NAVLE Cardiovascular

Canine Valvular Heart Disease – NAVLE Study Guide

Valvular heart disease represents the most common category of acquired cardiovascular disease in dogs, accounting for approximately 75% of all canine heart disease cases.

Overview and Clinical Importance

Valvular heart disease represents the most common category of acquired cardiovascular disease in dogs, accounting for approximately 75% of all canine heart disease cases. The most prevalent form is myxomatous mitral valve disease (MMVD), also known as degenerative valve disease, endocardiosis, or chronic valvular heart disease. Understanding the pathophysiology, diagnosis, staging, and treatment is essential for NAVLE success.

Figure 1 - Canine heart anatomy diagram showing all four cardiac valves - mitral, tricuspid, aortic, and pulmonic - with labeled chambers.

High-Risk Breeds Clinical Notes
Cavalier King Charles Spaniel Highest prevalence; inherited trait; early onset; breeding restrictions recommended
Dachshund Inherited trait; mitral valve prolapse common
Miniature/Toy Poodle, Chihuahua, Maltese High prevalence in all small breeds; age-related

Myxomatous Mitral Valve Disease (MMVD)

Epidemiology and Breed Predisposition

MMVD is predominantly a disease of small to medium-sized dogs, with prevalence increasing markedly with age. Up to 85% of dogs in predisposed breeds show evidence of valve lesions by 13 years of age. The disease affects the mitral valve alone in approximately 60% of cases, both mitral and tricuspid in 30%, and tricuspid alone in less than 10%.

High-YieldOn the NAVLE, when you see a geriatric small-breed dog with a left apical systolic murmur, MMVD should be at the top of your differential list. The Cavalier King Charles Spaniel is the classic breed association.

Pathophysiology

The pathophysiology involves progressive myxomatous degeneration characterized by: expansion of extracellular matrix with glycosaminoglycans; valvular interstitial cell transformation to myofibroblast phenotype; attenuation of the collagen-laden fibrosa layer; and chordae tendineae changes with potential rupture.

Figure 2 - Gross pathology of myxomatous mitral valve showing thickened, nodular valve leaflets

Reference: Menciotti G, Borgarelli M. Review of Diagnostic and Therapeutic Approach to Canine Myxomatous Mitral Valve Disease. Vet Sci. 2017 Sep 26;4(4):47. doi: 10.3390/vetsci4040047. PMID: 29056705; PMCID: PMC5753627.

Hemodynamic Cascade

  • Systolic regurgitation from LV into LA creates volume overload
  • Compensatory LA and LV dilation (eccentric hypertrophy)
  • Increased LA pressure transmitted to pulmonary veins
  • Pulmonary venous congestion and pulmonary edema (left-sided CHF)
  • Secondary pulmonary hypertension may develop

Clinical Presentation

  • Murmur: Left apical systolic (holosystolic); intensity correlates with severity
  • PMI: Left 5th-6th intercostal space
  • CHF signs: Cough (nocturnal), tachypnea, dyspnea, exercise intolerance, syncope
High-YieldSleeping respiratory rate (SRR) monitoring is critical. Normal SRR is less than 30 breaths/min. SRR greater than 40 suggests CHF.
Stage Description Treatment
A At-risk breeds; no murmur No treatment; annual screening
B1 Murmur present; no cardiac remodeling; LA:Ao less than 1.6 and/or LVIDdN less than 1.7 No medication; monitor 6-12 months
B2 Asymptomatic with remodeling. ALL 4 criteria: Murmur ≥3/6, LA:Ao ≥1.6, LVIDdN ≥1.7, VHS greater than 10.5 Pimobendan 0.25-0.3 mg/kg PO q12h; dietary modification
C Current/past CHF signs; pulmonary edema Triple therapy: Furosemide + Pimobendan + ACE-I; add spironolactone
D Refractory CHF; furosemide greater than 8 mg/kg/day Increase diuretics; add torsemide/HCTZ; amlodipine; consider surgery

ACVIM Staging System for MMVD

The ACVIM consensus staging system (2019 update) guides diagnosis and treatment. This is essential knowledge for the NAVLE.

NAVLE TipThe EPIC study showed pimobendan at Stage B2 delays CHF onset by ~15 months and reduces cardiac death risk by one-third. This landmark study is frequently referenced!
Parameter B2 Criterion Notes
VHS Greater than 10.5 Greater than 11.5 = significant cardiomegaly (can substitute for echo)
VLAS ≥2.5 suggests LA enlargement Useful when echo unavailable; 87% specific for LA:Ao ≥1.6
LA:Ao Ratio ≥1.6 Right parasternal short-axis at AV level; early diastole
LVIDdN ≥1.7 Formula: LVIDd (cm) / BW (kg)^0.294

Diagnostic Evaluation

Key Parameters

Figure 3 - Echocardiographic LA:Ao measurement in right parasternal short-axis view. The method for measurement of left atrial to aortic root ratio (LA/Ao). (A) A LA/Ao obtained from a right parasternal short axis (LA/AoSx) by method 1 (see text). (B) A LA/Ao obtained from a right parasternal short axis (LA/AoSx) by method 2 (see text). (C and D) A LA/Ao obtained from a right parasternal long axis (LA/AoLx). For LA diameter (C), the measurement was made at end-systole 1 to 2 frames before the opening of the mitral valve leaflets. The measurement bisects the atrium extending from the mid-atrial septum in the near field to the bright pericardial echo of the LA lateral wall in the far field and is roughly parallel to the mitral annulus. For Ao diameter (D), the measurement of the aortic valve was made between the opened aortic valve leaflets in an early systolic frame when the Ao diameter is the greatest.

Reference: https://www.intechopen.com/chapters/71522 DOI: 10.5772/intechopen.91819

Treatment of MMVD

Pimobendan (Vetmedin)

An inodilator combining positive inotropic effects with vasodilation via calcium sensitization and PDE-III inhibition. Dose: 0.25-0.3 mg/kg PO every 12 hours. Give 1 hour before or 2 hours after food. Start at Stage B2 or C/D.

Stage C Triple Therapy

  • Furosemide: Loop diuretic; 2-4 mg/kg PO BID-TID maintenance
  • Pimobendan: 0.25-0.3 mg/kg PO q12h
  • ACE inhibitor: Enalapril/benazepril 0.5 mg/kg PO q12-24h
  • Spironolactone: 2 mg/kg PO q12-24h (quadruple therapy)
High-YieldDo NOT start beta-blockers in dogs actively showing CHF signs - this is a common exam pitfall!

Prognosis

  • Stage B1: Excellent; many never progress
  • Stage B2 with pimobendan: ~3.5 years to CHF
  • Stage C: Median 9-15 months survival
  • Stage D: 3-6 months survival

Congenital Valvular Diseases

Tricuspid Valve Dysplasia (TVD)

Congenital malformation causing tricuspid regurgitation and right heart volume overload. Labrador Retrievers have highest predisposition (heritable - chromosome 9). Presents with ascites, jugular distension, right-sided murmur. Treatment: medical management of right-sided CHF.

High-YieldYoung Labrador with ascites and right-sided systolic murmur = think TVD. Affected dogs should not be bred.

Pulmonic Stenosis (PS)

Third most common congenital defect. Breeds: English/French Bulldogs, Boston Terriers, Samoyeds, Labs. Type A (dome-shaped, fused leaflets) vs Type B (hypoplastic annulus in brachycephalics). Severity by gradient: less than 50 mmHg (mild), 50-80 mmHg (moderate), greater than 80 mmHg (severe - balloon valvuloplasty indicated).

Infective Endocarditis

Bacterial infection of heart valves (usually aortic/mitral). Predisposing factors: subaortic stenosis (most important), immunosuppression, chronic infections. Common organisms: Staph, Strep, E. coli, Bartonella. Clinical signs: fever, shifting leg lameness, new murmur, weight loss. Echocardiography shows vegetations. Treatment: prolonged IV antibiotics (6-8 weeks).

NAVLE TipAntimicrobial prophylaxis IS indicated for dogs with SAS undergoing procedures. It is NOT indicated for dogs with MMVD - they are not at increased IE risk!

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