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