Feline Congenital Cardiac Abnormalities Study Guide

Overview and Clinical Importance

Congenital heart disease (CHD) in cats is relatively uncommon, with a prevalence of approximately 0.1-0.2% of the feline population and accounting for about 8% of cats diagnosed with heart disease. Unlike acquired cardiomyopathies, these defects are present from birth and result from abnormal cardiac development during gestation.

The most common indication of CHD in kittens is detection of a heart murmur at the first vaccination visit. Understanding feline congenital cardiac abnormalities is essential for NAVLE success, as these conditions require accurate diagnosis and appropriate management decisions.

Prevalence of Feline Congenital Heart Defects

Patent Ductus Arteriosus (PDA)

Embryology and Pathophysiology

The ductus arteriosus is a normal fetal blood vessel derived from the sixth aortic arch that connects the pulmonary artery to the descending aorta. In utero, it allows blood to bypass the non-functioning fetal lungs by shunting blood from the pulmonary artery directly into the systemic circulation.

Normal closure: At birth, lung expansion causes a dramatic decrease in pulmonary vascular resistance. Combined with increased oxygen tension and decreased circulating prostaglandins, the ductal smooth muscle constricts. Functional closure occurs within hours of birth, with complete anatomic closure (forming the ligamentum arteriosum) by 2-4 weeks of age.

PDA pathophysiology: When the ductus fails to close, blood flows from the higher-pressure aorta to the lower-pressure pulmonary artery (left-to-right shunt). This causes pulmonary overcirculation, left atrial and ventricular volume overload, and eventually left-sided congestive heart failure if untreated.

Feline-Specific PDA Considerations

PDA presentation in cats differs significantly from dogs. Key differences include:

• Murmur character: Only 55% of cats with PDA have the classic continuous (machinery) murmur; 45% have only a systolic murmur
• Asymptomatic presentation: Approximately 70% of cats with PDA show no clinical signs at presentation
• Concurrent defects: Cats have a higher incidence of concurrent cardiac anomalies (up to 82% in some studies)
• Pulmonary hypertension: Higher prevalence compared to dogs; right-to-left shunting found in 17.5% of feline PDA cases

Clinical Signs and Physical Examination

Diagnostic Findings

Radiographic Findings

• Left atrial and left ventricular enlargement (left-to-right shunt)
• Pulmonary overcirculation (increased pulmonary vascularity)
• Ductal aneurysm or ductus diverticulum (bulge at aorta-ductus junction)
• Pulmonary edema if CHF present
• Reverse PDA: Normal or mildly enlarged right heart; normal pulmonary vasculature

Echocardiographic Findings

• Direct visualization of PDA between descending aorta and main pulmonary artery
• Color Doppler: Continuous turbulent flow in pulmonary artery
• Left atrial dilation (LA:Ao ratio greater than 1.5)
• Left ventricular volume overload with eccentric hypertrophy
• Bubble study: Agitated saline injection shows bubbles in descending aorta (confirms R-to-L shunt)

Treatment Options

Exam Focus: NEVER surgically correct a reverse (right-to-left) PDA! Surgery is contraindicated as it would remove the only route for blood to bypass the high pulmonary resistance and reach systemic circulation, causing acute right heart failure.

Ventricular Septal Defect (VSD)

Ventricular septal defect is the most common congenital cardiac defect in cats, accounting for 46-50% of feline CHD. It results from incomplete development of the interventricular septum, creating an abnormal communication between the left and right ventricles.

Classification by Location

Pathophysiology and Clinical Features

Restrictive VSD (small defect): Maintains pressure gradient between ventricles. Blood shunts L-to-R during systole. Creates loud (Grade III-V/VI) holosystolic murmur best heard right sternal border. Most cats have restrictive VSDs with good long-term prognosis.

Non-restrictive VSD (large defect): Equalizes ventricular pressures. Causes significant volume overload. Risk of Eisenmenger syndrome (pulmonary hypertension with shunt reversal) developing by 6 months of age in cats. Soft or absent murmur when pressures equalize.

Eisenmenger syndrome: Chronic L-to-R shunting causes pulmonary vascular changes and pulmonary hypertension. When pulmonary pressure exceeds systemic, shunt reverses to R-to-L causing cyanosis and polycythemia. This is irreversible and surgical closure is contraindicated.

Clinical Signs by VSD Size

Atrioventricular Valve Dysplasia

Atrioventricular valve dysplasia is one of the most common congenital cardiac abnormalities in cats. Both mitral valve dysplasia (MVD) and tricuspid valve dysplasia (TVD) involve malformation of valve leaflets, chordae tendineae, and/or papillary muscles, resulting in valvular regurgitation.

Breed Predispositions

• Mitral Valve Dysplasia: Sphynx cats, Maine Coons, Ragdolls
• Tricuspid Valve Dysplasia: Chartreux, Siamese cats

Clinical Features Comparison

Treatment

Treatment is medical management focused on controlling CHF symptoms:

• Diuretics: Furosemide (1-2 mg/kg PO q12-24h) for fluid removal
• Pimobendan: 0.25-0.3 mg/kg PO q12h (inodilator)
• ACE inhibitors: Enalapril or benazepril (0.25-0.5 mg/kg PO q12-24h)
• Antithrombotic therapy: Clopidogrel (18.75 mg/cat PO q24h) for ATE prevention
• Activity restriction: Limit exertion based on exercise tolerance

Outflow Tract Stenosis

Aortic Stenosis

Aortic stenosis (AS) causes obstruction to left ventricular outflow. In cats, subvalvular stenosis (fibrous ring below aortic valve) is most common, though valvular and supravalvular forms occur.

• Clinical signs: Exercise intolerance, syncope, sudden death
• Murmur: Systolic ejection murmur, left heart base (radiates to thoracic inlet)
• Echo findings: LV concentric hypertrophy, increased aortic flow velocity (greater than 2.0 m/s), subvalvular ring
• Treatment: Beta-blockers (atenolol); Surgery rarely performed in cats

Pulmonic Stenosis

Pulmonic stenosis (PS) is rare in cats as an isolated defect. It causes right ventricular outflow obstruction leading to RV pressure overload and concentric hypertrophy.

• Clinical signs: Often asymptomatic; Severe cases show exercise intolerance, syncope, right CHF
• Murmur: Systolic ejection murmur, left heart base
• Echo findings: RV hypertrophy, post-stenotic dilation of pulmonary artery, increased pulmonic flow velocity
• Treatment: Beta-blockers; Balloon valvuloplasty for severe cases

Tetralogy of Fallot

Tetralogy of Fallot (TOF) is the most common cyanotic congenital heart defect in cats, comprising approximately 6% of feline CHD. It results from a single conotruncal malformation during embryonic development.

Four Components

• Pulmonic stenosis - Valvular, subvalvular, or both (primary defect)
• Ventricular septal defect - Large, non-restrictive, subaortic
• Overriding (dextropositioned) aorta - Aorta positioned over the VSD
• Right ventricular hypertrophy - Secondary to PS (compensatory response)

Pathophysiology

The severity of clinical signs depends on the degree of pulmonic stenosis. Severe PS causes elevated RV pressure that exceeds LV pressure, resulting in right-to-left shunting of deoxygenated blood through the VSD into the systemic circulation. This causes:

• Systemic hypoxemia and cyanosis (blue mucous membranes)
• Secondary polycythemia (erythropoietin response to hypoxia)
• Hyperviscosity syndrome (sludging, thrombosis risk)

Pink TOF: In cases with mild PS, shunting may be predominantly L-to-R, resulting in an acyanotic presentation. These cats have better prognosis and may survive to adulthood.

Clinical Signs and Diagnosis

• Stunted growth, failure to thrive
• Cyanosis of mucous membranes (gums, tongue)
• Severe exercise intolerance, collapse with exertion
• Seizures (hyperviscosity, paradoxical emboli)
• Systolic murmur (from PS); May have palpable thrill
• Lab findings: Polycythemia (PCV often greater than 65%)
• Radiographs: Right-sided cardiomegaly, decreased pulmonary vascularity
• Echocardiography: All four defects visualized; R-to-L shunt on color Doppler

Treatment and Prognosis

Surgical correction is rarely attempted in cats due to high mortality. Management is palliative:

• Activity restriction: Strict indoor confinement, avoid stress/exertion
• Beta-blockers: Atenolol (6.25-12.5 mg/cat PO q12-24h) reduces oxygen demand
• Phlebotomy: Remove blood and replace with crystalloid if PCV greater than 65-70%
• Hydroxyurea: May reduce RBC production in severe polycythemia

Prognosis: Generally poor to grave. Most affected cats do not survive beyond 1-3 years without intervention. Pink TOF has better prognosis.

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