Felis ISSN 2398-2950

Thromboembolism: aorta

Synonym(s): Feline aortic thromboembolism; FATE

Contributor(s): Serena Brownlie, Phil Fox, Philip K Nicholls, Penny Watson

Introduction

  • Aortic thromboembolism is a common clinical entity in cats with cardiomyopathy.
  • Cause: usually cardiomyopathies, occasionally hypercoagulable states.
  • Signs: depends on site of embolus lodging.
  • Diagnosis: signs.
  • Treatment: supportive, anticoagulation therapy, treatment of underlying condition.
  • Prognosis: guarded.
    Print off the owner factsheet Feline aortic thromboembolism Feline aortic thromboembolism to give to your client.

Pathogenesis

Etiology

Pathophysiology

  • Thrombus lodges in vessels (usually distal aorta) and obstructs circulation.

Thrombus formation

  • Dilated left atrium (dilated cardiomyopathy Heart: dilated cardiomyopathy (DCM)) or high left atrial pressure with resistance to outflow (hypertrophic cardiomyopathy Heart: hypertrophic cardiomyopathy)   →   stasis of blood flow in left atrium   →   thrombus formation.
  • Damage to endocardium, eg mitral regurgitant jets, also predisposes to thrombus formation.
  • Platelet hyperaggregability may predispose some cats to disease.

Embolic effects

  • Subendothelial collagen is exposed   →    von Willebrands factor   →    adherence of platelets   →    release adenosine diphosphate (ADP)   →    production of thromboxane A from the platelet membrane   →    vasoconstriction and recruitment of more platelets   →    clot formation.
  • Skeletal muscle is more susceptible to ischemic-reperfusion damage than the nerve. Ischemic myopathy usually affects the cranial tibial muscle but the gastrocnemius muscle can be severely damaged. Depletion of ATP in muscle causes muscle to contract.
  • When autolysis occurs the muscle proteins breakdown and the muscles soften at about 36 hours.
  • Nerve fibers may not have ischemic changes until 5 hours post-thromboembolism compared to muscle damage 2-3 hours later.
  • It is not blockage of the artery that causes the ischemic neuromyopathy (collateral circulation opens up). It is the reopening of these collateral vessels in the 12-24 hours after the thromboembolic event that result in the reperfusion injury that kills many cats.

Timecourse

  • Acute onset signs.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Welch K M, Rozanski E A, Freeman L M et al (2009) Prospective evaluation of tissue plasminogen activator in 11 cats with arterial thromboembolism. J Feline Med Surg 12 (2), 122-128 PubMed.
  • Alwood A J, Downend A B, Brooks M B et al (2007) Anticoagulant effects of low-molecular weight heparins in healthy cats. JVIM 21 (3), 378-387 PubMed.
  • Hogan D F, Andrews D A, Green H W et al (2004) Antiplatelet effects and pharmacodynamics of clopidogrel in cats. JAVMA 225 (9), 1406-1411 PubMed.
  • Norris C R, Griffey S M & Samii V F (2000) Pulmonary thromboembolism in cats - 29 cases (1987-1997). JAVMA 215 (11), 1650-1654 PubMed.
  • Schoeman J P (1999) Feline distal aortic thromboembolism - a review of 44 cases (1990-1998). J Fel Med Surg (4), 221-231 PubMed.
  • Sottiaux J & Franck M (1999) Pulmonary embolism and cor pulmonale in a cat. JSAP 40 (2), 88-91 PubMed.
  • Atkins C E, Gallo A M, Kurzman I D et al (1992) Risk factors, clinical signs, and survival in cats with a clinical diagnosis of idiopathic hypertrophic cardiomyopathy: 74 cases (1985-1989). JAVMA 201 (4), 613-618 PubMed.
  • Pion P D (1988) Feline aortic thromboemboli and the potential utility of thrombolytic therapy with tisssue plasminogen activator. Vet Clin North Am Small Anim Pract 18 (1), 79-86 PubMed.


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