Feline Cardiac Disease Flashcards
Pathophys of feline HCM
Primary myocardial disease caused by sarcomeric defect within cardiac myocytes. Mutations in sarcomeric genes result in increased LV wall thickness but enhanced myocyte contractility.
→ myocardium becomes stiff, thick or weak (or some combination) altering anatomic structure and mechanical function
→ Reduced diastolic function (decrease preload) due to LV noncompliance
→ increased LA afterload → LA enlargement
Altered structure → MV regurgitation → further LA enlargement
→ compromised myocardial blood supply → myocyte death, ischaemia, fibrosis → arrhythmias, syncope and weakness
Breeds with mutations associated with HCM
Significance of these mutations
Mutations in the same gene can cause different phenotypes, and mutations in different genes can cause the same phenotype.
Maine Coon - cardiac myosin binding protein C Autosomal Dominant
30-45% breed prevalence, 10% homozygous (but only 7-10% get severe phenotype). Heterozygotes usually not clinical (mild changes) though some will still get HCM
Ragdoll - R820W myosin binding protein C mutation Autosomal Dominant
Homozygotes have thicker LV wall than heterozygotes. Mutation prevalence is 27.4%, 1.4% homozygotes.
Sphynx - ALMS1 alstrom syndrome, present in many cats with HCM but have not assessed prevalence in cats without HCM so uncertain significance as a test
For other breeds genetic testing not recommended as these mutations have not been identified in other breeds with HCM
DDx for hypertrophic phenotype
DDX for hypertrophic phenotype = hypertension; hyperTH, reduced preload, neoplastic cardiac infiltrate; transient myocardial thickening, acromegaly
Taurine deficiency -> DCM
Cause of Obstructive HCM
Systolic anterior motion (SAM) of the MV can cause both dynamic LVOTO and MVR
SAM occurs due to hypertrophied and cranially displaced papillary muscles pulling a part of the anterior leaflet of the MV into a normal or narrowed LVOT
Once in the LVOT the tip of the leaflet is pushed further towards the septum by blood flowing from the apex of the left ventricle during systole, often with part of the leaflet touching the septum
This is dynamic LVOTO (a form of subaortic stenosis) that progressively worsens throughout systole
Due to distortion of the mitral valve there is also subsequent mitral regurgitation
Higher prevalence of false tendons in cats with OHCM
Findings associated with increased risk of HF in HCM
Moderate to severe LA enlargement is consistently associated with a negative effect on survival time in both occult and overt disease.
Severe LV hypertrophy, decreased systolic function and ↓ LA function, and RV enlargement are all associated with poor prognosis.
A gallop sound or arrhythmia on PE
Decreased LA fractional shortening
Decreased LV systolic function
Regional wall thinning with hypokinesis or restrictive diastolic LV filling pattern
Acute stress, anaesthesia, IV fluid therapy or steroid administration have all been reported to tip a cat from being subclinical into clinical heart failure.
Although, most cats presenting with CHF have no history of precipitating event and no exacerbating disease present
Accuracy of NT-proBNP in differentiating cardiogenic and noncardiogenic pleural effusion
Quantitative NT-proBNP laboratory test is reasonably accurate at differentiating cardiogenic PLE from other causes of PLE when either plasma (sensitivity, 95%; specificity, 82%) or pleural fluid (sensitivity, 100%; specificity, 76%) is used. The point of-care test (SNAP; IdEXX) is also reasonably accurate for this purpose if plasma is used (sensitivity, 100%; specificity, 79%) or if pleural fluid is used (sensitivity, 100%; specificity 86%)
Utility of NT-proBNP for screening HCM
Serum or plasma NT-proBNP concentration using the quantitative test is reasonably accurate at identifying subclinical HCM in cats referred to a veterinary cardiologist.
For example, a cut-off value of 99 pmol/l has been associated with 71% sensitivity and 100% specificity when screening cats for cardiomyopathy in a cardiology referral population.
sensitivity is significantly lower (51%) when the screened population is cats in general practice. The specificity, however, remains high (92%)
So, if the value is <99 pmol/l, the test result is much less meaningful since approximately 50% of cats in general practice with a negative test result will have a left-sided cardiomyopathy
similar situation exists for the point-of-care assay when comparing results in a referral practice population (sensitivity and specificity of 65–84% and 83–100%, respectively) with those in a general practice population (sensitivity of 43% and specificity of 96%)
Sensitivity increased to 71% when only used on cats with heart murmur
Recommendations for stage B HCM
Therefore, the best that can be done is to: Monitor the cat for the development of severe LA enlargement (so that antiplatelet/ anticoagulant therapy can be started);
< Avoid treatments that can trigger heart failure iatrogenically (eg, injudicious fluid therapy);
< Not breed the cat if it is sexually intact;
< Monitor for the onset of left heart failure (PE and/or PLE), if the LA is moderately to severely enlarged.
Recommendations for stage C HCM
administering a loop diuretic during all phases of treatment,
supportive therapy (oxygen, warming blanket) during the emergent phase
Antiplatelet/anticoagulant medication when there is severe LA enlargement
Possibly administering oral pimobendan and an angiotensin converting enzyme (ACE) inhibitor,
(limited evidence for either - in fact recent studies suggest no benefit in survival/outcome)
B blockers only in severe LVOTO - even then evidence of benefit is limited, more theoretical.
Reducing, or preferably eliminating, high-sodium foods and treats to avoid negating the natriuretic purpose of diuretics, will be undertaken regardless of the underlying type of cardiomyopathy
factors contributing to ATE
Endothelial injury is evident as an increase in the amount of von Willebrand factor in the endothelium of enlarged feline left atria and by its integral presence in LA thrombi from cats with severe cardiomyopathy.
blood flow stasis predisposes to red cell clumping which can be visualised on echocardiography as ‘smoke’ in the left atrium
Prognosis in ATE
Time (48–72 h) can be allowed to see if the cat can lyse its own thromboembolus via activation of plasmin. In one study of 127 cats presented with ATE, 89 were treated with supportive care and 39 (45%) survived to discharge HOWEVER: median survival time for that group of 39 cats was only 117 days. In another study, only around 30% survived to hospital discharge.
Up to 80% of cats with one affected limb will survive.
Overall 1-year survival for the entire population of cats with ATE is only around 10%
Evidence for thromboprophylaxis Txs in FATE
No prospective evidence of thromboprophylaxis reducing risk of ATE in cats with subclinical HCM - but makes physiological sense to try with anti-plt drugs.
No single treatment proven more effetcive in acute setting: traditionally used LMWH but combination with plt antagonism also often used (does not lyse thrombus but prevents it getting bigger). No prospective trials comparing these methods exist. Hampered by low survival
Matter of then waiting to see if patients thrombolytic system can break down the clot.
FATCAT - clopidogrel superior to aspirin at reducing risk of ATE and longer time to recurrence
JFMS 22 - retrospective case series. Clopidogrel + rivaroxaban in cats post ATE - reduced incidence of recurrence compared to prior single agent studies. Minor haemorrhage reported in some. Retrospective
JVIM 23 - synergistic effect of clop + riva on plt funct tests and plt dependent thrombin generation. Combined therapy was more effective than either drug alone at reducing these variables.
Diagnosis of OHCM
Aortic blood flow velocity determines severity of >50mmHg is abnormal, >80mmHg is severe
Obstruction worsens through systole
Systolic anterior motion of MV - develops due to abnormal papillary muscle size and narrowing of outflow tract → LVOTO.
Often causes a murmur, louder when stressed
Midventricular obstruction - phenotypic variant of HCM associated with LVOTO. Hypertrophy of papillary muscle. May be associated with murmur
Other cardiomyopathies in cats and their features
OHCM - Hypertrophy of the IVS > FW - obstructs LVOT and increases LV afterload further → reduced CO further
REVEAL - no significant difference in risk of CHF/ATE or cardiac death in cats with HCM or OHCM.
RCM - Impaired ventricular filling due to increased stiffness of myocardium
→ decreased ventricular filling and increased end diastolic filling pressure → pressure overload of LA
Later in disease there is also altered systolic function
Echo: normal appearing LV with LAE.
NO MYOCARDIAL THICKENING - major difference with HCM, but diastolic function is impaired
Diastolic dysfunction in absence of HCM
Identification of fibrous bands
Possible association with Bartonella hensela (50% of affected cats) causing endomyocarditis
DCM - Inherent myocardial disease resulting in reduced contractility and myocardial systolic failure
To compensate → LV volume increases (eccentric hypertrophy)
Dilation → altered MV annulus and MVR → atrial dilation and risk of ATE or CHF
LV dilation and depressed myocardial performance in absence of systemic hypertension or valvular/congenital defects
Echo: increased end systolic LV internal diameter (>11mm)
ECG: most have abnormal ventricular traces.
ARVC - Fibrofatty replacement of RV conductive myocardium. Arrhythmogeneic - formation of macro-reentrant circuits in fibrofatty replacement tissue,.
Present with RSCHF more commonly
May hear right sided tricuspid murmur
Echo: marked thinning of the RV free wall, nearly completely replaced with fibrous tissue; RAE. , increased RV diastolic pressure; tricuspid regurg
