title: Hypercoagulability in cats with cardiomyopathy.
abstract: BACKGROUND
  Arterial thromboembolism (ATE) is a common complication of feline cardiomyopathy; however, the pathogenesis of ATE is unknown.
  
  
  OBJECTIVE
  Systemic activation of the coagulation cascade (hypercoagulability) and endothelial injury promote ATE in cardiomyopathic cats.
  
  
  METHODS
  Healthy cats (n = 30) and 3 groups of cardiomyopathic cats: Group (1) left atrial enlargement only (LAE [n = 11]), ie, left atrial to aortic ratio >1.4; Group (2) LAE with spontaneous echocardiographic contrast, atrial thrombi or both (SEC-T [n = 16]); and Group (3) acute ATE with LAE (n = 16).
  
  
  METHODS
  Hypercoagulability was defined by 2 or more laboratory abnormalities reflecting coagulation factor excess (high fibrinogen concentration or Factor VIII coagulant activity), inhibitor deficiency (low antithrombin activity), or thrombin generation (high thrombin-antithrombin complex [TAT] and d-dimer concentrations). High von Willebrand factor antigen concentration (vWF : Ag) was considered a marker of endothelial injury. Data were analyzed using nonparametric statistics.
  
  
  RESULTS
  The 3 groups of cats with cardiac disease had higher median fibrinogen concentrations than did the healthy cats. Criteria of hypercoagulability were found exclusively in cats with SEC-T (50%) and ATE (56%). Hypercoagulability was not associated with left atrial size or congestive heart failure (CHF). ATE cats had significantly higher median vWF : Ag concentration than did the other groups.
  
  
  CONCLUSIONS
  Systemic hypercoagulability is evident in many cardiomyopathic cats, often without concurrent CHF or overt ATE. Hypercoagulabilty may represent a risk factor for ATE. High vWF : Ag in ATE cats was attributed to downstream endothelial injury from the occlusive thrombus.
authors.affiliation: Department of Population Medicine and Diagnostic Sciences, Cornell University, Ithaca, NY 14853, USA. ts23@cornell.edu
authors.forename: T
authors.initials: T
authors.lastname: Stokol
authors.forename: M
authors.initials: M
authors.lastname: Brooks
authors.forename: J E
authors.initials: JE
authors.lastname: Rush
authors.forename: M
authors.initials: M
authors.lastname: Rishniw
authors.forename: H
authors.initials: H
authors.lastname: Erb
authors.forename: E
authors.initials: E
authors.lastname: Rozanski
authors.forename: M S
authors.initials: MS
authors.lastname: Kraus
authors.forename: A R
authors.initials: AR
authors.lastname: Gelzer
authors.forename: A L
authors.initials: AL
authors.lastname: Gelzer
mesh_terms: D000818:Animals; D000941:Antigens / Q000378:metabolism; D000990:Antithrombin III / Q000378:metabolism; D009202:Cardiomyopathies / Q000097:blood / Q000150:complications / Q000662:veterinary*; D002371:Cat Diseases / Q000097:blood*; D002415:Cats; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology; D005169:Factor VIII / Q000378:metabolism; D005260:Female; D005337:Fibrin / Q000378:metabolism; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005340:Fibrinogen / Q000378:metabolism; D008297:Male; D010447:Peptide Hydrolases / Q000378:metabolism; D012307:Risk Factors; D019851:Thrombophilia / Q000097:blood / Q000150:complications / Q000662:veterinary*; D014841:von Willebrand Factor / Q000276:immunology
chemical_list: D000941:Antigens; D005338:Fibrin Fibrinogen Degradation Products; C029417:Von Willebrand antigen; C046193:antithrombin III-protease complex; C036309:fibrin fragment D; D014841:von Willebrand Factor; D000990:Antithrombin III; D005169:Factor VIII; D005337:Fibrin; D005340:Fibrinogen; D010447:Peptide Hydrolases