Feline and Canine Cardiomyopathy Flashcards
Types of canine cardiomyopathies
1) Dilated cardiomyopathy- primary (idiopathic/genetic) vs secondary
2) Arrhythmogenic right ventricular (arrhythmic) cardiomyopathy (boxers and bulldogs)
3) Hypertrophic cardiomyopathy -rare
4) secondary myocardial diseases (tachycardia-induces CM, myocarditis)
What breeds typically get Arrhythmogenic right ventricular (arrhythmic) cardiomyopathy
boxers and bulldogs
What is a primary cardiomyopathy
an acquired, adult onset primary myocardial disease associated with functional impairment, electrical abnormalities (ie. tachyarrhythmias) or both
in the absence of any other cardiovascular disease to cause the myocardial abnormality
an acquired, adult onset primary myocardial disease associated with functional impairment, electrical abnormalities (ie. tachyarrhythmias) or both
in the absence of any other cardiovascular disease to cause the myocardial abnormality
What is a primary cardiomyopathy
When do you use the term DCM phenotype
Idiopathic DCM that we’ve recognized on echo or clinically but we do not know if it is primary or secondary
implies that the cardiomyopathy is idiopathic
default diagnosis and not sure if primary (idiopathic or genetic) vs secondary
Are cardiomyopathies congenital?
NO- usually adult onset, some juvenile forms report but very rare
What is the second most common heart disease in dogs
DCM
(MMVD is #1)
How do recognize cardiomyopathies
1) Breed screenings (echo, ECG/holter, or both)
2) Cardiac auscultation- left sided systolic murmur, gallop sounds, arrhythmia auscultated
3) Clinical signs associated with CV disease
-Exercise intolerance
-syncope
-breathing difficulty
-abdominal distension
4) Signalment
What breeds have primary dilated cardiomyopathy (genetic/ familial/ idiopathic)
*Dobermans in US (PDK4) and titan gene
Dobermans in Europe (chromosome 5)
Great Dane
Irish Wolfhound
Newfoundland
Cocker spaniel
Portugese water dog (rare juvenile DCM)
Toy Manchester terrier (rare juvenile DCM)
Standard schnauzer (RBM20 mutation)
*more common in large or giant breeds
Why do Dobermans get dilated cardiomyopathy
it is primary (genetic, familial, or idiopathic- presumed to be genetic)
IN the US- PDK4 gene- involved in mitochondrial energy production and titan (sarcomeric gene)
In Europe-> Chromosome 5
What genes are mutated in the Doberman (US) that makes them get primary dilated cardiomyopathy
1) PDK4 (mitochondrial energy production)
2) Titan (sarcomeric gene)
What is the pathophysiology of DCM
1) Decrease in contractility (systolic function)
2) Increased ESV and Increased EDV (chamber dilation) to normalize stroke volume
3) Triggers eccentric hypertrophy to compensate
*Compensates up to a point
Why does the heart dilate in DCM
Because due to decreased contractility (systolic function drop off) there is increased End-Systolic Volume. This makes the heart increase its chamber size (Increased EDV) to normalize the stroke volume and ejection fraction
How are the sarcomeres added in DCM
added in series (eccentric hypertrophy)
How are sarcomeres added in eccentric hypertrophy
added in series
What are the adverse effects of eccentric hypertrophy
1) Neurohormones (NE, RAAS) increase preload but also trigger pathways resulting in hypertrophy, cell death and fibrosis leading to replacement or interstitial fibrosis (Increased myocardial collagen)- connective tissue cells (fibroblasts) can proliferate but cardiomyocytes cannot
2) Chamber dilation is progressive. With increased EDV, SV remains normal despite decrease in ejection fraction but increased chamber size impacts wall stress (LaPlace’s Law)
3) Predisposed functional mitral valve regurgitation due to remodeling of ventricle contributing to wall stress
-
What are the effects of neurohormones after eccentric hypertrophy
1) Neurohormones (NE, RAAS) increase preload but also trigger pathways resulting in hypertrophy, cell death and fibrosis leading to replacement or interstitial fibrosis (Increased myocardial collagen)- connective tissue cells (fibroblasts) can proliferate but cardiomyocytes cannot
2) they also cause fluid retention (increased preload) leading to pulmonary edema, pleural effusion, abdominal effusion
leading to congstive heart failure
How does LV eccentric hypertrophy lead to mitral valve regurgitation
because there is remodeling of the ventricle (papillary muscle displacement and annular stretch) which contributes to increased wall stress and increased chamber size (progressive LV dilation) and left atrial enlargement
What is the trigger for primary DCM
decreased contractility and interstitial fibrosis
How does DCM lead to congestive heart failure
Neurohormonal activation (RAAS hormones, NE) cause fluid retention (increased preload) leading to pulmonary edema, pleural effusion, abdominal effusion
What are the effects of primary DCM
*Progressive LV dilation secondary to systolic dysfunction:
1) Congestive heart failure (pulmonary edema, pleural effusion, abdominal effusion)
2) Arrhythmias (at any stage): ventricular tachyarrhythmias, A fib- with atrial dilation), VPC
3) Dilation without systolic dysfunction
4) Systolic dysfunction without dilation possible
What are common arrhythmias with DCM
ventricular tachyarrhythmias, A fib- with atrial dilation
*Can happen at any stage
What are some secondary cardiomyopathies with systolic dysfunction that can lead to a dilated cardiomyopathy phenotype
1) Nutritionally-mediated/diet (taurine or L-carnitine)
2) Cardiotoxicities (doxorubicin generates ROS)
3) Tachycardia-induced CM (TICM) or tachycardiomyopathy
4) Myocarditis (infectious, inflammatory, immune mediated, idiopathic)
5) Ischemic CM
6) Endocrinopathies (Hypothyroidism is unlikely)
Nutritional deficiencies in _______ can lead to DCM phenotype
taurine or L-carnitine
-specifically in Cockerspaniels
What chemotherapeutic drug can lead to DCM phenotype
Doxorubicin
T/F: Hypothyroidism can commonly cause DCM phenotype
False- it has been linked but not very likely that it is the cause
What diet is associated with DCM
“grain free” diet
avoid boutique, exotic, grain free (pulse main ingredient)
specifically lentils, peas, and beans as the main ingredient
*encourage diets backed by diet trials
Grain free diets with ____________ as the main ingredient may have a link to the development of DCM
lentils, peas, and beans
What are some criteria for the diagnosis of primary DCM in the Doberman
1) Echo: LV dilation and systolic dysfunction
2) >300 VPC in 24 hour Holter monitor
3) Troponin-I >0.22ng/mL
4) NT-proBNP>500 pmol/L
What causes increases of Troponin-I
myocardial death causes the release of troponin-I into the bloodstream
How do you diagnosis primary DCM in large breed dogs (not Doberman)
pre-clinical may be challenging
dx of clinical DCM is straightforward -> do echo and look for LV dilation and systolic dysfunction
How do you manage preclinical DCM
PIMOBENDAN +/- ACE inhibitors, spironolactone, betablockers? (but evidence is week in preclinical patients)
treat arrhythmias as needed (sotalol, mexiletine, amiodarone, etc)
treat secondary DCM by underlying cause - nutritional (change diet and supplement taurine if low)
T/F: Pimobendan increases the onset time of CHF/SD in preclinical DCM patients
true- it increases the time to 718 days instead of 441 days
increases survival to 623 increased of 466 days
How do you manage clinical DCM
-If CHF treat with furosemide, pimobendan, ACE inhibitors, spironolactone
-treat arrhythmias as needed (sotalol, mexiletine, amiodarone, etc)
-treat underlying arrhythmias (sotalol, mexiletine, amiodarone)
-Treat A-fib with Diltiazem +/- digoxin
change diet if BEG/nontraditional and supplement taurine if low
How do you treat Atrial Fibrillation due to DCM
you dont want to just stop A-fib otherwise they will just go back in.
you want to treat with drugs that slow AV node conduction (Diltiazem +/- digoxin)
Diltiazem is a ____________ used to treat _________ by slowing __________
Diltiazem is a calcium channel blocker used to treat Atrial fibrillation caused by DCM by slowing AV node conducton
What is the prognosis of DCM
unless you kind the reversible cause it has a very poor prognosis because it can cause sudden cardiac death, refractory CHF
need to increase furosemide dose a lot until it doesnt work or kidneys affected
Preclinical 2-4 years until clinical signs (syncope,CHF)- increased by pimobendan
Clinical 6-12 months
Bad clinical findings: <5 years +clinical signs, CHF (pulmonary edema) + ascites or pleural effusion, Frequent VPCs+CHF, A fib +CHF
What breed typically gets arrhthymogenic right ventricular cardiomyopathy
Boxers or Bulldog
What are the stages of arrhthymogenic right ventricular cardiomyopathy
Stage I: Asymptomatic with VAs
Stage II: Symptomatic with VAs
Stage III: LV systolic dysfunction/DCM phenotype -> more severe form associated with CHF and sudden death
Boxers that are asymptomatic with ventricular arrhythmias
Stage I: arrhthymogenic right ventricular cardiomyopathy
Boxers that are symptomatic with ventricular arrhythmias
Stage II: arrhthymogenic right ventricular cardiomyopathy
Boxers that have LV systolic dysfunction/DCM phenotype due to ventricular arrhythmias
associated with CHF and sudden death
Stage III: arrhthymogenic right ventricular cardiomyopathy
What causes Stage arrhthymogenic right ventricular cardiomyopathy in Boxers
Desmosopathy- a Striatin gene mutation leading to abnormal intercellular adhesion -> myocyte death -> myocardial fibrofatty infiltration -> intolerance to mechanical stress -> tacchyarrhythmias, impaired systolic function -> DCM phenotype
arrhthymogenic right ventricular cardiomyopathy in boxers is caused by a mutation in
a Striatin gene mutation leading to abnormal intercellular adhesion
“Desmosomopathy”
Homozygous is associated with type III and worse prognosis
Boxers that are ________ for the _________ are associated
homozygous for Striatin gene associated with type III and worse prognosis
How do you recognize ARVC
1) Boxer of Bulldog
2) Arrhythmia noted on PE
3) Syncope, exercise intolerance, lethargy, breathing difficulty, abdominal distension (CHF)
4) Right sided (LBBB-morphology) premature ventricular complexes
*Exclude ventricular arrhythmias
Will the premature ventricular complexes seen in boxers be positive or negative on lead II
positive on lead II
originating from the right ventricle
How do you manage ARVC
1) avoid strenuous exercise and excessive excitement
2) Antiarrythmogenics if symptomatic (Type II)
3) Pimobendan for type III -> if CHF add furosemide, ACE inhibitor, spironolactone +/- antiarrhythmics
How do you diagnose ARVC?
-Incidental arrhythmia, syncope, pre-syncope, exercise intolerance
-Diagnosis of exclusion (rule out other ventricular arrhythmias- heart disease, electrolytes, adrenergic, drigs, surgical disease)
-Largely based on ECG and 24 hour Holter
-Echocardiography- DCM phenotype (Boxers) but overt RV structural and function changes are uncommon
T/F: With ARVC the right ventricle typically enlarges
False- there is a LV enlargement DCM
functional (nonpathological) murmurs that are more common in cats (40-60%) without structural cardiac disease
stress-related murmurs
Almost all dogs with a murmur have CV disease but with cats
40-60% of cats have murmurs without structural cardiac disease and many cats with CV disease do not have abnormalities on cardiac auscultation (up to 30%)
Unlike dogs with CV, cats with CV rarely
cough
What is often the first clinical sign of CV disease in cats
breathing difficulty (CHF), then vomiting, hyporexia, hiding
Cats manifest left sided CHF as
pulmonary edema and or pleural effusion +/- pericardial effusion
*Dogs only get pulmonary edema
T/F: cats commonly get clinically significant acquired degenerative valve disease
false
What are the 3 broad categories of differentials for cat with a grade 3/6 left caudal parasternal systolic murmur
1) Congenital heart disease (pathological)
ex: ventricular septal defect, mitral valve dysplasia, atrioventricular septal defect
2) Acquired heart disease (pathologic) ex: cardiomyopathy (HCM -> primary vs secondary CM) or infective endocarditis (rare)
3) Functional/physiologic murmur (non-pathological) - Stressed cat
What is the most common congenital heart disease in cats
ventricular septal defect (VSD)
What kind of heart murmur would you hear in a patient with a PDA
continuous heart murmur
T/F: Calming or sedation techniques are helpful to differentiate pathological vs nonpathological murmur
false - doesnt tell you cause
What breeds of cats are predisposed to cardiac disease
Maine Coon + Ragdoll
What are indications that a heart murmur in a cat is not stress induced
1) Predisposed breed (Maine Coon or Ragdoll)
2) Clinical signs
3) Any additional abnormal heart sounds other than systolic murmur -> summation gallop sound, arrhythmia -> premature beats often auscultated as short pause, diastolic/continuous murmur
4) Loud murmur (>grade 4 murmuers) = pathologic
Stressed induced heart murmurs in cats are typically
Systolic
Grade 3 or less
Summation gallops
due to the cat’s fast heart rate. the gallops (low pitched, diastolic heart sounds) are summated
often difficult to tell the type (S3 vs S4) due to higher HRs in cats
What is the check list you should go through to tell if a murmur is functional or secondary CM in cats
1) Anemia?
2) Systemic hypertension? (comorbid disease)
3) Hyperthyroidism (old cats)
4) Biomarker NT-proBNP
*Refer to echo at any point
a marker of cardiomyocyte stress or stretch
stimulate vasodilation and renal natriuresis
specific specific test
used plasma (or pleural effusion)
NT-pro BNP (natriuretic peptide)
What sample do you need to submit NT-pro BNP in a cat
plasma (or pleural effusion)
what sample do you need to submit for cardiac troponin I (cTni) in a cat?
Serum Sample
marker of ongoing (short half-life) cardiomyocyte damage/injury -> ischemia, cell death -> ischemia or myocarditis
not species specific
cardiac troponin I (cTni)
T/F: NT-pro BNP and cardiac tropinin I tell you the cause of cardiomyocyte stress or injury
False- neither tell you cause of injury but tell you if the heart is the problem
When is running NT-proBNP on a cat a good idea?
It is a great idea if systolic murmur grade <4/6 and you arent sure if it is stressed induced or pathological
T/F: Thoracic radiographs are helpful to determining the cause of murmurs in cats when asymptomatic
False- unlike incidental murmurs in dogs
*Not going to pick up much cardiomegaly in an asymptomatic cat
What value of NT-proBNP in asymptomatic cats shows a high likelihood of clinically significant cardiac disease
> 100 pmol/L
*Makes an echo much more worthwhile, especially if cat is not azotemic
Cats with what disease might falsely elevate NT-proBNP
Cats with renal disease- excreted through the urine
Why might you get a false positive for NT-proBNP measurement?
if the cat is azotemic - renal disease
A cat with <100 pmol/L NT-proBNP means:
you can be confident that the cat does not have clinically significant cardiac disease (might have mild disease)
-echo not necessary but may be ideal if performed general anesthesia, elective surgery, spay/neuter, dental, etc
Symptomatic Cats with NT-proBNP >270pmol/L means
CHF
Two types of NT-proBNP in cats
1) Quantitative send out test -> ideal if not in rush
2) SNAP -> ideal in symptomatic cats
cut off is >100pmol/L
many false positives in symptomatic cats
normal/negative value most help in symptomatic cats
How do you interpret a cat with a NT-proBNP of 160pmol/L
Tells you there is cardiomyocyte stress or stretch (>100pmol/L)
1) Make sure it is not falsely elevated with renal disease
2) Follow up with echo or cautious approach to anesthesia
How do you interpret a cat with a NT-proBNP of 48 pmol/L
Tells you that the cat does not have heart disease and any murmur you hear might be non-pathological
What cardiomyopathy is most common in cats?
What are less uncommon?
Hypertrophic cardiomyopathy is msot common
*Restricitive CM, Arrhythmogenic right ventricular CM, and DCM are all uncommon in the cat
Two forms of restrictive cardiomyopathy in cats (RCM)
1) Endomyocardial form- fibrosis lining typically on LV and IV septum; La or biatrial enlargement is present
2) Myocardial form - Normal LV dimensions (including wall thickness with LA or biatrial enlargement)
T/F: Restrictive cardiomyopathy is uncommon in cats
True- challenging to definitively diagnose
What do you see with restrictive cardiomyopathy in cats
diastolic dysfunction with near normal wall thickness
LA or biatrial enlargement
What will you see on echo in a cat with restrictive
Diastolic dysfunction with near normal wall thickness (LA or biatrial enlargement)
Is restrictive cardiomyopathy in cats systolic or diastolic dysfunction
Diastolic dysfunction with near normal wall thickness (LA or biatrial enlargement)
T/F: Dilated cardiomyopathy is rare in cats
True
LV (+/- RV) systolic dysfunction (normal wall thickness) leading to chamber dilation in dogs
very rare in cats but often idiopathic
Dilated cardiomyopathy
Cats with a taurine deficiency develop
Dilated cardiomyopathy
LV (+/- RV) systolic dysfunction (normal wall thickness) leading to chamber dilation in dogs
very rare in cats but often idiopathic
T/F ARVC is rare in cats
true
How is ARVC different in the cat vs the dog
they often have severe RA and RV dilation and often idiopathic RV systolic dysfunction and RV wall thinning leading to ascites
dogs typically only get arrhythmias
What is a clinical sign of feline (A)RVC
Idiopathic RV systolic dysfunction and dilation leading to right sided congestive heart failure
*Ascites
Nonspecific CM in cats
Left of bi-atrial enlargement with
-Normal wall thickness
-Seemingly normal systolic function
-RV not overtly dialted/dysfuctional
-Often unable to assess diastolic function
-+/- Tachyarrhythmias (eg. Afub)
*Not adequately described by other categories
Left of bi-atrial enlargement with
-Normal wall thickness
-Seemingly normal systolic function
-RV not overtly dialted/dysfuctional
-Often unable to assess diastolic function
-+/- Tachyarrhythmias (eg. Afub)
*Not adequately described by other categories
Nonspecific cardiomyopathy
Diffuse or regional increase in LV wall thickness with nondilated LV chamber in cats
Hypertrophic cardiomyopathy
Hypertrophic CM in cats is a disease of (Systolic/Diastolic) dysfunction
Systolic Dysfunction
How do you diagnose the HCM phenotype in cats?
Echo: End-diastolic wall thickness measurements >6mm
*Mild HCM can be challenging to diagnose
What are causes of a HCM phenotype in a cat?
1) Primary (genetic/idiopathic) HCM = diagnosis of exclusion
2) Secondary HCM:
a)Systemic Hypertension
b) Hyperthyroidism
c) Infiltrative disease (lymphoma, myocarditis)
d) Acromegaly (very rare)
e) Aortic stenosis/LVOTO
f) Pseudohypertrophy (hypovolemia/dehydration)
What should you do if you notice a cat with hypertrophic cardiomyopathy phenotype on echo?
Find the cause
1) Check Blood Pressure- was it caused by systemic hypertension?
2) Total T4- Was it caused by hypertrhyroidism?
3) Rule out infiltrative disease (lymphoma, myocarditis)
4) Was it caused by acromegaly?
5) Did you see aortic stenosis/ LVOTO on echo?
6) Was their pseudohypertrophy? Was the patient hypovolemic or dehydrated?
Why might a dehydrated patient show a HCM phenotype
Due to hypovolemia- the chamber sizes shrink and give the appearance that there is HCM appearance
What can give a false appearance of a HCM phenotype
Dehydration
Due to hypovolemia- the chamber sizes shrink and give the appearance that there is HCM appearance
What are mutations known to cause HCM in cats?
1) Myosin binding protein: C3-A31P (Maine Coon)
2) Myosin binding protein C3-R820W (Ragdoll)
*both are autosomal dominant with incomplete penetrance
Primary HCM in the Maine Coon is due to
Autosomal dominant with incomplete penetrance mutation in Myosin binding protein: C3-A31P
Primary HCM in the Ragdoll is due to
Autosomal dominant with incomplete penetrance mutation in Myosin binding protein C3-R820W
Different phenotype diversity in HCM
1) Mostly see just thickening of the intervertebral
2) also can just see thickening of free wall (less common)
3) Hypertrophy of basal IVS
4) Apical Hypertrophy
5) Diffuse symmetric LVH
*Just need thickening of any wall >6mm to be diagnosed
Obstructive form of HCM
secondary to HCM and systolic anterior motion of mitral valve
in some cats with HCM you get laxity of chordae tendinae and the anterior leaf of mitral valve gets pushed towards left ventricular outflow tract
*Obstructs outflow out of aorta and mitral valve regurgitation
secondary to HCM and systolic anterior motion of mitral valve
in some cats with HCM you get laxity of chordae tendinae and the anterior leaf of mitral valve gets pushed towards left ventricular outflow tract
*Obstructs outflow out of aorta and mitral valve regurgitation
Obstructive form of HCM
Pathophysiology of primary HCM
1) Defective sarcomere due to mutation
2) Increased myocardial mass and myofiber disorganization
3) Demands more oxygen and leads to myocardial ischemia and fibrosis
a) Ventricular arrhythmias
b) Impaired RV relaxation
c) Alteration in calcium kinetics
*Overall: impaired myocardial relaxation and decreased chamber compliant
*Diastolic Dysfunction
Overall, what is the effect of primary HCM
impaired myocardial relaxation and decreased chamber compliant
*Diastolic Dysfunction
leads to increased pulmonary venous pressure from left atrial enlargement and dysfunction
Why do you get pulmonary capillary pressure with HCM and RCM
there is increased LV filling pressure (diastolic dysfunction) leading to left atrial enlargement and dysfunction
this increases pulmonary venous pressure and pulmonary capillary pressure
How do you diagnose HCM on echo
1) End-diastolic wall thickness measurements >6mm
2) Diastolic (and systolic) function assessment
3) atrial size assessment (will be increased due to diastolic dysfunction)
Stage A (cat)
A cat that is predisposed to cardiomyopathy
ex: Maine Coon or Ragdoll
Stage B1 (cat)
A cat that is low risk
subclinical
norma;/mild atrial enlargement
*Asymptomatic
Stage B2 (cat)
a cat that is subclinical but has moderate/severe atrial enlargement
*Asymptomatic
Stage C (cat)
a cat that has current or previous congestive heart failure or arterial thromboembolism and is going through or previously treated
Stage D (cat)
a cat that has refractory CHF
How do you treat cats that are subclinical for cardiomyopathies
most drugs have not shown a clinical benefit to delay the onset but treatment options should be based on risk assessment (echo findings) and pillability
-Pimobendan (for systolic dysfunction-really rare) and antiarrhythias (limited options)
When might you treat a cat with Pimobendan for subclinical HCM
when there is wall thinning from myocardial infarction/scar
*Very rare
What are the 3 adverse outcomes of cardiomyopathies in cats
1) Sudden cardiac death from systolic dysfunction and ventricular arrhythmias
2) Heart failure - atrial enlargement and decreased atrial pump function
3) Arterial thromboembolism from atrial enlargement and decreased atrial pump function
why might you get spontaneous echogenic contrast “smoke” seen on echo in a cat with HCM
atrial enlargement leading to decreased atrial pump function causing formation of atrial/aurciular thrombus that can dislodge and travel to LV and out aorta
What should you do when you see spontaneous echogenic contrast “smoke” seen on echo in a cat with HCM
Clopidogrel (Plavix)- makes platelts less sticky
+/- Factor Xa inhibitor (ex: rivaroxaban) - anti-thrombotic drug
Rivaroxaban is a
factor Xa inhibitor that is antithrombic
added with Clopidogrel when you see spontaneous echogenic “smoke” material in atrium/aurcular
What worsens the SAM (Systolic Anterior Motion) seen in obstructive HCM
A fast heart rate and increases in contractility (stressed cat)
Treat with a betablocker like atenolol
Beta-blockers typically arent used to subclinical HCM. However when are they indicated
Anmial is syncopic due to SAM- Systolic Anterior Motion and affects of obstructive HCM
A fast heart rate and increases in contractility (stressed cat)
need to treat tachycardia and increased in contractility
Cats with subclinical feline CM (Stage B2) need to be treated with
Clopidogrel (Plavix)
Cats with Stage C cardiomyopathy develop showing signs. What are they
1) Usually breathing difficulty, tachypnea +/- GI/sick cat signs)
2) Cardiogenic pleural effusion +/- pericardial effusion (Do POCUS prior to thoracic radiographs or thoracocentesis if present) and/or
3) Cardiogenic pulmonary edema
T/F: Furosemide does a great job at removing pleural effusion seen in HCM
False- it only prevents against future buildup of fluid
you need to remove it with a thoracocentesis
*it is good if there is pulmonary edema (fluid within the lungs)
T/F: you always need to remove pericardial effusion in cats
False - furosemide will prevent it
T/F: you always need to remove pleural effusion in cats
True
T/F: radiography is important to identify pleural effusion
False- you wont see anything
you will just see soft tissue opacity
*Do ultrasound first
*Tap them
*Then radiograph to check for pulmonary edema
In cats, cardiogenic pleural effusion might be
Chylous or Modified Transudate
How does one determine pleural/pericardial effusion or pulmonary edema is cardiogenic in a cat
Look for Left Atrial Enlargement (or biatrial enlargement) via Echo
If you notice atrial enlargement then start empircial furosemide (when associated with breathing difficulty)
What should you do if you dont have an ultrasound that can help you rule out cardiogenic causes of dyspnea
SNAP NT-proBNP
>270pmol/L is associated with cardiogenic causes of dyspnea
-False positive possible (renal disease)
How do you treat acute CHF in cats
-Sedation and oxygen
-Empirical furosemide
-Thoracocentesis? -pleural effusion
-Minimize stress, step-wise diagnostics
How do you treat chronic CHF in cats, after treatment of acute CHF
Stage C/D
1) Furosemide
2) Clopidogrel (Plavix) +/- factor Xa inhibitor (rivaroxaban, apixaban)
Possibly:
-ACE Inhibitor (most likely), spironolactone (ideal)
-Pimobendan -> not usually unless DCM or refractory CHF (Not good evidence
-Diltiazem, atenolol, or sotalol for A fib and rapid heart beat
4 possible outcomes of HCM in cats
1) Nothing (live normal life)
2) Death or euthanasia related to CHF/refractory CHF or even organ failure (renal)
3) Death or euthanasia related to ATE
4) Sudden cardiac death
What is the prognosis of a cat with subclinical HCM if no atrial enlargement
normal life to years if no atrial enlargement
What is the prognosis of a cat with congestive heart failure
can be months to 1.5 years (owner dependent)
What factors make the prognosis for CMs in cats significantly worse
1) Older cat
2) LA enlargement/dysfunction
3) LV systolic dysfunction (myocardial infarction)
4) ATE
What is the pathophysiology of feline arterial thromboembolism (FATE)
1) Left Atrial enlargement leading to blood stasis and endothelial/ endocardial injury and blood clumping
2) Large thrombus formation in Left Auricle
3) Dislodge/Embolize to systemic artery
-Often aortic trifurfcation (saddle thrombus) due to size
T/F: feline arterial thromboembolism is always cardiogenic
False- it mostly is but it can also be pulmonary neoplasia
How else, besides CM might a cat get thromboembolism
Pulmonary neoplasia (rare) -> get chest rads
Hypercoagulability
3 factors that predispose animal to thrombosis
1) Blood stasis
2) Vessel wall injury
3) Hyper coagulability
the 5 P’s of clinical signs of cats with arterial thromboembolism *
1) Pulselessness or very weak femoral pulses
2) Pale (acute) and/or blue/purple HL nail beds/foot pads
3) Pain leading to vocalization/agonizing (subsides 12-24 hours)
4) Paresis/paralysis of hindlimbs (distal to knee), tail
5) Poiklothermia: cold limbs
*also contracted/firm gastrocnemius muscles
What muscle will be contracted/firm with FATE
gastrocnemius muscles
How do you treat FATE
1) Potent Analgesia (Pure mu agonist like Fentanyl or Methadone) +/- anxiolytic (acepromazine)
2) Check electrolytes -to rule out hyperkalemia (reperfusion injury)
3) Antithrombotic drugs- prevent clot formation-> parenteral heparin and clopidogrel initially then clopidogrel and factor Xa inhibitor
ECG monitoring for hyperkalemia
Rule out CHF
Confirm ATE (particularly if not all 5P/s)
What analgesic should you use for FATE management
Potent Analgesia (Pure mu agonist like Fentanyl or Methadone) +/- anxiolytic (acepromazine)
T/F thrombolytic drugs are controversial for FATE management
true, drugs like tissue plasminogen activator might worsen repurfusion but this is controversial
What should you do if you suspect feline ATE, if not all 5P’s are not present
-Lack of Doppler BP
-Abdominal/vascular ultrasound with Doppler
-Serum CK (and AST and ALT) are always elevated usually >10K or 100K
-Paired glucose and lactate
What biochem value rules out suspected ATE
Serum Creatine Kinase (if low)
Management of feline ATE is commonly euthanasia but when might you advise the owners to consider 24-72 hours of treatment
-No CHF, single limb, forelimb, not hypothermic (CHF, bilateral HL, hypothermic = bad prognosis)
*Support through reperfusion injury and endogenous thrombolysis
