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Myxomatous Mitral Valve Disease - Coggle Diagram
Myxomatous Mitral Valve Disease
incidence and pathogenesis
most common heart disease of dogs (75% of heart disease cases seen in dogs)
affects left AV (mitral) valve and in 30% of cases the right AV (tricuspid) valve is also affected
more common in males than females
higher prevalence in smaller <20kg dogs
larger breeds sometimes are affected: faster disease progression with more apparent myocardial dysfunction and a more guarded prognosis
causes unknown, but inherited component in some breeds
changes in cellular constituents and intercellular matrix of the valve apparatus (including the valve leaflets and chordae tendinae)
changes involve the collagen content and alignment of the collagen fibrils within the valve
expansion of the spongiosa layer due to changes in the proteoglycan content of the layer
predictors of the rate of progression of MMVD and risk of impending heart failure
age
progressive heart enlargement of LA and ventricle
increased transmitral E wave blood flow velocities
increased serum N-terminal pro-B type natriuretic peptide (NT-proBNP) concentrations
increases in resting heart rate
staging system for MMVD
stage A
high risk for developing heart disease but no identifiable structural disorder of heart
every CKCS or other predisposed breed without a heart murmur
stage B
dogs with structural heart disease e.g. the typical murmur of mitral valve regurgitation accompanied by some typical valve pathology
no heart failure clinical signs
strong evidence to support initiating treatment in this stage
to delay the onset of clinical signs of heart failure
B1
asymptomatic dogs that have no radiographic or echo evidence of cardiac remodelling in response to their MMVD
B2
asymptomatic dogs which have more advance mitral valve regurgitation that is haemodynamically severe and long standing enough to cause radiographic and echocardiographic findings
left atrial and ventricular enlargement
stage C
current or past clinical signs of heart failure caused by MMVD
stage D
end stage MMVD in which clinical signs of heart failure are refractory to standard treatment
at some point efforts become futile without surgical repair of the valve
stage A
yearly auscultation
screening events by board-certified cardiologists participating in an ACVIM-approved disease registry.
no drug or dietary recommendations
do not breed from animal if murmur/echocardiographic evidence of mitral regurgitation is identified
stage B
recommendations for diagnosis
thoracic radiography
useful to obtain a baseline when patient asymptomatic
patients with MMVD often have concurrent tracheal or bronchial diseases
enhances ability to radiographically differentiate cardiac from non-cardiac causes of cough in face of future clinical signs
blood pressure
rule out concurrent systemic hypertension and establish baseline blood pressure
echocardiography
B1
asymptomatic dogs with mitral valve regurgitation caused by MMVD that is not severe enough to meet criteria for medical treatment
radiographically and echocardiographically normal left atrial and ventricular dimensions with normal LV systolic function and normal radiohtaphic vertebral heart score
recommendations for treatment
not recommended as heart failure is uncertain at this point
no drug or dietary treatment
re-evaluate by echo (or radio) in 6-12 months, depending on imaging results
stage B2
asymptomatic MMVD causing MR severe enough to result in cardiac remodelling (LA and LV enlargement)
likely to benefit substantially from treatment before onset of clinical signs of heart faulure
criteria
murmur intensity over 3/6
echocardiographic LA:Ao ratio in right sided short axis view in early diastole >1.6
left ventricular internal diameter in diastole, normalised for body weight (LVIDDN) >1.7
breed-adjusted radiographic VHS >10.5
treatment is a lifelong commitment
pimobendan 0.25-0.3mg/kg PO q12h
diet
mild dietary sodium restriction and provide a highly palatable diet with adequate protein and calories for maintaining optimal body condition
angiotensin converting enzyme inhibitors for patients in B2 on itial exam or if the LA has increased markedly in size on successive monitoring
no benefit of beta blockers or spironolactone at this stage
cough suppressants may be useful in some patients in advanced B2 when their cough is though to be result of pressure from cardiac enlargement (without pulmonary oedema) on adjacent bronchi
surgical intervention (mitral valve repair)
possible
Stage C
current or past clinical signs of heart failure
acute care of heart failure
regulating the patients haemodynamic status
tissue oxygen delivery
monitor and optimise patient's preload, after load, heart rate, contractility and oxygenation, whilst decreasing oxygen demand
goals
improve cardiac output
decrease mitral valve regurgitation
relieve clinical signs associated with either low cardiac output or excessively increased venous pressures (congestion) esp. pulmonary dysfunction
broad goals of chronic managment
maintaining haemodynamic improvements while providing additional treatments aimed at slowing the progression of disease, prolonging survival, decreasing the clinical signs of CHF, enhancing exercise capacity, maintaining body weight and improve quality of life
typical clinical presentation
clinical signs of left sided CHF
tachypnoea
restlessness
respiratory distress
cough
. As a group, dogs with clinical signs caused by heart failure have higher serum NT-proBNP concentrations than do dogs in which clinical signs are caused by primary pulmonary disease
A normal or near normal NT-proBNP concentration in a dog with clinical signs of cough, dyspnea, or exercise intolerance strongly suggests that heart failure is not the cause of the clinical signs.
Most symptomatic dogs with MMVD are middle-aged or older, and it is prudent to complete the clinical database with a blood pres- sure assessment, CBC, serum biochemical profile, and urinalysis, especially if treatment for CHF is anticipated.
acute hospital-based treatment
furosemide 2mg/kg IV/IM then hourly until respiratory signs are substantially improved or a total dosage of 8mg/kg reached over 4h
furosemide also may be adminis- tered as a constant rate infusion (CRI) at a dosage of 0.66-1 mg/kg/ hour after the initial bolus.
life threatening pulmonary oedema
signs
expectoration of froth associated with severe dyspnea
radiographic white-out lung
poor initial response to furosemide bolus with failure of respiratory effort and rate to improve over 2 hours
allow patient free access to water once diuresis begun
Pimobendan 0.25-0.3mg/kg PO q12h
oxygen supplementation
abdominal paracentesis, thoracocentesis
anxiety associated with dyspnoea --> sedation
butorphanol 0.2-0.25mg/kg IM or IV
buprenorphine (0.0075-0.01mg/kg) and acepromazine 0.01-0.03mg/kg IV, IM or SC
Sternal posture for sedated patients
dobutamine CRI
improve LV function
continuous ECG monitoring
reduce dose if tachycardia or ectopic beats occur
constant IV infusion of sodium nitroprusside
useful for life-threatening poorly responsive pulmonary oedema
ACEI e.g. enalapril or benazepril 0.5mg/kg PO q12h
for chronic stage C heart failure
Nitroglycerin ointment
approximately half an inch paste/10 kg BW, applied to an unhaired or shaved area of skin, can be used for the first 24 to 36 hours of hospitalization
chronic (home-based) treatment of stage C
PO furosemide to effect 2mg/kg q12h or as needed to maintain patient comfort
known causes of diuretic resistance
non-compliance
high sodium intake
slow absorption e.g. gut oedema
impaired secretion into the renal tubular lumen
chronic kidney disease
advanced age
concurrent NSAID use
hypoproteinaemia
hypotension
nephron remodelling
neurohormonal activation
add in torsemide if no longer adequately responsive to furosemide
diet
cardiac cachexia
loss of muscle or lean body mass associated with heart failure +/- clinically relevant accompanying weight loss
negative prognostic implications
easier to prevent than treat
maintain adequate calorie intake
60kcal/kg BW
improve appetite e.g.warm food, mix wet and dry food, variety of foods
BCS and weight regularly
ensure adequate protein intake
avoid low protein diets designed to treat chronic kidney disease unless severe concurrent renal failure is present
moderately restrict sodium intake
monitor for electrolyte imbalances e.g. hypokalaemia
stage D treatment
Sildenafil 1-2mg/kgPOq8h
Pimobendan dosage may be increased (off-label use) to include a third 0.3 mg/kg daily PO dose (ie, 0.3 mg/kg PO q8h)
Furosemide (or torsemide) dosage should be increased as needed to decrease the accumulation of pulmonary edema or body cavity effusions, if not limited by renal dysfunction (indicators of which generally should be monitored 12-48 hours after dosage increases). Inappetence may increase the risk of development of azotemia associated with medications for heart failure
digoxin
treatment of atrial fibrillation, including those in sinus rhythm
