Cardio3- HCM

  1. What is HCM?
    primary yocardial disease of unknown origin characterized by concentric hypertrophy and diastolic dysfunction of the LV and rarely the RV (thought to be genetic)
  2. What is a sign that dogs with CHF usually have that cats usually DO NOT?
  3. ____________ are very sensitive are relatively specific for cardiac abnormalities/ myocardial dz in cats.
    gallops and murmurs
  4. Is heart rate a good indicator of cardiac dz in cats?
    no- cats tend to have high sympathetic tone during PE
  5. What are primary idiopathic cardiomyopathies in cats? (4)
    HCM**, restrictive cardiomyopathy, DCM, arrhythmogenic RV CM (more a dog thing)
  6. What are common causes of secondary cardiomyopathies in cats? (7)
    hyperthyroidism, hypertension, chronic anemia, ischemia/infarction, taurine deficiency, myocarditis, acromegaly
  7. End-stage HCM has a(n) ___________ phenotype because...
    mixed hypertrophy; the heart dilates to try and compensate (increase SV and CO).
  8. What breeds of cat commonly are associated with HCM?
    Maine Coon (4-7 years old), Ragdolls (early onset- 6-12 months old)
  9. Males are _________ commonly affected with HCM than females.
  10. Describe the pathogenesis of HCM.
    genetic abnormality--> mutation causing impaired structure and sarcomere assembly--> contractile dysfunction and compensatory peripheral repair--> pressure, modifier genes, lifestyle--> hypertrophy, myofiber disarray, fibrosis, and small vessel dz--> HCM--> burn out--> DCM
  11. What is the mutation associated with HCM?
    impaired structure and assembly of sarcomeres (poison peptides), causing contractile dysfunction
  12. What pathological processes are associated with HCM? (5)
    concentric hypertrophy, myofiber disarray, fibrosis, small vessel disease (narrow lumen--> ischemia); end stage/ burn out- DCM
  13. Abnormalities of LV diastolic function. (3)
    abnormal filling (diastolic dysfunction), abnormal relaxation, increased stiffness/ decreased compliance
  14. What are potential presentations/ prognostic profiles of HCM? (5)
    sudden death, CHF, end-stage (DCM), FATE, benign/stable/ normal longevity (majority)
  15. What are PE findings commonly associated w/ HCM? (7)
    systolic murmur, gallop sounds (use bell to hear this), arrhythmia, systolic click, syncope, signs of ATE, CHF
  16. What clinical signs are always seen with HCM?
    none- cats may have no outward signs of disease at all
  17. What are ECG findings common with HCM? (5)
    [may be normal] increased R amplitude (LV enlargement), left axis deviation (LV hypertrophy or left fascicular block), wider P waves (LA enlargement), arrhythmias, ST segment depression (ischemia)
  18. What are signs of LV enlargement on ECG? (2)
    increased amplitude R waves, left axis deviation
  19. What are signs of LA enlargement on ECG? (1)
    wider P waves
  20. What are signs of ischemia on ECG? (1)
    ST segment depression
  21. __________ on ECG is relatively specific for myocardial disease in cats.
    Ventricular ectopy
  22. What might be radiographic findings with HCM? (3)
    [may be normal!] LV elongation, LA enlargement, evidence of CHF
  23. What are echo findings that are common with ECG? (8)
    • LV hypertrophy (diastolic wall thickness >6mm)
    • LA enlargement, dynamic LVOT obstruction, secondary mitral regurg, LV diastolic dysfunction (Doppler),increased LV systolic dysfunction, rare LV dilation (end stage), +/- RV involvement
  24. What is hypertrophic obstructive cardiomyopathy?
    dynamic obstruction of the LVOT, causing flow turbulence, flow acceleration, dagger shaped flow signal, mitral regurg; grave prognosis
  25. LV systolic function is ___________ in HCM.
    normal or increased
  26. Describe the Doppler profile with HCM.
    • LV relaxation delay-┬ásmaller E, large A wave
    • Endstage--> restrictive filling- huge E wave and almost no A wave
  27. Is serum cTI useful in diagnosing HCM?
    may help you identify patients that are fully compensated (no value in patients with heart failure or decompensated); indicates myocardial necrosis due to infarction, myocarditis, reperfusion; NOT A USEFUL SCREENING TEST
  28. __________ is a useful screening test for cats with murmurs.
  29. How is NT-proBNP used in the workup of HCM?
    • Postive snap test--> move forward with echo
    • Negative snap test--> rule out HCM
  30. What is the cutoff for NT-proBNP for ruling out HCM in cats?
    normal < 100pmol/L
  31. NT-proBNP snap test has high ________.
    NPV (negatives are very reliable; positive, need to go to echo to confirm)
  32. When is genetic testing used in the setting of HCM?
    [this is not recommended ever] mouth swab in Maine Coon and Ragdoll cats; negative test does not tell you that the cat will never develop HCM; positive test does not predict how the cat will progress (some cats never develop clinical decompensation)
  33. What are differentials for concentric hypertrophy in a cat? (7)
    • HCM, systemic hypertension, feline hyperthyroidism
    • mitral valve dysplasia w/ dynamic LVOT obstruction
    • aortic stenosis
    • pseudohypertrophy (dehydration)
    • infiltration
  34. Management of acute CHF in a cat with HCM. (6)
    • Furosemide
    • Oxygen
    • Nitroglycerine paste (ear pinnae)
    • Sedation
    • Tap (if there is pleural effusion)
    • reduce stress/ stabilize before more procedures (re-assess every 30 min)
  35. When managing acute CHF in a cat with HCM, HR should be around ________ within a few hours of initiating treatment.
  36. If __(2)__, the cat is in cardiogenic shock, and you must administer __________.
    hypothermia and hypotension; Dobutamine +/- Pimobendan +/- Dopamine
  37. Describe the management of postclinical HCM (chronic management after stabilization). (3)
    Furosemide, ACEi, Plavix (unless a contraindication exists for one of these)
  38. Do NOT give _________ to cats with CHF.
  39. How is preclinical HCM managed?
    usually "watchful waiting" and annual re-checks, advise owner on what to expect with decompensation
  40. Preclinical HCM cat with moderate-severe LVOT obstruction; use ___________.
  41. Preclinical HCM cat with moderate-severe LA enlargement; use __________.
    Aspirin or Plavix
  42. Preclinical HCM cat with atrial fibrillation; use ___________.
  43. Preclinical HCM cat with DCM phenotype; use __________.
    Taurine supplementation
  44. What are contraindications for Atenolol? (3)
    CHF, very large LA, bradycardia
  45. What is prognosis for HCM?
    • Good for most
    • Asymptomatic- up to 10 years
    • FATE- grave
  46. What are the morphological characteristics of "burn-out" HCM? (2)
    restrictive AND dilated CM
  47. What is "SAM" and how is it treated?
    • systolic anterior motion of the septal mitral valve leaflet, causing dynamic obstruction of the LVOT
    • Atenolol (decreases dynamic obstruction)
  48. What are the 2 main reasons for dynamic outflow tract obstruction in HCM? What are the hemodynamic consequences of this?
    • SAM of septal MV leaflet; LV hypertrophy or pseudohypertrophy
    • pressure overload of LV--> concentric hypertrophy--> decreased CO--> exercise intolerance, syncope
  49. What are differentials for concentric hypertrophy in cats? (5)
    HCM, systemic hypertension, pulmonic/ aortic stenosis, pulmonary hypertension, hyperthyroidism
  50. How can the definitive diagnosis of FATE be made? (3)
    strong clinical suspicion and: cardiac and abdominal US (distal aorta), Doppler to confirm absence of flow in femoral arteries, elevation of skeletal muscle enzymes and K+
Card Set
Cardio3- HCM
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