Feline Cardiomyopathy Past Paper PDF

Myocardial Disease II: Feline Cardiomyopathy Lauren Markovic, DVM, DACVIM (Cardiology), FACVIM (Interventional Cardiology)  Learning Objectives Be able to describe the following for hypertrophic cardiomyopathy Pathophysiology of this disease and how the d...

Myocardial Disease II: Feline Cardiomyopathy Lauren Markovic, DVM, DACVIM (Cardiology), FACVIM (Interventional Cardiology)  Learning Objectives Be able to describe the following for hypertrophic cardiomyopathy Pathophysiology of this disease and how the disease leads to heart failure Appropriate diagnostic testing Etiologies for primary and secondary feline cardiomyopathies and differential diagnoses Understand what type of clinical signs, examination and diagnostic imaging findings can be seen in cats with cardiomyopathy, with and without congestive heart failure (CHF) Understand appropriate therapies for CHF Understand what medication is available for thromboprophylaxis for arterial thromboembolism Feline Cardiomyopathy – Case Study Fernando 10 yo MN DSH 2 week history of lethargy and decreased activity 48 hour history tachypnea Fernando – Physical Exam RR 80br/min HR 220bpm, gallop sound Temp 99.9 F MM: pale pink, CRT ~2sec Distended jugular veins Bilateral crackles II/VI left parasternal systolic murmur Strong, synchronous femoral pulses  Fernando… What is the cause of Fernando’s tachypnea? What are the clinical signs and physical exam findings of congestive heart failure? What are differential diagnosis for heart failure in this patient? Understand radiographic and echocardiographic abnormalities?  Feline Cardiomyopathies Primary disease of the cardiac muscle Hypertrophic cardiomyopathy (HCM) Restrictive cardiomyopathy Dilated cardiomyopathy Arrhythmogenic RV cardiomyopathy Nonspecific Secondary disease of the cardiac muscle Hyperthyroidism Systemic hypertension Dietary Tachycardia-related JVIM Volume: 34, Issue: 3, Pages: 1062-1077, 2020 Acromegaly  Hypertrophic cardiomyopathy (HCM) The most common feline cardiomyopathy! HCM - Pathology Ventricular thickening Typically LV wall and IVS Papillary hypertrophy May be asymmetric hypertrophy LA enlargement 10 yo MC DSH  HCM Pathophysiology Thickened, noncompliant ventricular wallsà diastolic dysfunction Decreased cardiac output from reduced diastolic filling Geometric changes in the ventricle and papillary muscles à MR Increased LA pressure à congestion (pulmonary edema, pleural effusion, pericardial effusion) Increased myocardial O2 consumption/decreased perfusion à myocardial ischemia LV outflow obstruction may occur  Pathophysiology Diastolic dysfunction à increased LA pressureà CHF  Clinical findings – HCM Review Fernando’s clinical signs… Compensated Cats may have “clinically silent” disease Murmur, typically sternal or parasternal Gallop Arrhythmias, femoral pulse deficits Decompensated Panting, tachypnea, dyspnea Cyanosis Jugular vein MM color variable (normal, pale, cyanotic) Crackles (if pulmonary edema) Decreased/muffled lung sounds (if pleural effusion) Ascites is rare Evidence of arterial thromboembolism  Dog vs. Cat? Feline cardiac disease/heart failure has several characteristics that differ from dogs  Dog vs. Cat DOGS CATS Primary valvular disease most common Cardiomyopathies (CM) most common CM – Systolic dysfunction CM – Diastolic dysfunction Cough – frequent presenting sign Very rare to cough with cardiac disease Signs gradually worsen Signs appear acutely Frequently ascites, less often pleural effusion Frequently pleural effusion, less often ascites Echo may not be needed for diagnosis Echo typically is necessary for definitive diagnosis Normal feline radiographs Normal VHS 7.75 to 8.0 Heart ~ 2.5 to 3.5 ICS  Radiographic findings Generalized cardiomegaly left atrial enlargement left ventricular enlargement CHF Distended pulmonary veins Interstitial, alveolar infiltrates Pleural effusion Rare ascites  Electrocardiography Look for… Conduction abnormalities Axis shifts Signs of chamber enlargement  Genetics - HCM Maine Coon and Ragdoll cats Mutations MYBPC3 – A31P, R820W  Echocardiography LV wall and septal thickening may be asymmetric or regional +/- LVOT obstruction fixed or dynamic (systolic anterior motion) +/- LA enlargement +/- Smoke or intracardiac thrombus  Echocardiography What are differentials of LV concentric hypertrophy? 1) Systemic hypertension 2) Hyperthyroid heart disease Measure blood pressure and obtain T4 Systolic anterior motion (SAM) Mitral regurgitation due to SAM Normal aortic outflow profile vs. LVOT obstruction  Acute therapy – Congestive heart failure Oxygen supplementation IV furosemide – decrease preload +/- pimobendan (PO) or dobutamine (IV) – increase contractility +/- sedation Thoracocentesis if pleural effusion Chronic CHF therapy Furosemide Loop diuretic ACE-inhibitor Enalapril or benazepril +/- Pimobendan Inodilator +/- Spironolactone Aldosteone antagonist  Fernando Day 1 CHF Follow-up Recheck visit 5-7 days Thoracic radiographs Renal panel Blood pressure Fernando 1 week post therapy  Additional Considerations - NT-proBNP 114 normal cats; 113 occult cardiomyopathy History, physical exam, and echocardiography NT-proBNP 100% specific in distinguishing healthy from cardiomyopathy Feline CM RCM – Myocardial form End-Stage HCM Normal wall thickness Walls may be normal Atrial enlargement Dilated chambers Diastolic dysfunction +/- myocardial infarction  Dilated Cardiomyopathy (DCM) Left ventricular dilation and systolic dysfunction Primary DCM is rare Secondary Taurine deficiency  CM Sequelae – Feline arterial thromboembolism (FATE) introduction… Pathophysiology - ATE Commonly associated with feline CM Damaged cardiac endothelium Hypercoagulable state Intracardiac blood stasis Thrombus leaves the heart and embolizes to the peripheral vasculature Distal blood supply disrupted Thrombi cause release of vasoactive substances Acute event à pain à Ischemia leads to necrosis of muscles or organs Reperfusion injury  In the heart… Impaired relaxation à Left atrial enlargement Left auricular enlargement Blood stasis à Smoke = spontaneous echogenic contrast Thrombus formation Endothelial injury, platelet activation  Arterial thromboembolism Superficial portions of an intracavitary thrombus can break off Most common site = terminal abdominal aorta (Saddle thrombus) Alternate sites… Brachial infarction Cerebral infarction Renal infarction Splanchnic infarction  The 5 P’s… Pain Pulselessness Pallor Paresis Polar (cold extremities)  Clinical Signs - ATE Cats may regain some to all motor function within 4-6 weeks Reestablishment of a collateral vascular network Intrinsic dissolution of the embolus Recanalization of the obstructed aorta Chronic complications from aortic infarction Self-mutilation Limb necrosis requiring amputation  Clinical Signs – Renal or Splanchnic Renal Mesenteric Acute renal failure, renal pain Severe abdominal pain Vomiting Central neurologic Stupor Seizures Sudden death  Additional clinical signs Hypothermia Murmur Gallop Arrhythmia Congestive heart failure Reported in up to 60% of cases  Diagnostic Tests Chemistry findings Chest radiographs Hyperglycemia (stress) Rule CHF in/out Hypoglycemia affected limb Azotemia Hypoperfusion, embolism Echocardiogram Increased CK LA size and content Increased AST/ALT Hyperkalemia  Prevention Severe left atrial enlargement Spontaneous echo contrast in LA Clopidogrel superior to aspirin Longer median time to ATE with clopidogrel  Management strategies Analgesia! Maintain hydration/perfusion Judicious use of fluids, however caution if px has CHF Manage CHF Thrombolytic therapy (tPA) – hemorrhage, reperfusion injury, $$ Anticoagulant therapy – heparin, low molecular weight heparin  Anticoagulants Heparin Unfractionated heparin (UH) Inhibits Xa and IIa Low molecular weight heparin – alternative to UH dalteparin, enoxaparin $  Prognosis Guarded Survival rates 33-39% Single limb affected – improved survival compared to bilateral pelvic limb infarction Acute prognosis is more clear after 24-72 hours