Feline Myocardial Disease Flashcards
Cardiomyopathies
Diseases affecting the heart muscle with unknown/ uncertain etiology
ACVIM Cardiology consensus staging
A: predisposed (genetic/congenital)
B1 (low risk): subclinical- normal/ mild atrial enlargement
B2: (higher risk): subclinical- moderate to severe atrial enlargement
C: current/ previous CHF/ atrial thoraco embolism
D: refractory CHF
Hypertrophic cardiomyopathy
Most common acquired heart dz in cats
Concentric hypertrophy asymmetrical or generalized ( maine coon, shorthair)
Obstructive/ HOCM (murmurs)and non/ HCM forms
Genetics of HCM
Mutations in genes that encode proteins of the cardiac sarcomere → phenotypic HCM
Breed predispostion of HCM
Maine coon and ragdoll
Maine coon and ragdoll
Mutation of myosin-binding protein C (30%)
Most cats that are heterozygous for mutation won’t get sick
Homozygous= sick after 3y of age (maine coon), 1-2y old (ragdoll)
HCM pathophysiology
Diastolic dysfunction (↑ LV relaxation, LA pressure, and LV filling pressure)
Thromboembolic events
Arrhythmias secondary to ischemia
Signalment of cats with HCM
Most between 4-7y
Male predominance
CS associated with HCM
Often normal
Signs of L-CHF (rarely cough)
Systemic arterial thromboembolism
Syncope, sudden death from arrythmias
What’s seen on a PE of a cat with HCM
Auscultation (S4 gallop, systolic murmur)
CHF: resp. ditress
Most murmurs associated with HCM
Systolic
L-or-right parasternal
What causes a mumur with HCM
Dynamic left outflow tract obstruction/ systolic anterior motion of the mitral valve (SAM)
HOCM
HCM thoracic rads
Modest cardiomegaly
Bi-atrial enlargement
Pulm. venous congestion/ edema, pleural effusion
HCM ECG
Concentric hypertrophy of LV
LA dilation +/- thormbi
DSAS from SAM (obstructive)
Abnormal LV filling pattern
DX HCM
Dx of exclusion (rule out physiologic causes of concentric hypertrophy- hyperthyroid, hypertension and obstruction)
ProBNP (confirm with echo, helpful if - or slightly elevated)
Clin path of HCM
↑ CK, LDH and AST with emboli
K+ with reperfusion
Myofiber disarray
Tx of HCM (asymptomatic)
No tx (A-B1)
Beta-blocker in case of HOCM (atenolol)
Emergency tx for dyspneic patient with HCM
FOT: furosemide, oxygen then thoracocentesis (if pleural effusion)
Nitroglycerin ointment
Clinical management for HCM
Chr. oral therapy:
ACE inhibitors and diuretics (stage C-D)
Beta-blockers (complete HOCM)
Anticoagulant therapy (advanced B2-D)
Restrictive cardiomyopathy phenotype
Restrictive LV filling
Myocardial (idiopathic, non-infiltrative) and endomyocardial forms
Pathophysiology of restrictive cardiomypathy phenotype
Impaired diastolic filling
Severely dilated atria (mickey mouse heart)
Thryrotoxic cardiomyopathy
Hyperthyroidism: tropic effect →hypertrophy and tachycardia
focus on treating the underlying hyperthyroidism
What’s seen with Thyrotoxic cardiomyopathy ?
Arrhythmias, DSAS, DSPS
High output, vol expansion: systolic pump failure and high output heart failure
Dilated cardiomyopathy phenotype
Dietary taurine deficiency
Left ventricular eccentric hypertrophy
Decreased systolic function
How to tx DCM
Taurine supplements
Pimobedan (systolic dysfunction)
Placid for thromboprophylaxis
Standard therapy for CHF
Thrombus formation
Left atrial formation (LA)
Virchow’s triad (hypercoagulable state, endothelial injury, blood stasis)
Thrombus formation on U/S
Spontaneous echogenic contrast “smoke”
Increased blood echogencity (RBC aggregates)
Forms under low flow conditions
Marker of a prothombotic state
Thromboembolism in feline cardiomyopathies
Risk of thrombus formation in dilated atrium or distal aorta (saddle thrombus)
Acute paresis
Ischemic neuropathy
Activated platelets within the the thromboembolism →release vasoactive substance → serotonin and thromboxane A2→ collateral vasoconstriction
CS of thromboembolism
Acute hindlimb, pain, cold extremities, absence of femoral pulses, shock and hypothermia, dyspnea from pain or CHF
Dx of thromboembolism
Auscultation: murmur, gallop, arrhythmia, normal
Rads
Echocardiogram
Managing thromboembolism
Pain management (opioid)
CHF management
Limited thrombus progression (alter coagulation- heparin and decrease platelet aggregation- plavix)
Oral direct Xa inhibitors (rivaroxaban ans apixaban)
Plavix (clopidogrel)
Prevents platelet aggregation, protects collateral circulation
Decreased risk of 2nd thromboembolic event
Risk if perfusion
12-24 hrs after thromboembolism
Reperfusion of ischemic tissue
Release of K+ in the blood stream
Hyperkalemia
Further consequences of hyperkalemia
Bradycardia, ventricular arrhythmias (risk of sudden death)
Tx: rapid acting insuline + dextrose
