Introduction

• Aortic thromboembolism is a common clinical entity in cats with cardiomyopathy.
• Cause: usually cardiomyopathies, occasionally hypercoagulable states and pulmonary primary neoplasia.
• 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

• Cardiomyopathy Heart: hypertrophic cardiomyopathy.
• Hyperthyroidism Hyperthyroidism (rare).
• Hypercoagulable conditions, eg neoplasia, liver disease Liver: chronic disease, DIC Disseminated intravascular coagulation.
• Pulmonary neoplasia Lung: pulmonary neoplasia.
• Aberrant migration of adult heart worm Cardiopulmonary dirofilariasis.

Pathophysiology

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

Thrombus formation

• Dilated left atrium (any underlying cardiomyopathy leading to elevated left atrial with incomplete atrial diastolic filling of the left ventricle and aggregation of red blood cells, 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 h.
• Nerve fibers may not have ischemic changes until 5 h post-thromboembolism compared to muscle damage 2-3 h 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 h after the thromboembolic event that result in the reperfusion injury (and subsequent and rapid development of hyperkalemia and arrhythmias) that kills many cats.

Timecourse

• Acute onset signs.

Diagnosis

Treatment

Prevention

Outcomes