Hypercoagulability in cats with cardiomyopathy.
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.
Stokol
T
T
Department of Population Medicine and Diagnostic Sciences, Cornell University, Ithaca, NY 14853, USA. ts23@cornell.edu
Brooks
M
M
Rush
J E
JE
Rishniw
M
M
Erb
H
H
Rozanski
E
E
Kraus
M S
MS
Gelzer
A R
AR
Gelzer
A L
AL
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
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