Feline CMs Flashcards
Features of HCM
- Hypertrophied, non dilated LV
o Absence of other cardiac or systemic abnormalities causing LVH
Extracardiac causes of LVH
HyperT4, hypertension
Hypertension + RCM may resemble HCM
SAS or AS
Etiology HCM
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
Histopath HCM
- 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
History HCM
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)
Signalment/breeds HCM
- 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
PE HCM
soft systolic murmur
o Syncope can occur from tachyarrhythmias (not common)
o Gallop: usually represent S4
ECG HCM
Left anterior fascicular block reported In 11%, 30% and 33% of cats
o Signs of LVE/LAE
Clinical significance HCM
- Diastolic dysfct
- Dynamic ventricular outflow obstruction
- Myocardial ischemia
- Ventricular/SV arrhythmias
- Myocardial failure
Pathophysio HCM
- 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
Angio HCM
- 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
Echo changes HCM
- LVH: end diastolic wall thickness >6mm
o ↓LV chamber
o Hypertrophied pap muscles
o LAE - Dynamic LVOTO
o +/- SAM
Fibrous plaque on IVS
MR
Evaluation of myocardial fct on echo HCM
o Normal to ↑ FS%
o Myocardial infarcts:
Regional LV hypo/ dyskinesis
LVFW thinning (<2mm)
ST segment changes on ECG
Detect thrombi/prethrombic condition on echo HCM
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
Treatment HCM
- 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
Natural history HCM
- 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
Prevalence of dLVOTO
67% of cats with HCM
Features of LVOTO
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
Consequences of LVOTO
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
Conditions that can exacerbate LVOTO
o ↓ LV volume (preload)
o ↓ afterload
o ↑ contractility
Proposed mechanisms for mid LVOTO
Hypertrophied pap muscles
Hyperdynamic contractility
Mechanisms for DRVOTO
o Muscular hypertrophy of crista terminalis, moderator band, trabeculae
Proposed mechanisms for LVOTO
- Systolic anterior motion of anterior MV leaflet
- Septal hypertorphy
- Ventricular isometric contraction
What is SAM
- Anterior MV leaflet moves into LVOTO in mid-late systole
o Apposition w IVS
o OT turbulence
o MR
Mechanisms of SAM
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
Mechanism for septal hypertrophy and DLVOTO
- 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
Mechanism for Ventricular isometric contraction and DLVOTO
- 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
Pathophys RCM
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
What are the two major forms of fibrosis found in “restrictive” feline CM (according to Fox et al.)
Myocardial
Endomyocardial
RCM signalement
o No sex predilection
o Variable age: middle age to older most common
Etiology RCM
Idiopathic for both forms
Features of myocardial RCM
- Most prevalent
- Non infiltrative in cats
o Idiopathic
o Hu: amyloid infiltration → deposition of metabolic storage material
NOT documented in cats
Gross pathology myocardial RCM
o ↑ heart weight
o Biatrial enlargement
o Normal to mild ↑ LV wall thickness
o Normal systolic function
Histopath myocardial RCM
o Patchy endocardial fibrosis
o Myocyte necrosis
Etiology endomyocardial RCM
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
Gross pathology endomyocardial RCM
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
Histopathology endomyocardial RCM
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
4 major pathophysiologic categories of primary myocardial disease in cats
HCM, RCM, DCM, ARVC
Feature of HCM
- Idiopathic concentric LVH with small LV chamber
- Diastolic dysfct/failure from impaired relaxation
Other causes of hypertrophy causing reversible LVH
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
HCM prevalence
58-68%
HCM 2D echo changes LV
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
HCM 2D echo changes LA
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
HCM 2D echo changes systolic fct
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
HCM 2D echo changes DLVOTO
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
HCM Doppler echo changes DLVOTO
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
HCM Doppler echo changes MR
can be present if SAM → pull leaflet from closed position
o Jet toward lateral wall of LA → away from OT
HCM Doppler echo changes diastolic fct
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
HCM Doppler echo changes TDI
↓ 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
Complications associated w/ HCM
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
Features of RCM
- Marked diastolic dysfction with normal LV size, no LVH, normal systolic fct
Prevalence RCM
5-21%
Endomyocardial RCM 2D echo changes
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
Endomyocardial RCM Doppler echo changes
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
Myocardial RCM 2D echo changes
LA/RAE or both
Normal IVS/LVFW thickness
Normal LV chamber
Lack of L sided volume overload
Myocardial RCM Doppler echo changes
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
RCM angio changes
- 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
Features of myocardial infarcts
- 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
Echo features of mycardial infarct
- ↓ 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
Gross pathology myocardial infarct
- Well circumcised pale tan to red areas in myocardium
- Distinct red rim
Histology myocardial infarct
- 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
Most common localization of myocardial infarct
subendocardial region
o Wide lesion adjacent to endocardium
o Narrow adjacent to epicardium
o Reflect distribution of blood supply w/I myocardium
Etiology ARVC
unknown
Prevalence ARVC
2-4% according to 1 report
Gross pathology ARVC
RAE/RVE
Focal or diffuse wall thinning
Aneurysmal bulges may be observed in apical, sub TV, infundibular regions
Histology ARVC
- 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
Px ARVC
poor: many cats euthanized for RCHF after 4months
2D echo ARVC
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
Doppler ARVC
o TR: TV annular dilation
ARVC: how to differentiate between TVD
- Abnormal valvular morphology
- Normal RV systolic fct
- Age
- ↑TR velocity → normal systolic fct
UCM features/prevalence
- Distinction clinically negligible → same tx
- Prevalence: 10%
Etiology of ATE
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
Risk factors for thrombus formation
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
Components of virchow’s triad
Endothelial injury
Circulatory stasis
Altered blood coagulability
ATE: virchow: endothelial injury
- 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
ATE: virchow: circulatory stasis
- ↑ chamber dimension and ↓ contractility → ↑ end diastolic volume → blood stasis
o May lead to RBC aggregation - Impaired blood flow → ↓ clearance of clotting activated factors
ATE: virchow: altered blood coag
- 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
Prevalence of ATE
o Male cats overrepensented → may be because increased risk for HCM
Etiology of ATE in cats
o Cardiogenic: 89-92% of cats
o Neoplasia: bronchogenic carcinoma in 5%
o Idiopathic: 3%
Pathophys ATE
- Most involve L heart and systemic arteries
o Obstruction of artery
o Vasoactive mediator release → vasoconstriction of collateral circulation
Major cause of c/s
Gross pathology ATE
o Saddle thrombi have redish appearance
o Coagulative necrosis of tissues
o Pale affected surrounding muscles
Reperfusion syndrome ATE
o Ischemic rhabdomyolysis and reperfusion
Acute K+ release into systemic circulation
↑ lactactemia and acidosis
o Hours to several days after TE event
Px ATE
poor outcome associated with
o Hypothermia
o Azotemia
o 1 affected limb
Echo risks factor ATE
LAE
SEC
↓ flow in LAA
Most common location of ATE and why
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
How to assess 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
LAE w/ ATE
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
SEC ATE
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
Role of mitral septal contact in HCM
- Dynamic LVOT obstruction
o Mid systolic obstruction, after most of LV SV ejected (80-90%)
Rapid rise in arterial pulse
o Narrowed LVOT
Hypertrophied IVS
Anterior MV leaflet - Large high-pressure region below contact area
o Smaller, low-pressure region beyond point of contact
Mechanisms proposed for mitral septal contact w/ HCM
o Narrowing of subaortic outlet
o Longer anterior/posterior MV leaflets
o SAM of MV
o Anteriorly displaced papillary muscles
o Leaflets drawn into OT by Venturi forces from rapid blood flow
Consequences of mitral septal contact w/ HCM
o ↑wall stress
o ↑ myocardial O2 consumption
o ↓ coronary blood flow
o Myocardial ischemia
SAM
- HOCM → L parasternal systolic murmur
- Papillary muscle hypertropy → anterior displacement → pulling MV into LVOT → dynamic SAS
o Mid to late systolic ↑ LVP → ↑ blood flow velocity
o Worsen LVH → worsen diastolic fct
SAM exacerbated by
o Severe basilar septal knob
o ↑ contractility
o Tachycardia
