Heart murmur previously detected as an incidental finding.
Cough.
Breathlessness, especially at night.
Recent weight loss (even if still obese) .
Exercise intolerance.
Syncope.
Tussive syncope.
Inappetence.
Clinical signs
Heart murmur of mitral incompetence .
In early stages of the disease, duration and grade of murmur and extent of radiation roughly correspond with severity of mitral regurgitation. Murmur can be very localized; grade 1/6 and early systolic in very mild lesions and progress to high grade, widely radiating pansystolic harsh, plateau-shaped murmurs in severe disease.
In late disease, intensity of murmur may decrease due to decrease in left ventricular systolic pressure (reduced contractility) and raised left atrial pressure. These pressure changes reduce the pressure gradient between left atrium and ventricle thereby reducing the velocity of the regurgitant jet.
Signs of cardiac output are good until late in the disease:
Good color good with brisk capillary refill.
Good pulse.
Strong precordial impulse.
Loud heart sounds.
Good peripheral perfusion.
Signs of left-sided failure
Evidence of loss in condition.
Sinus arrhythmia abolished and increased heart rate (sinus tachycardia).
Tachypnea.
Adventitious respiratory sounds.
Dysrhythmias  : single or paroxysms of premature beats (supraventricular or occasionally ventricular), atrial fibrillation  , especially in large breeds.
Murmur may occasionally be very musical, high-pitched or squeaky - often reflecting mitral valve prolapse (grade of murmur does NOT correlate with severity of disease in this instance). Systolic clicks may also be associated with mitral valve prolapse.
Signs of myocardial failure
Large breed dogs almost always have myocardial failure at the time of onset of CHF.
Late in the course.
Heart murmur less loud; softer heart sounds.
Weak precordial impulse.
Variable pulse.
Diagnostic investigation
Radiography
Dorsoventral and lateral thoracic radiography  :
Left atrial and left ventricular enlargement  - progressive.
Method of choice in determining whether patient is in left-sided CHF.
Left atrial enlargement.
Pulmonary venous congestion .
Pulmonary infiltrate, predominantly perihilar, consistent with pulmonary edema.
2-D Echocardiography  
Mitral valve thickened, irregular and nodular . Both leaflets uniformly affected. Valve cusps may look normal in large breed dogs.
Left atrial and left ventricular enlargement due to left-sided volume overload.
Mitral valve prolapse is common.
Dilated pulmonary veins entering LA.
Visible gap between valve cusps.
M-mode echocardiography
Increased LA size - depends on severity.
Hyperkinetic left ventricle (increased fractional shortening and ejection fraction) in small breeds.
Mycocardial failure more common in large breed dogs with severe disease.
Increased LA:Ao ratio.
Increased EPSS.
Color flow and spectral Dopper echocardiography
Mitral regurgitation.
Electrocardiography
See ECG overview  :
Left atrial enlargement (wide, tall or notched p-wave).
Left ventricular enlargement (tall R-wave in lead II).
Documents any arrhythmia present - usually supraventricular premature complexes.
Atrial fibrillation   if severe, or in large breed dogs.
Biochemistry
With severe disease compromising cardiac output or if patients on high doses of diuretics, may have pre-renal azotemia  - increased urea  and creatinine .
Confirmation of diagnosis Discriminatory diagnostic features
Signalment: age, breed, sex.
Murmur consistent with mitral regurgitation.
Radiography.
Electrocardiography (insensitive indicator of chamber enlargement).
Definitive diagnostic features
2-D echocardiography.
Doppler echocardiography (color flow and spectral).
Gross autopsy findings
Mitral valve leaflets thickened, nodular, curled.
Chordae tendinae also affected, occasionally ruptured .
Valve obviously incompetent when closed.
Left atrial and left ventricular enlargement.
Eccentric hypertrophy of left ventricle.
If in left-sided CHF
Pulmonary congestion.
Pulmonary edema.
Histopathology findings
Myxomatous degeneration of mitral valve   .
Differential diagnosis
Other causes of cough :
Chronic airway disease.
Chronic bronchitis .
Tracheal collapse .
Bronchopneumonia .
Other causes of CHF, eg DCM  or endocarditis .
ACE inhibitors   not shown to delay or prevent onset of CHF if administered early in the course of disease.
Hydralazine  (an arteriodilator) has largely been superseded by the ACEI due to the sometimes profound hypotension caused by hydralazine. Hydralazine is occasionally useful in the treatment of severe acute onset pulmonary edema.
Strategy for treatment of early CHF
Vasodilation improves venous capacitance  diverts blood away from the cardiopulmonary circuit  helps control pulmonary edema.
Reduce the deleterious effects of activation of the rennin-angiotensin-aldosterone system.
Diuretics to reduce circulating volume thereby optimizing preload.
Positive inotropic agents to stimulate severely depressed myocardium.
Standard therapy for Class III and IV CHF due to mitral valve disease:
Diuretics
Frusemide  (2-4 mg/kg BID-TID PO). In class IV CHF can give <8 mg/kg IV for rapid diuresis.
Refractory cases may respond to the addition of another class of diuretic such as spironolactone  or thiazide    rather than increased doses of frusemide. AND
ACE inhibitor.
Pimobendan :
An inodilator:
Increases the sensitivity of the myofibrils to calcium  improvement in systolic (contractile) function.
Phosphodiesterase III inhibitor thereby causing vasodilation  afterload reduction.
Effect on survival time unclear.
Improves cerebral blood flow which often makes dogs appear more alert. The actions of ACE1 and pimobendan are complimentary. The timing of introducing pimobendan in this disease is controversial - many cardiologists do not introduce pimobendan until there are clear echocardiographic signs of systolic failure. However, this recommendations may change as the results of further studies are published.
And, if atrial fibrillation present:
Digoxin
Digoxin  dose based on body surface area (0.22 mg/m2).
Reduce dose if pre-renal azotemia or overt renal dysfunction, ascites, cachexia or low plasma protein levels.
Digoxin slows AV nodal conduction, hence slows ventricular response to atrial fibrillation; may act as a mild positive inotrope; may improve baroreceptor sensitivity and function; neurohormonal modulator for CHF.
In Cavalier King Charles Spaniel  , breeding from dogs and bitches with no heart murmur who are as old as possible (dogs should be over 5 years old) and who have parents with a late onset of murmur, has been shown in Sweden to be effective at reducing age of onset and severity of murmurs in progeny.
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Roudebush P, Allen T A, Kuehn N F, Magerkurth J H & Bowers T L (1994) The effect of combined therapy with captopril, furosemide and a sodium-restricted diet on serum electrolyte concentrations and renal function in normal dogs and dogs with congestive heart failure.J Vet Intern Med8 , 337-342. (Importance of monitoring electrolytes and renal function in patients in CHF.)
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Other sources of information
Smith P J, French A et al (2002) Long term efficacy and safety of pimobendan in slight-to-moderate heart failure caused by myxomatous mitral valve disease in dogs. VCS Proceedings, November 2002. Loughborough.
Lombard C W et al (2000) Clinical experience with pimobendan.VCS Proceedings,Spring meeting. Birmingham.
Kittleson M & Kienle R (1998) Myxomatous atrioventricular valve degeneration. In: Small Animal Cardiovascular Medicine. 1st edition. Eds: M Kittleson and R Kienle. Mosby, St Louis pp 297-318.