Acquired CV disease of cats Flashcards
Commonest acquired cardiac disease - CATS
Myocardial - i.e. cardiomyopathy
Congenital - less common
Primary arrhythmias - also less common
Primary valvular disease - extremely rare
Pericardial disease - much less common than dogs
Types of cardiomyopathy
Same classification as humans: ****Hypertrophic - HCM**** Dilated - DCM Restrictive - RCM Arrhythmogenic - ARVC
Key features - HCM
Concentric LV hypertrophy (disatolic septum or free wall thickness > or equal to 6mm)
Poor LV relaxation
Stiff LV
Key features - DCM
Dilated LV with thin LV walls
Hypokinetic LV
Key features - RCM
Marked atrial dilation
No LV hypertrophy or dilation
Stiff LV
Key features - ARVC
Left heart relatively normal
Severe dilation of RA and RV
RV wall thinning
List examples of secondary myocardial disease
Hyperthyroid myocardial disease
Hypertensive myocardial disease
Cardiomyopathy secondary to hypersomatotropism (acromegaly)
When is it difficult to identify the original form of myocardial disease?
when pathological processes such as myocarditis or infarction are also present
Another name for HCM
Idiopathic (or genetic) left ventricular hypertrophyy (i.e. NOT due to systemic hypertension, aortic stenosis or hyperthyroidism)
Mutations - HCM
Human - usually associated with genetic mutations in sarcomeric proteins
Mutations in myosin binding protein C identified in Maine Coons and Ragdolls with HCM
Pathophysiology - HCM
MILD DISEASE: Impaired ventricular relaxation and increased ventricular stiffness. BOTH –> diastolic dysfunction
END STAGE: LA dilation, LA contractile dysfunction, LV systolic dysfunction (EFFECTS = increased atrial pressures, CHF, LA thrombus formation)
Also dynamic LVOTO
Define LVOTO
left ventricular outflow tract obstruction.
It describes the abnormal motion of the anterior mitral leaflet during systole (SAM)–> anterior leaflet moves towards OT during ejection –> OT obstruction and mitral regurgiatation –> worse with increased contractility, SNS stimulation or ventricular septal hypertrophy
Pathological findings - HCM
LV hypertrophy may affect any part of LV
LA dilates when filling pressures increased
Myocardial infarction may occur, appear as localised wall thinning with hypomobility and scarring.
Signalment - HCM
most common in young male adults
BUT all ages affected
Predisposition: maine coons, persians, ragdolls, cornish rexes and bengals. Most cats with HCM are moggies.
Presenting signs - HCM - 4
Asymptomatic - majority
Respiratory distress (CHF) - minority
HL paralysis due to ATE - minority
Sudden death - unknown prevalence
PE - HCM
** +/- variable intensity systolic murmur **
Prominent apical impulse
+/- gallop sounds (poor prognosis), arrhythmias
+/- tachypnoea, crackles
May be completely NORMAL
Radiography - HCM
LV hypertrophy (long cardiac silhouette on lateral view) Pulmonary oedema and/or pleural effusion (indicate CHF)
Echocardiography - HCM
LV hypertrophy = diastolic septal or free wall thickness greater than or equal to 6mm (focal or generalised)
SAM of mitral valve causes DLVOTO and murmur
Define SAM
Systolic anterior motion
Define DLVOTO
Dynamic left ventricular outflow tract obstruction
Prognosis - HCM
GOOD: short-medium term if LA normal size
POOR: if clinical signs present, LA enlargement, ATE
Describe DCM
Dilation of all 4 chambers, with thinning of the ventricular walls and hypokinesis (systolic dysfunction). Historically associated with taurine deficiency. Now uncommon - most cats diagnosed have normal serum taurine levels.
Clinical presentation - DCM
Middle-aged and older
Taurine-deficiency (if fed dog food)
Signs of output failure (hypotension, hypothermia, bradycardia)
Murmur quiet/absent but gallop often present
Thromboembolic disease - common
Echocardiography - DCM - 3
Dilated, spherical LV
FS < 30%
LV end-systolic diameter >14mm
Prognosis - DCM
Grave
Outline RCM
Severely impaired diastolic filling
Stiff LV
Relatively normal LV dimensions and systolic function
2 forms of RCM
Endomyocardial form - severe endomyocardial scarring such as a bridging scar across the LV.
Myocardial form - normal LV dimensions, non-infiltrative, patchy thickening of the LV walls
Severe atrial enlargement in both forms.
Clinical presentation - RCM
older cats dyspnoea from pleural effusion common \+/- low output signs \+/- ATE arrhythmias common
Echocardiography - RCM
severe bilateral enlargement
Endomyocardial form of RCM is distinctive - endomyocardial scarring is readily imaged
Myocardial form is more challenging
Outline ARVC
Arrhythmogenic right ventricular cardiomyopathy
Only recently characterised in cats - fibrofatty infiltration of the LV (scar tissue and adipose cells).
Marked right heart enlargement
May be asymptomatic
May be syncopal in association with arrhythmias
May have right-sided HF
Echocardiography - ARVC
Severe RV and RA dilation
Tricuspid regurgitation usually present
How is feline heart disease staged?
A = predisposed B1 = HCM, no CHF, normal LA B2 = HCM, no CHF, big LA C = HCM + CHF (past or present) D = HCM + CHF despite treatment
Treatment options - A - cats at risk of HCM
MBPC mutation test available - maine coons and ragdolls only
ANY cat could be at risk of HCM
Echocardiography provides a definitive diagnosis
Can consider NT-proBNP as initial step (>100picomols/litre)
Treatment options - B - asymptomatic cats (HCM)
Some affected cats are at low risk for complications and don’t need treatment (no gallop, no arrhythmia, normal LA size, low NT-porBNP/troponin-I)
LVOTO - give a beta-blocker such as atenolol, may control the obstruction, currently no proven survival benefit, eases angina pain in humans
High risk cats (LA dilation, systolic dysfuction, extreme hypertrophy) - consider anti-thrombotic to reduce risk of ATE (e.g. clopidogrel is better than aspirin)
What should you be aware of in cats with acute life-threatening HF?
Do everything to cause the least stress possible - echo is less stressful than radiographs
Treatment - C - past or present HF
IMPROVE OXYGENATION:
Administer CO2 - oxygen cages practical
SEDATION: since dyspnoeic cats often become very distressed (butophanol sometimes works well)
IV FUROSEMIDE TO EFFECT: initial dose lower than dogs (2mg/kg) with subsequent doses (1-2mg/kg) every 60 mins until RR increases
THORACOCENTESIS: generally with a butterfly cannula
INCREASE CO: Difficult! If BP normal –> just treat
congestive signs. AVOID IV fluids - won’t increase CO and will worsen CHF.
What are aims of home therapy for mild-moderate HF patients?
Eliminate abnormal fluid retention
Modulate neurohormonal activation
Optimise haemodynamic function
Prevent thromboembolism
How do you eliminate fluid retention
FUROSEMIDE (1-4mg/kg q12-24 hours PO) - use to effect - decrease once congestive signs clear
ACEI - target dose of benazepril (0.5mg/kg q24 h)
How can neurohormonal activation be modulated?
ACEI - benazepril preffered as licesned in cats - no evidence that abnormal hypertrophy is reveresed - Imidapril is difficult to pill cats with as it is a tasteless liquid.
How can haemodynamic function be optimised?
Pimobendan if systolic dysfunction present
Otherwise v difficult to improve diastolic function
Treatment - supraventricular tachycardia
Diltiazem
What are the thoughts on using negative inotropes for dynamic obstruction?
Negative inotropes may decrease LVOTO gradients and beta-blockers are more effective at this than diltiazem in cats. However, negative inotropes may worsen CHF.
Treatment - chronic refractory HF
If CHF persists despite therapy with furosemide and an ACEI, increase furosemide dose. If CHF continues desptite this, consider adding other diuretics:
Spironolactone - not licensed in cats - dosing similar to dogs - 1mg/kg q24h PO. Facial skin lesions
Thiazides - off label - combination used most commonly
For cats with systolic dysfunction, pimobendan can be added. Not licensed and should NOT be used in cats with DLVOTO.
When may ATE occur?
any cardiomyopathy
particularly when the LA is dilated and poorly contractile
A thrombus usually forms in the left auricle and when disolodge dis ejected into the systemic circulation only to lodge in a peripheral artery. The commonest site is the distal aorta, but other sites include subclavian artery or a cerebral, renal or mesenteric artery.
CS: peracute and severe, with HL paresis and pain associated with obstruction of the terminal aorta.
Rate of survival to discharge <45%.
Underlying myocardial disease predisposing to TE cannot usually be resolved.
Management - acute ATE - 5
Analgesia - methadone, fentanyl CRI
Manage electrolyte and acid-base abnormalities
Prevent thrombus extension - consider early use of clopidogrel
Pulses often return in 72h, thorough limb use longer (physio)
Thrombolysis can be associated with increased risk of reperfusion syndrome - therefore not usually attempted
How can systemic TE be prevented? 4
Clopidogrel (superior to aspirin)
Aspirin (high or low dose)
Warfarin - not recommended
LMW-heparins - not recommended, costly, SC injection
