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Published on: March 29, 2020
Hypercoagulability in cats with cardiomyopathy
1Department of Population Medicine and Diagnostic Sciences, Cornell University, Ithaca, NY 14853, USA. ts23@cornell.edu
Insights
Systemic hypercoagulability is a risk factor for arterial thromboembolism (ATE) in cats with cardiomyopathy. This hypercoagulability, indicated by coagulation abnormalities, occurs even without congestive heart failure or overt ATE.
Area of Science:
- Veterinary Cardiology
- Feline Medicine
- Thrombosis Research
Background:
- Arterial thromboembolism (ATE) is a frequent complication of feline cardiomyopathy, but its underlying causes remain unclear.
- Understanding the pathogenesis of ATE is crucial for managing affected cats.
Purpose of the Study:
- To investigate the role of systemic hypercoagulability and endothelial injury in the development of ATE in cardiomyopathic cats.
- To identify laboratory markers associated with ATE in this population.
Main Methods:
- Compared healthy cats (n=30) with three groups of cardiomyopathic cats: left atrial enlargement (LAE), LAE with spontaneous echocardiographic contrast/thrombi (SEC-T), and acute ATE with LAE.
- Assessed hypercoagulability via fibrinogen, Factor VIII, antithrombin, thrombin-antithrombin complex (TAT), and d-dimer levels.
- Measured von Willebrand factor antigen (vWF:Ag) as a marker of endothelial injury.
Main Results:
- Cats with cardiac disease showed higher fibrinogen levels than healthy controls.
- Hypercoagulability was present in 50% of SEC-T cats and 56% of ATE cats.
- ATE cats exhibited significantly higher vWF:Ag concentrations, suggesting endothelial injury.
Conclusions:
- Systemic hypercoagulability is common in cardiomyopathic cats, potentially preceding overt ATE or congestive heart failure (CHF).
- Hypercoagulability is identified as a significant risk factor for ATE in cats.
- Elevated vWF:Ag in ATE cats is likely due to endothelial damage caused by the thrombus.
Background:
Arterial thromboembolism (ATE) is a common complication of feline cardiomyopathy; however, the pathogenesis of ATE is unknown.
Hypothesis:
Systemic activation of the coagulation cascade (hypercoagulability) and endothelial injury promote ATE in cardiomyopathic cats.
Animals:
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.
Conclusion And Clinical Importance:
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.
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