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
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
26
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
27
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
28
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
29
What are the two major forms of fibrosis found in “restrictive” feline CM (according to Fox et al.)
Myocardial Endomyocardial
30
RCM signalement
o No sex predilection o Variable age: middle age to older most common
31
Etiology RCM
Idiopathic for both forms
32
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
33
Gross pathology myocardial RCM
o ↑ heart weight o Biatrial enlargement o Normal to mild ↑ LV wall thickness o Normal systolic function
34
Histopath myocardial RCM
o Patchy endocardial fibrosis o Myocyte necrosis
35
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
36
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
37
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
38
4 major pathophysiologic categories of primary myocardial disease in cats
HCM, RCM, DCM, ARVC
39
Feature of HCM
* Idiopathic concentric LVH with small LV chamber * Diastolic dysfct/failure from impaired relaxation
40
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
41
HCM prevalence
58-68%
42
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
43
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
44
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
45
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
46
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
47
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
48
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
49
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
50
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
51
Features of RCM
* Marked diastolic dysfction with normal LV size, no LVH, normal systolic fct
52
Prevalence RCM
5-21%
53
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
54
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
55
Myocardial RCM 2D echo changes
 LA/RAE or both  Normal IVS/LVFW thickness  Normal LV chamber  Lack of L sided volume overload
56
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
57
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
58
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
59
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
60
Gross pathology myocardial infarct
* Well circumcised pale tan to red areas in myocardium * Distinct red rim
61
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
62
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
63
Etiology ARVC
unknown
64
Prevalence ARVC
2-4% according to 1 report
65
Gross pathology ARVC
 RAE/RVE  Focal or diffuse wall thinning  Aneurysmal bulges may be observed in apical, sub TV, infundibular regions
66
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
67
Px ARVC
poor: many cats euthanized for RCHF after 4months
68
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
69
Doppler ARVC
o TR: TV annular dilation
70
ARVC: how to differentiate between TVD
* Abnormal valvular morphology * Normal RV systolic fct * Age * ↑TR velocity → normal systolic fct
71
UCM features/prevalence
* Distinction clinically negligible → same tx * Prevalence: 10%
72
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
73
Risk factors for thrombus formation
o Sluggish blood flow  Normal to ↓ blood flow through enlarged chamber * Exacerbated in LAA due to semi-isolated state * cats * Platelet reactivity > in cats * Volume of platelet/BW o Endothelial damage o Hypercoagulable state
74
Components of virchow's triad
Endothelial injury Circulatory stasis Altered blood coagulability
75
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
76
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
77
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
78
Prevalence of ATE
o Male cats overrepensented → may be because increased risk for HCM
79
Etiology of ATE in cats
o Cardiogenic: 89-92% of cats o Neoplasia: bronchogenic carcinoma in 5% o Idiopathic: 3%
80
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
81
Gross pathology ATE
o Saddle thrombi have redish appearance o Coagulative necrosis of tissues o Pale affected surrounding muscles
82
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
83
Px ATE
poor outcome associated with o Hypothermia o Azotemia o 1 affected limb
84
Echo risks factor ATE
LAE SEC ↓ flow in LAA
85
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
86
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
87
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
88
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
89
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
90
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
91
Consequences of mitral septal contact w/ HCM
o ↑wall stress o ↑ myocardial O2 consumption o ↓ coronary blood flow o Myocardial ischemia
92
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
93
SAM exacerbated by
o Severe basilar septal knob o ↑ contractility o Tachycardia