Canine Heart Diseases & Cardiomyopathies Flashcards
What valves are most commonly affected by endocarditis? What are the 4 most common causes?
mitral and aortic valves (left-sided!)
- Staph
- Strep
- E. coli
- Bartonella - can be negative on culture
What lesion is characteristic of endocarditis? What does this cause?
vegetative lesion - fibrin + platelets + bacteria
severe valvular regurgitation and spread of bacteria into systemic circulation
What is this most common origin of bacterial endocarditis? What perpetuates it?
recent/current infection of skin, mouth, urinary tract, prostate, or lungs
- chronic bacteremia
- diseased valves - SAS, mitral disease; damage causes poor protective barrier
What patients are most commonly affected by bacterial endocarditis? What signs are most common?
young, large breed dogs
- FEVER
- new, severe murmur
- hyperkinetic, bounding pulse
- polyarthritis
- thromboembolism
- CHF
What is required for diagnosing endocarditis?
blood culture
+/- echo
+/- thoracic radiographs
What treatment is used for endocarditis?
appropriate IV antibiotics for at at least 6-8 weeks - Ampicillin, Baytril —> guarded prognosis due to bacterial embolization
- address failure, arrhythmias, and underlying disease
What is the difference between primary and secondary DCM?
PRIMARY - idiopathic, genetic, inflammatory (arrhythmogenic right ventricular cardiomyopathy - ARVC)
SECONDARY - persistent tachycardia, toxicosis (doxorubicin, epirubicin), muscular dystrophy, infections (Parvo, Borreliosis, Trypanosomiasis), metabolic conditions, nutritional disorders (grain-free, taurine, carnitine)
What is DCM? What breeds are predisposed?
myocardial disease characterized by decreased contractility with secondary compensatory ventricular dilation
large/giant breeds - Doberman (pyruvate dehydrogenase, titan), St. Bernards, Irish Wolfhounds, Boxers (ARVC), Newfoundlands, Afghans, Dalmations, Great Danes (X-linked), Cocker Spaniels, Portuguese Water Dog (autosomal recessive)
What is the pathogenesis of DCM?
- systolic contractile failure
- neurohormonal activation causes sodium and water retention/vasoconstriction, which increases preload, and proliferation of myocytes/fibroblasts
- cardiac remodeling = hypertrophy, dilation, fibrosis, sphericity
- changes cause abnormal systolic and diastolic function and arrhythmias
What are the 5 stages of DCM?
- Stage A - unaffected dogs with increased risk (breed/genotype)
- Stage B1 - electrical changes (VPC, Afib), but NO structural changes
- Stage B2 - LV systolic dysfunction AND structural changes +/- electrical changes
- Stage C - electrical and structural changes with CHF
- Stage D - end-stage disease with CHF refractory to standard therapy
What are some signs of DCM?
- first sign can be sudden death
- weakness, lethargy
- tachypnea, dyspnea, exercise intolderance
- cough/gagging
- anorexia
- ascites
- syncope
- tall R waves
- ventricular enlargement
What is seen on PE in patients with DCM?
- systolic murmur or S3 gallop
- arrhythmia (pulse deficit)
- weak arterial pulse
- LS-CHF - pulmonary edema, cough
- RH-CHF - ascites, jugular pulses
- cardiac cachexia
What changes in EKG are expected with DCM? What diagnostic is considered more sensitive?
- atrial/ventricular enlargement patterns - abnormal P and R waves, APCs, VPCs, bundle branch blocks
- tachyarrhythmias - Afib, Vtach
- often normal
Holter monitor - <50 VPC/day
What is seen in thoracic radiographs in cases of DCM? How is this limited?
CHF = severe enlargement
cannot assess function unless CHF is present
How are biomarkers being used to diagnose DCM?
(DNA, NT-proBNP, troponin I) - NOT to diagnose —> indicate those at-risk, aid in screening and response to therapy
- echo is confirmatory
What is the diagnostic test of choice for DCM? What 3 things are seen?
echocardiography
- LV systolic dysfunction
- mitral regurgitation, annulus enlargement
- LA enlargement
What breed is most commonly affected by DCM? What are the 2 major outcomes?
Doberman Pinschers —> adult onset, left/biventricular failure, arrhythmias
- sudden death
- CHF
How do most Dobermans present with DCM? What is key to survival?
occult phase (Stage B2) at 2-4 years —> progressive LV dysfunction, sudden death before any signs
early intervention/detection —> screen at 3 years (q 1 y) with echo, holter, and NT-proBNP to determine if Pimobendan, ACEi +/- Sotalol are indicated
What is the difference in the causes of DCM in American and English Cocker Spaniels?
AMERICAN = low plasma taurine levels (poorer prognosis) —> taurine supplementation and L-carnitine may improve LV function, but will not be normal
ENGLISH = not taurine related, likely heritable
What is the most common cause of DCM in Great Danes? What is the most common finding? What monitoring is recommended?
X-linked recessive - males > female, especially sons of affected females, daughters of affected fathers likely silent carriers
atrial fibrillation before signs of myocardial changes
annual monitoring, especially with Afib
What is the most common cause of DCM in Irish Wolfhounds? What is the most common sign? What is not seen?
familial, males > females
- atrial fibrillation about 24 months prior to CHF
- long-term result = biventricular CHF
sudden death
How are Portuguese Water Dogs most commonly affected by DCM? What is the most common sign?
juvenile form —> autosomal recessive trait linked to chromosome 8
affected puppies commonly collapse and die between 2-32 weeks of age
How are Newfoundlands affected by DCM? What are the most common signs?
adult onset
- biventricular CHF
- heart murmurs rare, but AF and VPCs seen
What is arrhythmogenic right ventricular cardiomyopathy (ARVC)?
Boxer cardiomyopathy —> primary myocardial disease where fibro-fatty replacement of the RV myocardium causes ventricular arrhythmias
- English Bulldogs also affected!
What are the 5 most common results of ARVC?
- ventricular arrhythmias
- ventricular systolic dysfunction and dilation
- CHF
- syncope
- sudden death
What are the 3 types of ARVC? How do most Boxers present?
- Class I = asymptomatic
- Class II = collapse and syncope
- Class III = CHF (left AND right)
normal PE, arrhythmia may be auscultated but is commonly missed
What is the diagnostic test of choice for ARVC? Why?
Holter monitor
- biomarkers (troponin I, BNP) not helpful
- genetic testing only available for Boxers - negative result does not r/o possibility of developing gen
- majority of dogs have normal structure, so echocardiography is only helpful for dogs with overt signs of CHF
What is seen on ECGs and Holter monitors in cases of ARVC?
ECG - typically performed for 2-5 minutes —> VPCs (single, couplet, runs of VT), left bundle branch block
HOLTER - 24 hour hours, 300 VPC per day (always screen Boxers!)
What are the 3 stages of ARVC? How do they present on physical exams?
- ventricular arrhythmias with NO cardiac dysfunction and symptoms - 50-300 VPC/day is possible, >300 VPCs/day very likely
- ventricular arrhytmias progress, no cardiac dysfunction, SYNCOPE - normal PE and echo, Vtach on Holter (syncope when >300 bpm >8 s)
- ventricular arrhythmia, cardiac dysfunction, heart failure, syncope - CHF on PE, echo shows LV dilation and poor function, Vtach and Afib with hugh LA on Holter
When is treatment recommended for ARVC?
when VPCs > 1000/day or clincial signs of weakness/syncope —> must treat or will develop DCM morphology
What are the 2 major treatments of ARVC? When patient is in failure?
- Sotalol +/- Mexiletine
- fish oil
treat failure and add antiarrhythmic
What is the prognosis of ARVC like?
- sudden death always possible with arrhythmias
- can live for years on medication
- must find and treat CHF quickly
When can tachycardia cause DCM? What is indicative of tachycardia being the cause?
HR > 200 bpm for more than 2-6 weeks = myocardial failure —> if resolved early, can return to normal in 1-2 weeks
all 4 chambers will become enlarged —> true dilation and failure causes ascites and pulmonary edema
- hypoxia NOT mechanism for failure
What are some nutritional causes of DCM?
- DOGS = alcohol, Doxorubicin, Adriamycin, L-carnitine deficiency (Cockers, Goldens, Newfies)
- DOGS and CATS = grain-free, boutique diets deficient in taurine, thiamine, vitamin E, and selenium, while containing grapeseed oil, heavy metals, and monensin
Why is it especially important to screen for DCM in at-risk breeds?
occult disease most common in these breeds - early detection allows time to stop breeding and provide early treatment if arrhythmias or low contractility are detected
- average onset is 5-7 years, but can be as early as 2 years
What screening is recommended for DCM at-risk breeds?
start at 2 years and screen annually —> 24 Holter monitor looking for VPCs (expect ~50 single VPCs/day in healthy Dobermans, more = concern for occult disease)
What ancillary tests are commonly used while screening at-risk breeds for DCM?
- biomarkers - NT-proBNP
- genetic tests
- short ECGs
What are the 6 strategies for treating DCM?
- INOTROPIC SUPPORT - Pimobendan
- NEUROHORMONAL SUPPORT - ACEi, Spironolactone
- PRELOAD REDUCTION - Furosemide, low sodium diet
- AFTERLOAD REDUCTION - ACEi, Pimobendan
- VENT. ARRHYTHMIA - Lidocaine, Sotalol, Mexelitine
- SUPRAVENT. ARRHYTHMIA - Digoxin, Diltiazen (NO beta-blockers)
check diet, monitor RR
When has it been proven that ACEi and Pimobendan are beneficial for occult DCM?
in Dobermans and Irish Wolfhounds
What are 5 negative predictors for survival in patients with DCM?
- age of onset
- ascites
- atrial fibrillation
- decreased ejection fraction
- restrictive diastolic pattern
What causes myocarditis? What are the 7 most common etiologies?
mild/transient/fulminant immune response leads to heart abnormalities
- bacterial - Bartonella, Lyme
- fungal
- viral - Parvo, Herpes, Adenovirus, Distemper
- toxins - anthracyclines (doxorubicin)
- protozoal - trypanosoma (Chagas), Toxoplasma, Neospora, Babesia, Hepatozoan
- hypersensitivities - cephalosporins, Digoxin, diuretics
- immunologic - post-infectious, IBD, lupus
How is viral etiology of myocarditis unique?
multisystemic signs predominate
How does Doxorubicin cause myocarditis?
decreases CO and causes arrhythmias/myocyte damage, systolic dysfunction, CHF —> similar presentation to DCM
- cumulative dose!
What are 5 methods to reduce Doxorubicin toxicity?
- use lowest cumulative doses
- give drug slowly (CRI) —> rapid infusion causes peak plasma levels > toxic dose
- liposome-encapsulated forms
- pretreat with Dexrazoxane
- Carvedilol may minimize damage
What transmits Trypanosoma that can cause myocarditis? What are the 2 types of presentations?
Reduviid/kissing bugs (TEXAS/Southern US) carry Trypanosoma cruzi, which is spread from feces deposited by wounds or ingestion of bug
- ACUTE - tachyarrhythmias, AV conduction disturbances, and sudden death common in puppies and young dogs
- CHRONIC - progressive myocardial disease looks like DCM and causes bradyarrhythmias common in older dogs that survive the acute phase
(chronic myocarditis + cardiomegaly)
What are 3 ways to diagnose Trypanosomiasis?
- suspicion based on geography and uncommon breeds developing DCM
- antibody titers
- identification of trypomastigotes in peripheral blood or amastigotes on myocardial biopsy/necropsy
What treatments are used for Trypanosomiasis?
- no known treatment for cardiac signs in dogs
- supportive care for arrhythmias and CHF
- Benznidazole may benefit in acute phase
What endocrine disease is associated with DCM? How are they related?
hypothyroidism —> poor thyroid function can result in systolic dysfunction and LV dilation (minorly!)
DOES NOT CAUSE DCM, but can have an impact in dogs that are already declining in function
- hypothyroidism AND DCM common in Dobermans, screen for both!
