Canine Cardiomyopathies Flashcards
DCM phenotype
what we see with US: structural changes or arrhythmogenic changes seen on US
ex: ID a large dilated heart: all you can say is that the pt has a DCM phenotype: need workup to determine cause
what is primary myocardial disease
- functional impairement: not pumping or filling
- electrical abnormalities
- or both
IN THE ABSENCE of any other cardiovascular disease to cause the myocardial abnormality
occult
has the disease but no signs
signalment of cardiomyopathies in dogs
usually adult onset, some juvenile forms reported but very rare
typically 2-5 yrs onset
clinical/overt
has clinical signs with their disease
T/F: canine cardiomyopathies are common
true: 2nd most common heart disease in dogs
clinical recognition of cardiomyopathies
- breed screenings: dobies! echo, HCG, both
- cardiac auscultation: left sided systolic murmur, gallop sounds, arrhythmia auscultated
- clinical signs associated with CV disease: exercise intolerance, syncope, breathing difficulty (pulmonary edema/effusion), abdominal distension (R sided CHF)
- signalment: adult, larger breed dog. (if small dog, likely mitral valve disease)
primary dilated cardiomyopathy is predisposed in what breed?
dobermans!! PDK4: involved in mitochondrial energy production and titan (sercomeric gene)
primary dilated cardiomyopathy
genetic, familial or idiopathic
- dobermans in US: PDK4 and titan
- dobermans in europe: chromosome 5
- great dane, irish wolfhound, newfoundland, cocker spaniel, portuguese water dog, standard schnauzer (RBM 20 mutation)
what 2 mutations have been ID’d of predisposing dogs to primary dilated cardiomyopathy
dobermans in US: PDK4: involved in mitochondrial energy production
titan: sarcomeric gene
but: can have this mutation and not have DCM and vice versa
DCM pathophysiology
- CONTRACTILITY issue: systolic function impaired!!
- leads to increased ESV and increased EDV
- this then leads to decreased stroke volume because trying to normalize stroke volume
- leads to dilation as compensation (consequence)w
what is the consequence of DCM
dilation of the heart
compensatory chamber dilation with DCM
in the impaired/dilated heart, the EDV, ESV, and SV all increase, but the ejection fraction decreases. if it dilates, doesn’t have to contract as much to maintain filling
- this is really only a short term fix: get eccentric hypertrophy (sarcomeres added in series dilating the ventricle)
eccentric hypertrophy (chamber dilation) in DCM only compensates up to a point. what happens as severe consequences of DCM?
- cardiomyocytes not made to sustain prolonged stressors
- cost: “maladaptive hypertrophy”: neurohormones (NE, antiogensin, aldosteron) activated to augment/assist filing: these trigger pathways resulting in hypertrophy, cell death and fibrosis
- also act as growth factors: these cause the eccentric hypertrophy
pathology of DCM
- attenuated/wavy myofibers and replacement or interstitial fibrosis (increased myocardial collagen)
- heart is a terminally differentiated organ: when heart muscle cells die, that is all you get
- patchwork of body is inflammation and then fibrosis: get interstitial fibrosis
- in R ventricle can get fatty infiltration
adverse impact of eccentric hypertropy
- chamber dilation progressive
- enhanced filling (increased EDV) –> SV remains normal despite decreased ejection fraction
- but: dilated chamber diameter/radius INCREASES WALL STRESS
- LaPlace’s Law: wall stress = pressure x radius / 2x wall thickness
- increased chamber size increases wall stress
- mitral valve regurgitation from remodeling of ventricle
neurohormones with DCM
- activated to assist with increased filling (increased preload/pulmonary venous return)
- this will increased EDV and pressure: gets reflected back to atrium and pulmonary veins, and eventually pulmonary pressure increased = pulmonary edema, pleural effusion, abdominal effusion
what are the neurohormones associated with DCM
norepinephrine, angiotensin 2, aldosterone
T/F: eccentric hypertrophy/DCM causes mitral valve degeneration/regurgitation
true
T/F: you can get arrhythmias at any stage of DCM
true
what are causes of secondary CMs with systolic dysfunction?
- nutritionally-mediated/diet: increased pulses, decreased taurine, L-carnitine
- cardiotoxicities: doxorubicin creating ROS
- tachycardia induced CM or tachycardiomyopathy
- myocarditis: infx, inflamm, immune
- ischemic CM: rare
- endocrinopathies?
diagnosis of primary DCM
- DCM phenotype: doberman, etc
- diagnosis of exclusion:
- ECG, Holter (24 hr monitor on chest)
- CBC, chem, troponin, infx disease testing
- drug history
- DIET HISTORY! boutique, grain free, pulses (lentils, peas, beans)
- taurine, L carinitine deficiency? (goldens and cocker spaniels)
what are pulses in diet?
group of foods consisting of lentils, peas, beans
some dog foods have these as a primary list of ingredients, and some dogs can develop DCM from this. taking them off diet can help improve these
what doberman specific DCM tests can you do>
- troponin-I: biomarker/protein that’s part of contractile apparatus: specific to heart muscle. if increased = heart muscle cell damage
- NT-proBNP: biomarker of heart muscle stretch/stress
