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Flashcards in Acquired heart conditions Deck (52)
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1

Dilated cardiomyopathy--K9

General/lesions

  • Decreased myocardial contractiliy--systolic dysfunction--leading to progressive dilation of the L and/or R ventricle
  • Mild thinning of the walls
  • Can lead to eventual L or R-sided CHF
  • Histo lesions include
    • Lack of inflammation
    • Wavy myofibers
    • Fibro-fatty infiltration
    • Loss of myocytes and myocardial fibrosis

2

Dilated cardiomyopathy--K9

Pathophysiology

  • Idiopathic--diagnosis of exclusion, but poss. familial etiology in dobies, boxers, cockers, wolfhounds
  • End-stage of various other processes--L-carnitine or taurine deficiencies, toxicities (doxorubicin, alcohol), ischemia, infections, immunological, tachycardia and metabolic abnormalities

3

Dilated cardiomyopathy--K9

Doberman pinscher progression

 

  • Arrhythmogenic cardiomyoathy
    • Arrhythmias but normal L ventricular contractility
    • IWH may have lone AF
    • Dobies present w/ VDs, generally progresses to the next stage of dz
  • Occult DCM
    • Animals appear normal but have mophological changes (L ventricular enlargement), trending towards dec. contractility
    • Ventricular arrhythmias or AF common
  • Classic DCM: heart failure
    • L-sided more common
    • Ventricular enlargement, dec. contractility--systolic dysfunction
    • Ventricular arrhythmias or AF present

4

Dilated cardiomyopathy--K9

Taurine/L-carnitine deficiency

  • Bile acids are conjugated with taurine
  • Important moderator of Ca flux, reduces platelet aggregation, stabilizes neural membranes, + inotrope
  • Dogs can synthesize (those on lamb and rice diet have recently been diagnosed w/ deficiencies)
    • Recommend supplementing dogs on these diets w/ taurine and carnitine
    • Dogs which develop DCM can improve w/ medication and may eventually only need supplementation (will not reverse damage)

5

Dilated cardiomyopathy

Signalment

Usual history

  • Signalment
    • Seen in giant and some smaller breeds of dogs
    • Dif. gene pools may be over-represented in dif. countries
    • Most common in middle-aged males
  • History
    • Depends on ventricles involved
    • Wt. loss, exercise intolerance, weakness, syncope, etc.
    • Sudden death occurs in ~30% of dobies

6

Dilated cardiomyopathy--K9

Common abnormalities on PE

 

  • Poor BCS
  • Signs of heart failure
  • Muffled heart and lung sounds
  • Signs of A-fib
  • Systolic murmur from mitral regurg
  • S3 gallop sounds common

7

Dilated cardiomyopathy--K9

Abnormalities commonly found on special exam

  • Labwork
    • Pre-renal azotemia
    • Elevated liver enzymes
    • Low taurine or arnitine levels (rare)
    • Future--natriuretic and cardiac tropoin level testings (early diagnosis)
  • X-ray--generalized heart enlargement
  • Echo--definitive diagnosis
    • Ventricular enlargement w/ 'flabby,' thin walls
    • Reduced contractility and fractional shortening is decreased (~23% is normal for dobies)
  • M-mode--fractional shortening <20% (N = 25-45% in normal dogs)
  • Doppler--mitral valve insufficiency and reduced SV
  • ECG
    • VPDs--dobies
      • Up to 50/day ok
    • A-fib in other breeds
    • Signs of heart enlargement and ST segment depression

8

Dilated cardiomyopathy--K9

DDx

Prevention

Prognosis

 

  • DDx--pericardial effusion
  • Prevention--genetic markers should be available to detect animals at risk to keep them from breeding programs
    • Autosommal dominant in dobies--mutation in pyruvate dehydrogenase kinase (PDK4); commercial test available
    • Age of onset variable
  • Prognosis
    • Guarded to poor
    • Therapy will inc. quality of life
    • ACE inhibitors and pimobendan together improve life expectancy to 350 days
    • American cocker spaniels can recover completely w/ taurine and carnitine deficiency

9

Dilated cardiomyopathy--K9

Treatment: ACM

  • Arrhythmogenic CM
    • Treat if avg HR >90bpm or >250bpm w/ exercise
    • No evidence that treating will reduce risk of sudden death
    • Recommended to treat dogs w/ runs of VT, RonT phenomenon, or excessive VPDs
    • Lone A-fib
      • Beta blockers--atenolol, metoprolol
      • Control arrhythmias and 'cardio-protection'
      • Diltiazem--control HR
    • Ventricular arrhythmias
      • Beta-blockers: sotalol
      • Combination of mexiletine and atenolol--reduce frequency of ventricular beats and runs
      • Indication to delay onset of further stages

10

Dilated cardiomyopathy--K9

Treatment: OCM

  • Ace inhibitors in dobies seem to delay onset of DCM
  • Same effect possibly with beta-blockers
  • Treat arrhythmias and moitor for dz progression

11

Dilated cardiomyopathy--K9

Treatment--DCM and CHF

  • Mild failure: furosemide, ACE inhibitors, pimobendan, and antiarrhythmics
  • Severe failure: hospitalized, oxygenated, and treated w/ injectable furosemide (monitor for hypo- K, Na, and Cl); observe RR and change administration of furosemide accordingly
  • Dobutamine can be used in cases of hypotension and markedly decreased contractility
  • Reduced preload w/ nitroglycerine ointment or sodium nitroprusside
    • Control w/ ACE inhibitors after
  • Pimobendan--(+) inotrope, inc. sensitivity to existing Ca w/o an inc. in myocardial oxygen demand
    • PDE III inhibitor--inc. contractility, general vasodilator
  • Digoxin + diltiazem--slow ventricular response rate in dogs w/ A-fib
    • Hypotension and heart block may occur
  • Dogs w/ clinical signs from ventricular arrhythmias, runs of VT, numerous VPDs w/ tachy, or RonT phenomenon--lidocaine followed by long-term mexiletine
    • No evidence that this will prevent sudden death
    • Reserve this trtmt for dogs w/ VT
  • Beta-blockers--dec. # and complexity of ventricular arrhythmias at low doses
    • High doses are (-) inotropes and cause severe decompensation
      • Should not be initiated until heart failure is controlled and standard therapy is in place
    • Metoprolol or carvediolol--dose should be gradually inc. until decompensation occurs, then back off
      • Optimal dose is unknown--low dose better than nothing
  • After discharge from hospital animal should set own activity level + restricted Na diet
    • Taper to lowest poss. dose of furosemide, start ACE inhibitors low and gradually inc. to max over a few weeks
  • Renal fx should be monitored/assessed after 3-7d (furosemide doseage)--dec. if BUN, Cr elevated
  • Supplement for any deficiencies ID'd
  • Fish oil improves cachexia in dobies

12

Dilated cardiomyopathy--feline

Pathophysiology

  • Characterized by ventricular dilation, thinning of ventricular wall, and dec. contractility
  • Majority of cases are due to taurine deficiency
    • Rare disease now

13

Dilated cardiomyopathy--feline

Signalment

Usual history

  • Signalment
    • Middle aged to older males
    • Burmese, siamese, abyssinian predisposed
  • History
    • Acute onset of paresis/paralysis due to ATE
    • Dyspnea, anorexia, lethargy, vomiting, and lung sounds
    • Gallop rhythms and murmur from AV valvular insufficiency common 
    • Focal areas of retinal degeneration are suggestive of taurine deficiency

14

Dilated cardiomyopathy--feline

Common abnormalities on PE

DDx

Prevention

  • PE
    • Hypothermic, weak femoral pulses, poor CRT
    • Dyspnea, muffled heart and lung sounds
    • Gallop rhythms and murmur from AV valvular insufficiency common
    • Focal areas of retinal degeneration are suggestive of taurine deficiency
  • DDx--hypertrophic cardiomyopathy
  • Prevention--ensure cats receive adequate levels of taurine

15

Dilated cardiomyopathy--feline

Abnormalities on special exam

  • Labwork--low taurine or high T4
  • X-ray
    • Pleural effusion
    • Heart appears diffusely enlarged
    • Diffuse alveolar and interstitial patterns in lungs
  • Echo--definitive diagnosis
    • Dilated, thin-walled left ventricle w/ reduced contractility
  • M-mode
    • Inc. left atrial dimensions
    • Dec. ventricular wall thickness
    • Reduced fractional shortening
  • Doppler--mitral valve insufficiency, reduced stroke volume
  • ECG--normal or tall R waves in lead II

16

Dilated cardiomyopathy--feline

Treatment

Prognosis

  • Treatment
    • Treat pulmonary edema/pleural effusion if present
      • Oxygen, furosemide, venodilator therapy, thoracocentesis
    • ACE inhibitors can improve systolic fx
    • Treat ATE if present
    • Supplement taurine if found deficient
      • Will see echocardiographic improvement in ventricular performance by 6wks
    • Treat hyperthyroidism if present
  • Prognosis: fair if taurine deficient; if not, most cats die w/in 2 months regardless of treatment

17

Hypertrophic cardiomyopathy

Pathophysiology

  • Functional abnormalities in myocytes that leads to inc. cell stress and activation of trophic and mitotic factors--papillary musc. and left ventricular concentric hypertrophy (diffuse or focal)
  • Histo-myocytes are enlarged w/ fiber disarray
  • Intramural coronary arteriosclerosis and myocardial interstitial fibrosis 
  • Primary and idiopathic in most cases
  • Hypertrophied and fibrosed L ventricular wall lacks compliance and cannot fill during diastole--diastolic failure; ventricular chamber non-existent in systole
  • Dynamic outflow tract obstruction by hypertrophied ventricular septum
  • Systolic anterior motion of the anterior mitral valve leaflets--misalignment of the mitral valve; anterior leaflets blocking outflow tract during systole
    • Can cause mitral insufficiency and regurg of blood back into atrium during systole = murmur
  • Lack of diastolic filling in L ventricle = inc. pressure in the L atrium --> chamber enlargement -- L CHF signs
  • Blood stasis in the L atrium can predispose to clot formation
    • If dislodges--> iliac bifurcation of the aorta an dlodge--> ischemia in one/both hind limbs
      • Muscle necrosis, lameness

18

Hypertrophic cardiomyopathy

Signalment

Usual history

  • Signalment
    • Most common cardiomyopathy in cats; exclusion diagnosis
    • Middle-aged male cats
  • History
    • Most asymptomatic; only pick up murmur as incidental finding
    • Can trigger animal into heart failure if too stressful
    • Some may die suddenly--arrhythmias
    • Cats in heart failure resent w/ acute dyspnea--apear perfectly normal until then
    • Heart failure cats may also have painful hind limb lameness

19

Hypertrophic cardiomyopathy

Common findings on E

  • Pronounced apex beat on L side
  • S4 gallop rhythms and systolic murmurs common
  • Hind limbs may be cold to the touch, muscles hard and painful--lameness may be only sign
  • Remember that distress signs can mimic heart failure

20

Hypertrophic cardiomyopathy

Common abnormalities found on special exams

  • Labwork
    • Troponin-1 and pro-BNP biomarkers elevated
    • ATE--muscle necrosis and elevated ck AND ast
    • K+ may be elevated
    • Normal coag
  • X-ray
    • Valentine-shaped heart on DV
    • 50% have generalize heart enlargement--appear like DCM
    • Pulmonary edema present if in CHF
  • Echo
    • Marked thickening of the ventricular septum or L ventricular free wall
    • Papillary muscle hypertrophy
    • Reduced ventricular lumen
    • Can see regional or segmental hypertrophy
    • Can see dynamic outflow obstruction and SAM
  • Doppler
    • Turbulence in outflow tract
    • Can also see jets at mitral valve if insufficient
    • Spectral doppler will allow measurements of pressure gradients--determines severity of obstructions if resent
  • M-mode--thickened ventricular free wall and septum
  • Angio
    • Enlarged heart and septum, enlarged papillary muscles, dec. ventricular volume
    • Can be used to confirm ATE
  • ECG--normal or signs of L heart enlargement, dysrrhythmias or microscopic intramural myocardial infarction (MIMI)

21

Hypertrophic cardiomyopathy

DDx

Prevention

 

  • DDx--differentiate between primary and secondary HCM
  • Prevention--test for myosin binding protein 3 mutation in Maine Coon cats and 1 specific for Ragdolls--don't breed cats that are +
    • May be other genes that cause dz--(-) test for MyBPC doesn't mean the cats will never develop HCM

22

Hypertrophic cardiomyopathy

Treatment

  • May remain asymptomatic and live normal lifespan
  • Beta-blockers
    • Atenolol--reduce pressure gradient in cases of LVOT obstruction
      • ACE inhibitors are given in cases w/ atrial enlargement--usually alongside a beta-blocker or dilitazem
  • Cats that are close to heart failure can be placed on ACE inhibitor and low-dose furosemide
    • Can start anti-coag therapy if indicated by imaging ('swirling smoke' in atrium)
    • Heparin or aspirin and plavix
  • Cats presenting in acute failure should be sedated, placed on oxygen, warmed (cardiogenic shock), and given dobutamine via CRI (reduce dose as animal improves)
    • Remove effusion via thoracocentesis and administer furosemide--taer as soon as RR improves (cats very sensitive to electrollyte imbalances caused by the drug)
  • Once stabilized, blace cats on beta blockers--propranolol (unless asthmatic) or atenolol
    • Beta-blockers promote ventricular relaxation and slow heart--improves passive ventricular filling, inc. stroke volume, and reduces pulmonary edema
    • Increased CO and slower rate will also improve myocardial perfusion and decrease oxygen req.
  • Diltiazem--Ca channel blocker--improves relaxation and reduces HR and contractility and O2 demand
    • Less effective than atenolol and has adverse side effects
  • Spironoloactone contraindicated--ulcerative facial dermatitis
  • ATE: can spontaneously recover via recanalization or collateral circulation
    • Sedation and analgesia required--painful
    • Reperfusion is sketch--hyperkalemia and acidosis from muscle damage (control w/ sodium bicarb)
    • Acepromazine + ACE inhibitor = hypotension--caution
    • Acepromazine used for anxiety and arteriodilation to improve collateral circulation
  • Thrombolytic therapy may seed up clinical recovery--expensive trtmts, lots of complications
  • Can control further thrombus formation w/ short term unfractionated hearin, lavix, warfarin (sketch), or daily inj. of low mo. wt. heparin (none are 100%)
  • Aspirin--no evidence of improvement

23

Hypertrophic cardiomyopathy

Prognosis

  • Asymptomatic = guarded to good
    • Median 5 yr survival
    • Focal enlargements are better tolerated
    • Cats w/ more diffuse hypertrophies have worse prognosis
  • Cats presenting in heart failure have ~3mo
  • Cats w/ ATE and heart failure = very poor prognosis
    • Same w/ renal or celiac thromboembolism

24

Feline hyperthyroidism

All the things

  • L ventricular concentric hypertrophy--w/ hypertension
  • Most have eccentric hypertrophy--high output and volume overload
  • Signs resolve w/ appropriate thyroid treatment

25

Restrictive cardiomyopathy--feline

All the things

  • Endocardial, subendocardial or myocardial fibrosis or infiltrative disease which reduces diastolic filling
  • L ventricle involve--extreme L atrial enlargement
    • L heart failure signs
  • L atrium dilated, L ventricle relatively normal
  • Several etiologies
  • Poor prognosis

26

Arrhythmogenic R ventricular cardiomyopathy in Boxers

Pathophysiology

  • Familial disease, autosomal dominant; incomplete penetrance
  • Extensive changes in right myocardium--inflammation, fibrosis, fat infiltration
  • Ventricular arrhythmias
  • VPDs originate from R ventricle
  • Sudden death possible at any stage
  • Possible etiology from dysfunctional gap junctions and Ca leakage

27

Arrhythmic R ventricular cardiomyopathy of boxers

Signalment

Usual history

 

  • Signalment--boxers 1-15yrs (average 6-10yrs)
  • History
    • Sudden death
    • No abnormalities
    • Weakness
    • Syncope
    • Signs of R or L heart failure

28

Arrhythmic R ventricular cardiomyopathy in boxers

Common findings on PE

Comm abnormalities on special exams

  • PE--normal, may hear VPDs
  • Special tests
    • Definitive diagnosis can only be made during necropsy after sudden death
    • Probable diagnosis based on familial history and any ossible clinical signs--weakness, syncope, etc.
    • Serum cTn-1 conc. elevated in affected animals
    • Holter monitoring to detect VPDs--anything over 100 episodes/day is suggestive

29

Arrhythmogenic R ventricular cardiomyopathy in boxers

Treatment

Prevention

  • Treatment may decrease the complexity and # of VPDs--but no evidence this does anything to decrease risk of sudden death
  • Treat dogs w/ weakness and syncope, asymptomatic dogs with >1000 VPDs/day, VT, or RonT 
    • Sotalol or mexiletine + atenolol
    • Evaluate treatment w/ holtor monitoring--effective if VPDs decrease by 85%
      • Beware of proarrhythmic effects
    • Omega-3 FA's to help decrease # of VPDs
  • Prevention--dogs should be screened at ~1yr old and every year after to look for ARVC and sub-aortic stenosis
    • Dogs showing signs or suspect signs shouldn't be bred

30

Arrhythmogenic R ventricular cardiomyopathy in boxers

DDx

Prognosis

  • DDx--DCM or sub-aortic stenosis
  • Prognosis
    • Sudden death always possible
    • Severity of clinical signs does not correlate w/ # of VPDs (but more clinical signs are generally seen w/ inc. # of VPDs)