrin / Q000378:metabolism; D005340:Fibrinogen / Q000378:metabolism; D006325:Heart Atria; D006352:Heart Ventricles; D006801:Humans; D008297:Male; D008875:Middle Aged; D008946:Mitral Valve Stenosis / Q000097:blood / Q000150:complications* / Q000628:therapy; D019007:P-Selectin / Q000097:blood; D015539:Platelet Activation / Q000502:physiology; D011379:Prognosis; D012189:Retrospective Studies; D012307:Risk Factors; D019851:Thrombophilia / Q000097:blood* / Q000209:etiology; D001620:beta-Thromboglobulin / Q000378:metabolism
chemical_list: D015415:Biomarkers; D001779:Blood Coagulation Factors; D019007:P-Selectin; D001620:beta-Thromboglobulin; D005337:Fibrin; D005340:Fibrinogen