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11. Acquired heart dz > Feline CMs > Flashcards

Feline CMs Flashcards

1
Q

Features of HCM

A
  • Hypertrophied, non dilated LV
    o Absence of other cardiac or systemic abnormalities causing LVH
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2
Q

Extracardiac causes of LVH

A

HyperT4, hypertension
 Hypertension + RCM may resemble HCM
 SAS or AS

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3
Q

Etiology HCM

A

mutation in 1 of 7 genes encoding for cardiac sarcomere protein
o Cardiac B myosin heavy chain
o cTnI, cTnT
o Alpha-tropomyosin
o Cardiac myosin binding protein C
o Ventricular myosin essential light chain
o Ventricular myosin regulatory light chain

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4
Q

Histopath HCM

A
  • Myocardial/fiber disarray in LV and RV
  • Intramural coronary arterial sclerosis
  • Interstitial fibrosis (blue)
  • Contact lesions (SAM)
  • Connective tissue abnormalities: MV, intramural CAs, collagen matrix derangements
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5
Q

History HCM

A

o Asymptomatic with heart murmur, arrhythmia, gallop
o Acute signs of CHF
o Acute paresis → most common sign associated with ATE (hindlimbs > R front limb)

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6
Q

Signalment/breeds HCM

A
  • 3mo to 17y (mean 5-7y)
  • DSH most commonly reported, followed by DLH
    o Breed predisposition: Maine Coon, American Shorthairs, Persians
  • Male predominance
  • Non obstructive > obstructive
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7
Q

PE HCM

A

soft systolic murmur
o Syncope can occur from tachyarrhythmias (not common)
o Gallop: usually represent S4

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8
Q

ECG HCM

A

Left anterior fascicular block reported In 11%, 30% and 33% of cats
o Signs of LVE/LAE

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9
Q

Clinical significance HCM

A
  • Diastolic dysfct
  • Dynamic ventricular outflow obstruction
  • Myocardial ischemia
  • Ventricular/SV arrhythmias
  • Myocardial failure
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10
Q

Pathophysio HCM

A
  • Diastolic function: impaired diastolic filling
    o ↓ relaxation/compliance in early diastole = diastolic dysfct
    o Filling dynamics: influenced by extent of septal hypertrophy
    o Non uniform LV relaxation/stiffness
     → ↑ L sided filling P → LA dilation → ↑ PVP
     From abnormal Ca2+ kinetics
  • Abnormal cytosolic Ca2+ kinetics
    o Abnormal loading conditions
    o Fibrosis, myofiber disarray, hypoxia, ischemia
  • Myocardial ischemia → affect diastolic fct
    o CA remodeling: arteriosclerosis
     Thick arteriolar wall → ↓ lumen
  • Tachycardia: ↑HR → ↓ systolic/diastolic function → ↑ OT PG → ↓ CO
    o ↑ myocardial O2 consumption → ischemia → ↑ myocardial stiffness → ↓ ventricular filling
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11
Q

Angio HCM

A
  • LVFW hypertrophy
  • ↓ LV chamber size
    o Slitlike appearance
  • Hypertrophied pap muscles
  • Moderate to severe LAE/RAE
  • Distended PVs
  • Normal to accelerated transit time (contrast)
  • Thrombi in LA or LV
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12
Q

Echo changes HCM

A
  • LVH: end diastolic wall thickness >6mm
    o ↓LV chamber
    o Hypertrophied pap muscles
    o LAE
  • Dynamic LVOTO
    o +/- SAM
     Fibrous plaque on IVS
     MR
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13
Q

Evaluation of myocardial fct on echo HCM

A

o Normal to ↑ FS%
o Myocardial infarcts:
 Regional LV hypo/ dyskinesis
 LVFW thinning (<2mm)
 ST segment changes on ECG

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14
Q

Detect thrombi/prethrombic condition on echo HCM

A

o Spontaneous echo contrast: associated w LA blood stasis
 Erythrocyte aggregation at low shear rate
 Platelet aggregates
 Factors involved in thrombogenesis
* Blood stasis → areas of a/dyskinesis
* Systemic platelet activation from MR
o Abnormal valvular surface
o Hemodynamic irregularity
o *severe MR may have protective role

o Associated w ↑ thromboembolic risk

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15
Q

Treatment HCM

A
  • B blockers
    o HR control → indirect improvement in LV filling by ↑ diastole
     ↑ coronary blood flow
     ↓ myocardial ischemia
    o ↓ DLVOTO
    o ↓ myocardial O2 demand
    o Anti arrhythmic effect
    o Inhibit ∑ myocardial stimulation
  • B-blockers, Ca2+ blockers, ACEi, pimobendane may delay progression
    o No evidence
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16
Q

Natural history HCM

A
  • Most will achieve adulthood w/o c/s
  • Sudden death: recurrent syncope is a risk factor
    o Tachy/brady arrhythmias
    o DLVOTO: Most commonly associated w exercise
    o Altered baroreflexes
    o Ishemia
  • Acute pulmonary edema
  • Arterial thromboembolism
  • Myocardial failure: sometimes can progress to stage of chamber dilation and reduced contractility
    o Severe myocyte death and fibrosis replacement
    o Resemble DCM
    o Poor prognosis
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17
Q

Prevalence of dLVOTO

A

67% of cats with HCM

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18
Q

Features of LVOTO

A

o Obstruction in mid systole, after most of LV SV ejected → lead to
o Narrowing of LVOT
 Hypertrophied IVS
 Anterior MV leaflet:
* Thickened
* Elongated chordae tendinae
o Systolic anterior motion (SAM) of MV
 Apposition of MV leaflet on IVS
* Fibrous plaque on basal IVS
 Associated with MR → directed posterolaterally (eccentric)
* Usually small
* Should not be significant enough to cause CHF
* May contribute to ↑ LAP
o PG in LVOT in mid-late systole
 Asymmetric flow pattern shape: slow rise in early systole and abrupt increase and peak in mid systole (dagger shape)
 Associated high velocity turbulent flow in ascending Ao

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19
Q

Consequences of LVOTO

A

o ↑ systolic LV pressures → ↑ myocardial wall stress
o Exacerbated subendocardial ischemia
o ↑ myocardial O2 demand
o Stimulate LVH
o No studies showed a worse survival in cats with LVOTO

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20
Q

Conditions that can exacerbate LVOTO

A

o ↓ LV volume (preload)
o ↓ afterload
o ↑ contractility

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21
Q

Proposed mechanisms for mid LVOTO

A

 Hypertrophied pap muscles
 Hyperdynamic contractility

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22
Q

Mechanisms for DRVOTO

A

o Muscular hypertrophy of crista terminalis, moderator band, trabeculae

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23
Q

Proposed mechanisms for LVOTO

A
  1. Systolic anterior motion of anterior MV leaflet
  2. Septal hypertorphy
  3. Ventricular isometric contraction
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24
Q

What is SAM

A
  • Anterior MV leaflet moves into LVOTO in mid-late systole
    o Apposition w IVS
    o OT turbulence
    o MR
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25
Q

Mechanisms of SAM

A

o Narrowing of subaortic outlet: may contribute

o Elongated MV leaflets
 Echo and post mortem measurements of Hu MV leaflets with HCM showed longer MV leaflets than normal of non obstructive HCM Hu
 Possibly due to MV stretching from LVH and distorsion

o Anteriorly displaced pap muscles
 Change in ventricular geometry 2nd to LVH →anterior displacement → coaptation point of MV closer to LVOT
 Initial pulling of MV leaflet into LVOT
* Leaflet get caught into blood flow and slammed to IVS
 Studies showed that physical displacement of pap muscle toward IVS causes SAM

o Venturi effect w/I LVOT:
 ↑ LVOT velocity → Venturi effect sucking MV toward septum
* Leaflet has to be close to IVS to be drawn by the flow
* PG has to be present before the valve is drawn: high velocity flow → ↓ pressure → pull mobile valve
* In systole, MV is closed
* Cannot explain alone SAM

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26
Q

Mechanism for septal hypertrophy and DLVOTO

A
  • Basilar IVS hypertrophy present in most cases of HOCM
    o Abnormal systolic thickening → obstruction of LVOT in absence of SAM
    o Can produce high velocity flow in LVOT → venturi forces → SAM
  • Evidence of IVS hypertrophy contribution
    o ↓ obstruction in patients w HOCM by surgical resection/alcohol ablation of septal region
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27
Q

Mechanism for Ventricular isometric contraction and DLVOTO

A
  • Excessive emptying of LV w mid-end systolic isometric contraction
    o High LVP → PG across LVOT
    o Unable to obliterate its cavity because of different pressure/forces
    o Implausible according to Doppler studies
     Rapid blood flow in stenosis region
     Evidence of DLVOTO in early systole: chamber full of blood
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28
Q

Pathophys RCM

A

diastolic dysfct and ↑ myocardial stiffness
o Lead to ↑ LVP → L-CHF

  • Cardiomyopathic process restricting ventricular filling w/o LVH
    o Impaired diastolic filling
    o Normal to ↓ diastolic volume
    o Normal systolic function
    o Normal to ↑ ventricular wall thickness
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29
Q

What are the two major forms of fibrosis found in “restrictive” feline CM (according to Fox et al.)

A

Myocardial
Endomyocardial

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30
Q

RCM signalement

A

o No sex predilection
o Variable age: middle age to older most common

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31
Q

Etiology RCM

A

Idiopathic for both forms

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32
Q

Features of myocardial RCM

A
  • Most prevalent
  • Non infiltrative in cats
    o Idiopathic
    o Hu: amyloid infiltration → deposition of metabolic storage material
     NOT documented in cats
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33
Q

Gross pathology myocardial RCM

A

o ↑ heart weight
o Biatrial enlargement
o Normal to mild ↑ LV wall thickness
o Normal systolic function

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34
Q

Histopath myocardial RCM

A

o Patchy endocardial fibrosis
o Myocyte necrosis

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35
Q

Etiology endomyocardial RCM

A

endomyocardial fibrosis
o Associated with endomyocarditis
 Viral infection → direct invasion/myocardial toxins → myocardial tissue injury
* Possible parvoviral gene material from high % of feline hearts
o Immune mediated myocardial injury suggested
o Metastatic neoplasia → infiltrative dz (lymphosarcoma)
o Hypereosinophilic syndrome with multiorgan infiltration described
 Hu: Loffller’s endocarditis
* Marked eosinophilia with cardiac involvement
 Cats: small # of cases reported
* Focal mononuclear  in myocardium
* Subendocardial eosinophilic infiltration
* Endomyocarditis

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36
Q

Gross pathology endomyocardial RCM

A

o ↑ heart weight
o Severe endocardial scar
 Mid to apical cavity
 Obliterating distal chamber causing mid ventricular stenosis
* Bridging LVFW and IVS
 Diffuse scar also possible → can ↓/obliterates LV chamber size
o Can affect MV apparatus
 Fusingof pap muscles/chordae tendinae
 Distortion of MV apparatus
 Tethering of posterior MV leaflet
o Normal to mild ↑ LV wall thickness
o Severe LA, often RAE
 Atrial hypertrophy: diffuse endocardial thickening + white surface
 Atrial thinning: thin and translucent from loss of atrial myocytes and collagen replacement = fibrosis
o Myocardial infarction: focal, pale, depressed area

37
Q

Histopathology endomyocardial RCM

A

o Severe, extensive LV endocardial thickening and scar
* Rarely affects both ventricles
* RV only reported in Hu, not cats
 Hyaline, fibrous and granulation tissue
* Extend for variable distance into subendocardium and myocardium
 Myocardial interstitial fibrosis
 Chondroid metaplasia
o Intramural coronary artery atherosclerosis
o Endomyocardial necrosis/fibrosis
o Myocyte hypertrophy
o Endomyocarditis: varying degree of endomyocardial infiltration
 Neutrophils, macrophages > lymphocytes, plasma 
o Atria: diffuse endocardial thickening associated w ↑ collagen fibers
 Diffuse myocyte necrosis
 Replacement fibrosis
 Wall thinning

38
Q

4 major pathophysiologic categories of primary myocardial disease in cats

A

HCM, RCM, DCM, ARVC

39
Q

Feature of HCM

A
  • Idiopathic concentric LVH with small LV chamber
  • Diastolic dysfct/failure from impaired relaxation
40
Q

Other causes of hypertrophy causing reversible LVH

A

 Systemic hypertension
 Hypertrophic feline muscular dystrophy
 Infiltrative disorders
 Hyperthyroidism
* Hypertrophy of LVFW (72%), IVS (40%)
* LAE 70%
* Unusual presentation: biventricular dilation with poor systolic fct → reversible to certain degree w tx

41
Q

HCM prevalence

A

58-68%

42
Q

HCM 2D echo changes LV

A

o LVH → end diastolic LV wall thickness >6mm (equivocal 5.5-6mm)
 Mild 6-6.5mm
 Moderate 6.5-7.5mm
 Severe>7.5mm
o Symmetric hypertrophy of IVS and LVFW in most cats
 Asymmetric hypertrophy of IVS or LVFW (17%) in some cats
 Apical, mid ventricular, segmental areas of LVH also possible
 Basilar IVS → septal knob
* Frust form of HCM vs normal age related variant
o Large, prominent papillary muscles
 Area >0.2cm2
 Not specific for HCM

43
Q

HCM 2D echo changes LA

A

o May or may not be enlarged
 Determine staging dz severity
 LAE occurs from ↑ LV end diastolic P → transmitted to LA → ↑ LAP
* Risk for CHF and ATE
o Hu: indicator of severity/chronicity of diastolic dysfct
 Larger LA ↓ px

44
Q

HCM 2D echo changes systolic fct

A

o ↑FS%, hyperdynamic heart
 72% of cats with FS<30% were dead w/I 3 months in 1 study
o Hypercontractile septum → can worsen dynamic obstruction → can impede CO
o End systolic cavity obliteration possible

45
Q

HCM 2D echo changes DLVOTO

A

o SAM with moderate to severe DLVOTO
 Abnormal ventricular architecture + displaced pap muscles
 ↑ velocity in narrowed LVOT → venturi effect pulling MV leaflet
o Degree and duration of septal contact → correlates with severity of obstruction
o Easier to detect on M-mode
o Most frequent in cats w symmetric LVH or basal IVS hypertrophy
o Reported in patients with ↑RVP: PS, TOF, PH

46
Q

HCM Doppler echo changes DLVOTO

A

o PG across LVOT in Hu: predictor of complication, dz progression and death if >30mmHg
 Mild <50mmHg
 Moderate 50-80 mmHg
 Severe >80 mmHg
o Late systolic obstruction
 Dagger shape on spectral Doppler
 ↑ flow velocity as IVS narrows OT/SAM obstruct flow
o PW interrogation of mid ventricular region
 Suspect if murmur but no SAM or MR

47
Q

HCM Doppler echo changes MR

A

can be present if SAM → pull leaflet from closed position
o Jet toward lateral wall of LA → away from OT

48
Q

HCM Doppler echo changes diastolic fct

A

diastolic failure is major factor of CHF developemnt
o Impaired myocardial relaxation
 Rate of relaxation = IVRT will ↑
 ↓ Early filling
 Prolonged deceleration time of E wave → prolonged filling → delay filling to late diastole
 ↑ late filling from atrial contraction
* ↑ A wave
* ↑ duration and velocity of PV AR flow
o Restriction to LV filling → restrictive pattern may develop as ↑LV filling P
 E:A >2
 ↓IVRT
 ↓ deceleration time of E wave

49
Q

HCM Doppler echo changes TDI

A

↓ E’ and ↓ E’:A’ <1, ↓ S’
o ↓ early diastolic wall motion of LVFW and MV annulus
o E’ >7.2cm/s has spe = 87% and sens = 92% for normal heart

50
Q

Complications associated w/ HCM

A

Thrombus
* LAE → risk factor for ATE
* Form secondary to stasis of blood into LAA/LA
o Spontaneous echo contrast is a sign precursor of thrombus formation
o LAA flow can provide information: <0.25m/s correlated with blood stasis and ↑ risk

Ischemia
* Myocardial ischemia → seen occasionally with HCM cats
* Echo: ↓ systolic thickening of IVS/LVFW

Effusion
* Pericardial or pleural effusion → sign of CHF

51
Q

Features of RCM

A
  • Marked diastolic dysfction with normal LV size, no LVH, normal systolic fct
52
Q

Prevalence RCM

A

5-21%

53
Q

Endomyocardial RCM 2D echo changes

A

 Bright, dense echos on endocardial surfaces
* May be several mm thick
* Irregular endocardial surface
* Represent endocardial scars
 Obliteration of apical LV cavity may occur
 Mid LV scar: bridging band btw LVFW and IVS
* Narrowed, akinetic tube
 LA/biatrial enlargement
 Normal/↓ LV dimension
 Focal wall thinning or thickening may occur
* Non homogenous LVFW
 Normal systolic function

54
Q

Endomyocardial RCM Doppler echo changes

A

 Transmitral flow patterns: diastolic dysfct
* Restrictive filling
* Pseudonormal flow
 Diastolic and systolic PG can be observed with mid LV scar
 MR may occur if scar tether MV leaflets or affect chordae/pap muscles
 DLVOTO from SAM is uncommon
o Heterogenous dz

55
Q

Myocardial RCM 2D echo changes

A

 LA/RAE or both
 Normal IVS/LVFW thickness
 Normal LV chamber
 Lack of L sided volume overload

56
Q

Myocardial RCM Doppler echo changes

A

restrictive physiology
 Transmitral inflow
* Restrictive physiology: E:A>2
o ↑E wave >1m/s
o Rapid, early deceleration
 59+/14m/s
o ↓A wave <0.4m/s
o ↓IVRT (55+/-13ms)
* Impaired relaxation
o ↓ E wave
o Delayed E deceleration
o ↑ A wave

57
Q

RCM angio changes

A
  • Severe LAE
  • Irregular LV cavity
    o Partial mid ventricular constriction
    o Obliteration of apical cavity
    o LA/LV filling defects → thrombus
  • Antemortem diagnosis is hard
    o Identify endomyocardial scar on echo
    o Restrictive physiology is similar to constrictive pericarditis
     Associated with respiratory variation of peak mitral/tricuspid inflow velocities, PV flow and IVRT
58
Q

Features of myocardial infarcts

A
  • Not frequent in dogs/cats
    o Hu: acute myocardial infarction most important form of ischemic heart dz
     2nd to atherosclerosis of CAs
     Dogs naturally resistant to atherosclerosis
  • Can occur in hypoT4 dogs
  • Often 2nd to other cardiac dz
    o Aortic/pulmonic stenosis
    o PDA
    o Cardiomyopathy
     HCM
    o Neoplasia
    o Endocarditis
59
Q

Echo features of mycardial infarct

A
  • ↓ wall/septal systolic thickening
    o 2D or M-mode
    o Sudden change in wall thickness
    o Acute infarct
  • Systolic thinning (opposed to thickening) of wall
  • Dyskinetic/akinetic regional wall motion
    o ↓ motion toward LV center during systole on 2D transverse apical view
    o Paradoxical motion of affected area = dyskinesis
  • Echodense, thinner area → fibrosis
    o Chronic infarcts
60
Q

Gross pathology myocardial infarct

A
  • Well circumcised pale tan to red areas in myocardium
  • Distinct red rim
61
Q

Histology myocardial infarct

A
  • Acute: discrete focal/multifocal areas of acute myocardial necrosis
    o Inflammatory infiltrates, neutrophils +/- macrophages
    o 6h – 7 days/old
  • Hypereosinophilic myofibers
    o Loss of cross striation
    o Separated by edema
62
Q

Most common localization of myocardial infarct

A

subendocardial region
o Wide lesion adjacent to endocardium
o Narrow adjacent to epicardium
o Reflect distribution of blood supply w/I myocardium

63
Q

Etiology ARVC

A

unknown

64
Q

Prevalence ARVC

A

2-4% according to 1 report

65
Q

Gross pathology ARVC

A

 RAE/RVE
 Focal or diffuse wall thinning
 Aneurysmal bulges may be observed in apical, sub TV, infundibular regions

66
Q

Histology ARVC

A
  • Characterized by fibrofatty infiltration of RV myocardium
    o Predominantly R sided dz, but can also include LV or IVS

 RV myocardial atrophy
 Fibrous/fibrofatty replacement
 Lymphocytic infiltrates

67
Q

Px ARVC

A

poor: many cats euthanized for RCHF after 4months

68
Q

2D echo ARVC

A

o RAE
o RVE with thinning of RVFW
 ↓ wall motion
 Aneurysmal bulges are uncommon
o Paradoxical septal motion may be present
o RV systolic dysfct
 Mild myocardial LV dysfct can be present, but most commonly w/I normal limits

69
Q

Doppler ARVC

A

o TR: TV annular dilation

70
Q

ARVC: how to differentiate between TVD

A
  • Abnormal valvular morphology
  • Normal RV systolic fct
  • Age
  • ↑TR velocity → normal systolic fct
71
Q

UCM features/prevalence

A
  • Distinction clinically negligible → same tx
  • Prevalence: 10%
72
Q

Etiology of ATE

A

Thrombus formation = risk with any CM causing LAE
Aggregation of platelets and fibrin with entrapped in RBCs
* Form in some regions of L heart
o Most commonly LA or LAA
* Can break loose into systemic circulation

73
Q

Risk factors for thrombus formation

A

o Sluggish blood flow
 Normal to ↓ blood flow through enlarged chamber
* Exacerbated in LAA due to semi-isolated state
* <certain velocity → RBC + other factors clump together → SEC/smoke
 Allow cagulation factors to accumulate → induce plateket agreggation
 Rare formation of thrombus in DCM dogs → discrepancy → differences in
* RBC aggregability > cats
* Platelet reactivity > in cats
* Volume of platelet/BW
o Endothelial damage
o Hypercoagulable state

74
Q

Components of virchow’s triad

A

Endothelial injury
Circulatory stasis
Altered blood coagulability

75
Q

ATE: virchow: endothelial injury

A
  • Endomyocardial injury → endothelial fibrosis
    o Hyaline, fibrous, granular tissue
  • Reactive substrates to circulating blood → trigger thrombotic process
    o Induce platelet adhesion/aggregation
    o Activation of intrinsic clotting cascade
76
Q

ATE: virchow: circulatory stasis

A
  • ↑ chamber dimension and ↓ contractility → ↑ end diastolic volume → blood stasis
    o May lead to RBC aggregation
  • Impaired blood flow → ↓ clearance of clotting activated factors
77
Q

ATE: virchow: altered blood coag

A
  • 75% of cats will present
    o DIC associated with coagulopathy
    o Liver failure
    o TE
  • Feline reactive to:
    o ADP and other platelet aggregation agonists
    o Serotonin: released from platelets → ↑ platelet aggregation
  • Other possible factors
    o Resistance to factor V Leiden (APC)
    o Proteins C and S deficiency
    o AT III deficiency
    o Antiphospholipid syndrome
    o Hyperhomocysteinemia
78
Q

Prevalence of ATE

A

o Male cats overrepensented → may be because increased risk for HCM

79
Q

Etiology of ATE in cats

A

o Cardiogenic: 89-92% of cats
o Neoplasia: bronchogenic carcinoma in 5%
o Idiopathic: 3%

80
Q

Pathophys ATE

A
  • Most involve L heart and systemic arteries
    o Obstruction of artery
    o Vasoactive mediator release → vasoconstriction of collateral circulation
     Major cause of c/s
81
Q

Gross pathology ATE

A

o Saddle thrombi have redish appearance
o Coagulative necrosis of tissues
o Pale affected surrounding muscles

82
Q

Reperfusion syndrome ATE

A

o Ischemic rhabdomyolysis and reperfusion
 Acute K+ release into systemic circulation
 ↑ lactactemia and acidosis
o Hours to several days after TE event

83
Q

Px ATE

A

poor outcome associated with
o Hypothermia
o Azotemia
o 1 affected limb

84
Q

Echo risks factor ATE

A

LAE
SEC
↓ flow in LAA

85
Q

Most common location of ATE and why

A

LAA
o ↓ flow in LAA
o PW Doppler of LAA flow: evidence for potential formation of SEC/thrombus formation
 Flow velocity <0.25m/s correlated to stasis of blood flow and high possibility of thrombus formation

86
Q

How to assess flow in LAA

A

o PW Doppler of LAA flow: evidence for potential formation of SEC/thrombus formation
 Flow velocity <0.25m/s correlated to stasis of blood flow and high possibility of thrombus formation

87
Q

LAE w/ ATE

A

o Seems like a risk factor, but statistically not supported
 LA size >20mm thought to be predisposed
 Study found LA size as small as 14mm
o Primary myocardial dz: HCM, RCM, UCM, DCM with LAE

88
Q

SEC ATE

A

o Possible indicator of cats at increased risk
o Associated with blood stasis
 LAA flow velocity <0.20m/s marker for prediction of SEC in 1 study
o Considered as a marker for thrombi
o Attributed to RBC or platelet aggregation at low shear rate

11. Acquired heart dz (11 decks)

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