Feline Cardiomyopathies Flashcards
What is the dominant form of heart disease in cats?
CMOs, usually hypertrophic
Outline some causes for dilated feline CMO
Taurine deficiency (no longer common)
Hyperthyroidism is a very likely occurrence in older cats. What causes it to appear like HCM?
Regional vasoconstriction
Outline the aetiology of feline HCM
Idiopathic, but a strong genetic predisposition in some breeds
Which breeds have a strong genetic predisposition to HCM?
Maine coon (autosomal dominant; mutation in myosin-binding protein C) Persian Ragdoll (different mutation in myosin-binding protein C) American shorthair
What viral disease is though to relate to feline HCM?
Parvovirus
Explain the pathophysiology behind HCM
Thickening of LV wall and septum, small lumen
Stiff ventricular walls, diastolic dysfunction, poor LV filling, low SV, neurhohormonal activation, tachycardia, even poorer LV filling.
Progressively high LV filling pressures, enlarged LA
Possible common consequences of HCM as a result of the pathophysiology?
Pulmonary congestion
Thrombus formation in LA or LV
Arterial thromboembolism
List some pathophysiology cal complications of HCM
LV outflow tract obstruction Myocardial ischaemia Mitral insufficiency Atrial fibrillation (uncommon) Biventricular failure with pleural effusion
What are the clinical features of HCM cats (age, progression, signs, etc).
middle aged, male cats (can occur at any age and sex)
subclinical for years, murmur possible
Mostly present with resp. Signs or aortic thromboembolism.
Tachyponoea, panting with mild exertion, dyspnoea
List a common condition affecting the posterior of a cat with HCM following thromboembolism lodgement
Saddle thrombus.
Is a saddle thrombus painful? How does it present? What is the result?
Painful within the first hour and then ceases. Pulses become weaker, footpads cyanotic, muscles begin to feel tight and stiff. Support these animals, but expect a plantar grade stance with limited functionality (can’t jump well, aren’t happy).
Clinical features of HCM?
Disease onset may seem acute despite development of pathological changes
Acute development of CHF and or sudden death possible
Possible systolic (usually mitral) murmur
+/- gallop. Sound/rhythm +/- arrhythmia
Usually good pulses, strong precordial impulse (apex beat)
Maybe pulmonary crackles
Maybe muffling (if pleural effusion)
What leads you to a diagnosis of HCM (what findings)?
Radiograph:
Echocardiography
ECG
Ruling out secondary causes (hyperthyroidism, systemic hypertension, SAS, taurine deficiency)
Valentine shaped heart (not always present)
You radiograph a suspect HCM and notice a bronchoinsteretitial pattern heading towards becoming alveolar. After giving Frusemide and taking another RadX a few hours later, the substance disappears. hat time of substance was it likely to be? What do you suspect?
Low protein, watery fluid. Still HCM. Frusemide is good at fixing waterlogged lungs in HCM cases.