Myocardial disease NB: more being added Flashcards
Signalment of DCM in dogs
Large and giant breed dogs esp Doberman, Great Dane, Irish Wolfhounds
+ exception to rule = cocker spaniels
What is DCM
A primary myocardial disease characterised by left ventricular systolic dysfunction
What is the aetiology of DCM
Assumed familial
Mutations have been found in Dobermans
Pathology of DCM
There is ventricular systolic dysfunction, leads to left ventricular dilation –> get progressive left atrial dilation
In same cases get dilation and dysfunction of the right ventricle too
There is eccentric hypertrophy with thinner ventricular walls that normal
What is the pathophysiology of DCM
Cellular level metabolic dysfunction and contractility defects
–> Get systolic dysfunction
–> Reduction in stroke volume and CO which activates RAAS and sympt system causing remodelling, increased myocardial O2 demand and cell death leading towards CHF
+ reduced function and ventricular dilation leads to increases in LV end diastolic pressures and therefore rise in left atrial and venous pressures
So get left sided CHF
What are some potential sequelae of DCM
Left sided congestive heart failure
Forward failure
RIght sided CHF because of arrhythmias
Arrhythmias
at what point of DCM is the dog at risk of congestive heart failure
When the left atrium is enlarged
What arrhythmias can occur in DCM
Atrial fibrillation esp in giant breeds
Ventricular arrhythmias and sudden death
Current staging of DCM
Pre-clin = have DCM but not in heart failure
Clnical = in heart failure
What does pre-clinical DCM mean
Either echo or electrical changes or both
No signs of congestive heart failure
= typically a slowly proressive disease
How prevalent is DCM in dobermans
Up to 60% have it
History and clinical exam of pre-clin DCM
History = asymptomatic usually, but often family history
May show exercise intolerance, or collapse
Clin exam may be unremarkable; may head soft murmur or arrhythmia
Why might we hear a soft murmur with pre-clinical DCM
Due to ventricular dilation causing stretching of the mitral valve and some regurgitation occuring
History of clinical DCM
= of congestive heart failure
- Exercise intolerance
- Lethargy, weakness
- Collapse/syncope
Tachypnoea, dyspnoea
Cough
Abdominal distension
What clinical exam signs can we see with clinical DCM
Murmur
Tachycardia
Tachyarrhythmias
Pulse deficits/reduced pulse quality
Dyspnoea
PUlmonary crackles
Weakness, collapse
+ in some cases have signs of right sided CHF - abdominal distension, jugular distension
What do we look for on echo with DCM evaluation
LV systolic function
Assess LV and LA size
Identify any murmurs
Assess right side size and function too
Hallmarks = LV systolic dysfunction and dilation
What do we use the ECG holter for in DCM analysis
Assess ventricular arrhythmias for burden i.e number of VPCs in 24hrs, severity of arrhythmias e.g couplets/triplets etc
What are the ECG criteria for DCM
> 300 VPCs Or two wtihin 12 months showing 50-300
Frequent couplets or triplets are assocaited with higher risk of sudden death
What is the gold standard way to diagnose pulmonary oedema
Thoracic radiographs
What two cardiac biomarkers can we look at
NT-proBNP: tells us about myocardial stretch and strain
Cardiac troponin 1: indicator of myocardial cell damage
Advantages/disadvantages of NT-proBNP as DCM biomarker
Predicts pre-clinical DCM with echo changes well but not those with just arryhtmias
Can get false +ves in renal disease, sepsis, hypertension
Takes a while so not good for emergency
What do very high values of cardiac troponin 1 suggest
Myocarditis
How do we treat pre-clinical DCM
Pimobendan; PDE III inhibitor should be introduced now
Advise monitoring of respiratory rate for increases that indicate moving into heart failure
What is different about resting respiratory rate monitoring in large dogs with DCM vs small ones with mitral valve
They go intro heart failure at much lower RRs so very important to have a base level to spot increase (Can’t jsut use over 30 rule)
What imaging signs do we see as DCM progresses to clinical stage
Echo shows worse ventricular dysfunction, atria now may be dilated
X rays show pulmonary oedema
What drugs do we use once in clinical DCM
[already should be on pimobendan]
Add in diuretics until stable
Then spironolactone, ACE inhibitors
What drugs should we use to treat atrial fibrillation in DCM
Want to get HR back until 125bpm
Diltiazem
Digoxin
What do we need to remember about digoxin
Very narrow therapeutic window
How to treat sustained ventricular tachycardia in DCM
Lidocaine
Amiodarone
Then can move to chronic oral therapy later; amiodarone, sotalol, mexiletine
Primary vs secondary cardiomyopathy
Primary = no apparent cause; i.e genetic - this is most cases
Secondary = where systemic disease is causing damage to myocardium
What systemic diseases can cause secondary cardiomyopathy cat HCM phenocopies
Hypertension, hyperthyroidism, acromegaly, lymphoma, nutritional
What is the most common cardiomyopathy in cats
Hypertrophic cardiomyopathy
Up to 15% of cats have this and most are asymptomatic with normal life expectancy
Basic complications of HCM in cats
~30% get complications
> Congestive heart failure
> Thromboembolic events
> Sudden cardiac death
What is the aetiology of HCM
Disease of the sarcomere
Familial in several breeds and some mutations identified e.g in myosin binding protein
e.g Maine coon, ragdoll, DSH
How do we diagnose HCM
Echocardiography showing left ventricular hypertrophy (wall thickness >6mm in diastole)
What does a HCM phenocopy look like and what are the most common ones
Thick walls; but not necessarily hypertrophy could be oedema or infiltration
What are the most common causes of HCM phenotype
First one is HCM
Then systemic hypertension and hyperthyroidism
What are the categories of causes of increased left ventricular thickness
- Myocardial hypertrophy: from aortic stenosis, hypertension, HCM, acromegaly, hyperthyroidism
Pseudohypertrophy due to dehydration
Accumulation of cells of fluid e.g TMT, lymphoma
At what blood pressures can we get significant changes to the heart
> 180mmHg
What condition are acromegalic cardiomyopathy cats frequently presented with
Diabetes mellitus
If thick ventricular walls normalise after IV fluid therapy what does this tell us
It was pseudohypertrophy due to dehydration
What tumour can cause thickened left ventricle and HCM phenotype
Cardiac lymphoma
What is transient myocardial thickening
Present with thick walls and in congestive heart failure
- There is reverse remodelling over time to revert to normal
Good prognosis so can stop treatment evnetually unlike heart failure
What is the key difference between HCM and TMT
Typically young cats
Reverts to normal over time
Classifcally there is an antecedent stressful event a couple of weeks before the presentation in heart failure
What are two proposed ideas for transient myocardial thickening in cats
Acute myocarditis; causing myocardial oedema and cellular infiltration which makes walls thick causing acute dysfunction
- Then inflammation resolves
Broken heart syndrome = where severely stressful event causes catecholamine surge
Murmur frequency in HCM cats
~50 have systolic murmur
Up to 70% have normal sounds
What is systolic anterior motion of mitral valve
Where the mitral valve is pushed towards the outflow tract in systole, against the interventricular septum which creates an obstruction to blood flow
So blood accelerates to go round leaflet giving a murmur
+ this holds valve open so get regurgitation into atria
Also more likely in HCM bcecause ventricle very thick, longer leaflets and hypercontractive ventricle
What is the most common cause of systolic anterior motion of mitral valve
HCM
What other than HCM can cause SAM
Hypovolaemia because the empt ventricle creates conditions that can drag the vlve
MV dysplasia
Subaortic stenosis
What is the classic pulmonary oedema lung pattern in dogs with congestive heart failure and how is it different in cats
Dogs show alveolar pattern in caudo-dorsal region
In cats no pattern is followed; so cannot exclude pulmonary oedema based on X ray distribution
What is restrictive cardiomyopathy
= the second most common cardiomyopathy in cats
= due to replacement fibrosis in the ventircular walls so they are normal thickeness but fibrosed
This means high pressure in ventricles, atrial dilation, restrictive LV filling pattern
What are the two phenotypes of restrictive cardiomyopathy
Myocardial form = where myocardium very fibrotic; normal wall thickness; very large atria
Endomyocardial form = where muscle/scar tissue bridge in the middle of the left ventricle
What is the aetiology of restrictive cardiomyopathy
Unclear could be congenital, could be just very late stage HCM where walls become thinner due to fibrosis
What is presentation of restrictive cardiomyopathy like and what must we be aware of
Middle age/older cats typically
Around half have systolic murmurs
Gallop rhythms or arrhythmias are more specific
NB: many cats have no abnormalities on auscultation
Characteristics of dilated cardiomyopathy in cats
Severe LV dilation and systolic dysfunction (BUT there are other phenocopies of this e.g late stage HCM, L to R shunt, tachycardia induced]
What has dilated cardiomyopathy classically been assocaited with in cats
Taurine deficiency
What are the characteristics of arrhythmogenic RV cardiomyopathy
Fibrous and fatty infiltration into the right ventricle
Causes severe dilation of RV, thin RV wall
Associated with malignant ventricular arrhythmias due to scar tissue blocking normal conduction
What does B1 vs B2 stage of feline cardiomyopathy mean
Both are subclinical
But B1 = low risk of complications
B2 = high risk
These complications = heart failure, thromboembolic disease
How does a cat with thromboembolic disease from left atrium embolising into aorta often present
Suddenly paraparetic on hind limbs
Cold, painful legs with no pulse, pale toe MMs
What does the appearance of smoke in the atrium on ultrasound mean
Blood is flowing slowly in the large atrium, allowing RBCs to aggregate and form mini thrombi
This means there is a high risk for thrombus formation and thromboembolic disease
What should we do at stage B2 feline cardiomyopathy
Start clopidogrel blood thinner to reduce thromboembolism risk
Ask owners to start taking resting respiratory rates to help detect going into heart failure
What do we do in stage C of feline cardiomyopathy
Congestive heart failurue treatment
Oxygen
Furosemide
What should we do if a thromboembolic event has occured (e.g HCM in cats)
Antithrombotics e.g unfractionated heparin, clopidogrel etc
Pain management because this is very painful
But do NOT remove thrombus or attempt to lyse it; instead stop growth and give body time to make collateral circulation
Risk factors for poorer prognosis in HCM
LA dilation
LA thormbus
Smoke on U/S
Survival time of asymtomatic HCM cats
Normal i.e >10 years
What things can cause a DCM phenotype in dogs
Hypothyroidism, hypoadrenocorticim
SIRS
Chronic volume overload e.g anaemia, high fluids
Chronic myocarditis
Taurine deficiency
Grain free/legume rich diets
Long term arrhythmias
What is arrhythmogenic right ventricular cardiomyopathy and what breeds are commonly affected
Myocardiac disease mostly affecting right ventricle with progressive loss of myocytes and replacement with fatty/fibrous tissue
Can affect electrical systmon most and present with arrythmias
Seen in boxers and bulldogs
Treatment of arrhythmogenic right ventircular cardiomyopathy
Sotalol = first line oral treatment to manage arrhythmias
If there is systolic function add in pimobendan
What are the three forms of ARVC presentation
Asymptomatic; but see VPCs on holter
Symptomatic; synvope with arryhtmias but normal systolic function
DCM phenotype and arrhythmias
