Mitral valve disease (MVD), also known as chronic valvular disease, endocardiosis, or degenerative mitral valve disease (DMVD), represents the most common acquired cardiac disorder in dogs and a significant cardiovascular condition in cats. This disease process is characterized by progressive myxomatous degeneration of the mitral valve apparatus, leading to mitral regurgitation and potential congestive heart failure.
Pathophysiology #
The mitral valve complex consists of the valve leaflets, annulus, chordae tendineae, papillary muscles, and the left atrial and ventricular myocardium. In MVD, progressive myxomatous degeneration occurs, characterized by:
- Valvular changes: Thickening, nodular irregularities, and loss of collagen organization in the valve leaflets
- Chordal changes: Elongation, thinning, and potential rupture of chordae tendineae
- Annular dilation: Progressive enlargement of the mitral annulus
These structural alterations result in incomplete leaflet coaptation during systole, allowing retrograde blood flow from the left ventricle into the left atrium (mitral regurgitation). The pathologic cascade that follows includes:
- Volume overload of the left atrium and left ventricle
- Eccentric hypertrophy of the left ventricle (remodeling)
- Left atrial enlargement
- Increased left atrial pressure
- Pulmonary venous congestion and edema (in advanced stages)
- Right-sided heart failure (in severe cases with pulmonary hypertension)
At the cellular level, myxomatous degeneration involves excessive production of glycosaminoglycans and proteoglycans, disorganization of collagen fibrils, and abnormal activation of valvular interstitial cells.
Epidemiology #
Incidence and Prevalence #
- Dogs: MVD accounts for approximately 75-80% of canine cardiac disease
- Age-related progression: ~10% of dogs aged 5-8 years, ~25% at age 9-12 years, and ~35-40% in dogs over 13 years
- Cats: Less common, representing 5-15% of feline cardiac disease
Breed Predisposition #
- Small breed dogs: Highest predisposition
- Cavalier King Charles Spaniels (CKCS): Particularly susceptible, with over 50% affected by age 5 and nearly 100% by age 10
- Other predisposed breeds: Dachshunds, Miniature and Toy Poodles, Chihuahuas, Yorkshire Terriers, Maltese, Pomeranians, Shih Tzus
- Medium-sized breeds: Less common but seen in Cocker Spaniels and Beagles
- Large breeds: Uncommon, although German Shepherds have a higher incidence than other large breeds
- Cats: No clear breed predisposition, though may be more common in domestic shorthair and Siamese cats
Sex Predisposition #
- Males are affected earlier and more severely than females (1.5:1 ratio)
Classification #
The American College of Veterinary Internal Medicine (ACVIM) classification scheme for MVD includes:
- Stage A: Patients at high risk for developing heart disease but without structural abnormalities (e.g., predisposed breeds without murmurs)
- Stage B: Patients with structural heart disease but without clinical signs
- B1: No cardiac enlargement
- B2: Significant left atrial and/or ventricular enlargement
- Stage C: Patients with past or current clinical signs of heart failure associated with structural heart disease
- Stage D: Patients with end-stage disease with clinical signs of heart failure that are refractory to standard therapy
Clinical Presentation #
- Stage B1: Soft systolic murmur (typically grade I-III/VI) heard best at the left apex; no radiographic or echocardiographic evidence of cardiac enlargement
- Stage B2: Louder murmur (typically grade III-VI/VI); radiographic and echocardiographic evidence of left atrial and ventricular enlargement; no clinical signs
- Stage C: Coughing, exercise intolerance, tachypnea, respiratory distress; radiographic evidence of pulmonary edema
- Stage D: Persistent clinical signs despite optimal medical therapy; severe respiratory distress, ascites (right-sided heart failure), weakness, syncope
Prognosis #
Prognosis varies significantly based on disease stage:
- Stage B1: Generally excellent, with many dogs remaining asymptomatic for years
- Stage B2: Median time to onset of congestive heart failure approximately 700-900 days
- Stage C: Median survival time 1-2 years with appropriate therapy
- Stage D: Poor prognosis, with median survival time typically less than 6 months
Negative prognostic indicators include:
- Left atrium to aorta ratio >2.0
- Severe left ventricular enlargement
- Pulmonary hypertension
- Chordal rupture
- Arrhythmias (particularly atrial fibrillation)
- Renal dysfunction
- High NT-proBNP levels
Medical Management #
Treatment recommendations by ACVIM classification:
Stage A #
- No medical therapy recommended
- Regular monitoring for murmur development
Stage B1 #
- No consensus on pharmacologic therapy
- Regular monitoring (every 6-12 months)
Stage B2 #
- Pimobendan (0.25-0.3 mg/kg PO BID) recommended to delay onset of congestive heart failure
- ACE inhibitors (enalapril 0.5 mg/kg PO BID or benazepril 0.25-0.5 mg/kg PO SID-BID) may be considered
- Regular monitoring (every 3-6 months)
Stage C #
- Furosemide (2-4 mg/kg PO BID-TID)
- Pimobendan (0.25-0.3 mg/kg PO BID)
- ACE inhibitor (enalapril 0.5 mg/kg PO BID or benazepril 0.25-0.5 mg/kg PO SID-BID)
- Spironolactone (1-2 mg/kg PO SID-BID) may be considered
- Dietary sodium restriction
- Activity restriction (moderate)
- Regular monitoring (every 1-3 months)
Stage D #
- Increased furosemide dosage (up to 4-6 mg/kg PO TID-QID)
- Addition of thiazide diuretic (hydrochlorothiazide 1-2 mg/kg PO BID)
- Consideration of torsemide as an alternative to furosemide
- Pimobendan at increased frequency (0.3 mg/kg PO TID)
- ACE inhibitor
- Spironolactone
- Sildenafil if pulmonary hypertension is present (1-2 mg/kg PO BID-TID)
- Severe dietary sodium restriction
- Significant activity restriction
- Frequent monitoring (every 2-4 weeks)
Anesthetic Management #
General Considerations #
- Thorough pre-anesthetic assessment including echocardiography and thoracic radiographs
- Minimize stress and anxiety
- Maintain adequate preload while avoiding volume overload. Iterative titration of fluid volume using small (1-2 mL/kg) boluses at 5-10 min intervals may be useful in patients that have comorbities or are on diuretic therapy.
- Support myocardial contractility with inotropes such as dobutamine. Addition of dopamine at low doses may improve vascular constriction further improving afterload and preload
- Avoid drugs with significant negative inotropic effects or that increase afterload such as alpha-2 agonists
- Monitor blood pressure, ECG, and oxygenation continuously
- Have emergency drugs readily available
Stage B1 Considerations #
- Standard anesthetic protocols usually well-tolerated with the caveat that alpha-2 agonists may significantly worsen regurgitation secondary to increased afterload
- Maintain normotension and avoid tachycardia
- Fluid therapy at maintenance rates (2.5-3 ml/kg/hr)
- Consider pre-oxygenation before induction
Stage B2 Considerations #
- Avoid alpha-2 agonists (dexmedetomidine, xylazine)
- Consider opioids for sedation
- Induction with propofol or alfaxalone is generally well tolerated
- Maintain with isoflurane or sevoflurane
- Cautious fluid administration (2-3 ml/kg/hr)continuous blood pressure monitoring
- Have inotropic support available (dobutamine, dopamine)
Stage C/D Considerations #
- Postpone elective procedures if possible. Referral or consultation with a Veterinary Anesthesiologist is recommended if anesthesia is required
Careful anesthetic planning and vigilant monitoring are essential for successful outcomes in patients with mitral valve disease, with management strategies tailored to the disease stage and individual patient factors.
