Many humans with cardiomyopathy have systemic hypercoagulability.1,2 Results of other studies3,4 suggest that dogs and cats with cardiomyopathy may also have systemic hypercoagulability. Hypercoagulability in humans with heart failure may be associated with platelet activation, increased thrombin activity, and endothelial dysfunction.5 Moreover, hypercoagulability in humans with hypertrophic cardiomyopathy may be caused by left atrial enlargement, whereas hypercoagulability in humans with DCM may be caused by left ventricular enlargement and dysfunction.1 Both of those diseases are associated with formation of thromboembolisms. Although controversial, cats6 and humans7 with cardiac failure or left ventricular systolic dysfunction are sometimes treated with anticoagulants. Platelet aggregation inhibitors and warfarin are used as anticoagulant drugs in humans with heart failure.7
A major complication of anticoagulant treatment is hemorrhage. Despite the systemic hypercoagulable state in humans with cardiomyopathy,1,2 humans with severe heart disease who are treated orally with anticoagulant drugs have an increased risk of bleeding.8 However, to the authors' knowledge, ascites attributable to right-sided CHF has not been investigated as a risk factor for bleeding in such patients.
Fibrinolysis results in dissolution of fibrin, and hyperfibrinolysis (which compromises blood clot integrity) develops when the rate of fibrinolysis is greater than the rate of fibrin formation. Hyperfibrinolysis is classified as primary or secondary.9 Primary hyperfibrinolysis develops independently of intravascular activation of coagulation, and plasmin is formed without concomitant formation of thrombin. Lysis of preformed fibrin and fibrinogen will then occur.9–11 In addition to causing increased degradation of fibrinogen and preformed fibrin (if present), spontaneous formation of plasmin causes degradation of coagulation factors V, VIII, IX, and XI.10 Primary hyperfibrinogenolysis is a rare condition that develops in humans in association with acute conditions such as shock, surgical procedures, liver transplantation, acute leukemia, or administration of thrombolytic drugs. It can also be caused by chronic conditions, such as neoplasia or chronic liver disease.10 During PHF, production of FDPs is increased but production of D-dimer is not increased.10 Secondary hyperfibrinolysis is a consequence of activation of a coagulative process, often caused by DIC, which stimulates endothelium to increase production of tissue plasminogen activator, causing activation of plasminogen to form plasmin.9 Lysis of cross-linked fibrin during secondary hyperfibrinolysis generates FDPs and D-dimer.10,11 To the authors' knowledge, PHF has been reported only once in the veterinary medical literature,a and it has never been associated with congestive cardiac diseases in humans or other animals. Standard criteria for diagnosis of PHF have not been reported. Nevertheless, discordant FDPs and D-dimer assay results may be an indicator of PHF and such criteria have been used in a clinical setting to diagnose PHF in humans.10,12,13
We identified a 9-year-old sexually intact male CKCS (index dog) with a 2-week history of exercise intolerance and ascites attributable to right-sided CHF that was referred to the Small Animal Hospital of Glasgow University, Glasgow, Scotland, because of a progressively enlarging neck hematoma that developed following jugular venipuncture for blood collection. Results of the coagulation profile analysis were characterized by severe hypofibrinogenemia, prolonged aPTT and PT, discordant results between FDPs and D-dimer assays, and mild thrombocytopenia. Therefore, we conducted a retrospective study to determine whether other dogs with right-sided CHF and ascites had such hemostatic abnormalities. The objectives of this retrospective case-control study reported here were to determine whether dogs with right-sided CHF and ascites had hypofibrinogenemia, prolonged aPTT and PT, and discordant plasma FDPs and D-dimer assay results (ie, a circulating concentration of FDPs higher than the reference range and a circulating concentration of D-dimer within the reference range) and to determine whether such assay results were associated with bleeding rather than the more commonly reported thrombotic events in those dogs.
Activated partial thromboplastin time
Congestive heart failure
Cavalier King Charles Spaniel
Disseminated intravascular coagulation
Fibrin-fibrinogen degradation product
Caldin M, Furlamello T, Florio F, et al. Primary hyperfibrinogenolysis in dogs (abstr), in Proceedings. Eur Cong Comp Vet Clin Pathol 2005;27.
STA APTT Kaolin, Diagnostica Stago, Asnières sur Seine, France.
STA Neoplastin Plus, Diagnostica Stago, Asnières sur Seine, France.
STA Fibrinogen, Diagnostica Stago, Asnières sur Seine, France.
STA Compact, Diagnostica Stago, Rhoce, Bäsel, Switzerland.
FDPs plasma, Diagnostica Stago, Asnières sur Seine, France.
Caldin M, Fulanello T, Lubas G. Sensitivity and specificity of citrated plasma FDPs and D-dimer in the diagnosis of disseminated intravascular coagulation (DIC) in dogs (abstr). J Vet Intern Med 1998;12:236.
Tina-quant D-Dimer, Roche Diagnostic GMBH, Mannheim, Germany.
Olympus AU 640, Hamburg, Germany.
ADVIA 120, Bayer Heath Care, Tarrytown, NY.
Vetmedin, Boehringer Ingelheim Ltd, Bracknell, West Berkshire, England.
Fortekor, Novartis Animal Health UK Ltd, Camberley, Surrey, England.
Furosemide, TEVA UK Ltd, Eastburn, East Sussex, England.
Spironolactone, Dr Reddy's Laboratories Ltd, Beverly, North Humberside, England.
Cykelokapron, Pfizer Ltd, Walton-on-Hill, Surrey, England.
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