Congenital heart defects in dogs: symptoms and treatment

Overview

Congenital heart defects are estimated to affect fewer than 1% of dogs. A prevalence estimate of 0.13% has also been reported in crossbreeds. The frequency of individual defects varies geographically. Common defects include patent ductus arteriosus, pulmonic stenosis and aortic stenosis.

Openings can occur in the heart's dividing walls. Valves can have developmental abnormalities. The same dog may have several congenital defects. Their significance depends on type and effect on circulation. Congenital and inherited are not synonymous: heart disease appearing later can also be inherited.

Causes

Genetics and foetal development

An inherited predisposition is known or suspected for many defects. Environmental factors affecting foetal development may also contribute. Possible factors include infections and toxic substances. Maternal medication or nutritional deficiencies can also influence development. Several factors may act simultaneously.

Patent ductus arteriosus and septal defects

In patent ductus arteriosus, or PDA, the foetal connection between the aorta and pulmonary artery remains open after birth. In the foetus, this vessel directs blood past the not-yet-functioning lungs. After birth, the open connection usually carries blood from the aorta into the pulmonary artery. The pulmonary circulation and left heart consequently receive too much blood.

A ventricular septal defect, or VSD, is an opening between the ventricles. An atrial septal defect, or ASD, lies between the atria. A large left-to-right shunt can raise pulmonary artery pressure.

Narrowing and valve malformations

In pulmonic stenosis, or PS, blood outflow from the right ventricle is obstructed. Abnormal development or fusion of pulmonary valve leaflets is often responsible. The right ventricle must generate greater pressure than normal.

Aortic stenosis obstructs emptying of the left ventricle. The most common canine form is narrowing below the aortic valve, called subaortic stenosis or SAS. A fibrous ridge or ring forms beneath the valve. In valve dysplasia, structures develop abnormally and the valve may leak.

An abnormal vessel course

A persistent right aortic arch passes behind the oesophagus and trachea. It can form a vascular ring compressing the oesophagus near the heart.

Risk factors

Breed predisposition depends on the specific defect. SAS is more common in large dogs such as Boxers, Golden Retrievers, Rottweilers, German Shepherd Dogs and Newfoundlands. Breeds predisposed to PS include French Bulldogs, Bulldogs, Boxers and Beagles.

PDA occurs particularly in small breeds but also affects larger dogs. It is more common in females than males. However, sex predisposition differs between heart defects. Of 520 PDA patients, 16.2% were at least 24 months old at diagnosis.

Breeds predisposed to mitral dysplasia include Bull Terriers, German Shepherd Dogs and Great Danes.

Tricuspid valve dysplasia occurs particularly in Labrador Retrievers and German Shepherd Dogs.

Typical symptoms

A congenital heart defect may remain entirely symptom-free for a long time. PDA is often discovered during a routine examination of an apparently healthy puppy.

• A puppy grows or develops poorly.
• Your dog tires sooner than usual during exercise.
• Your dog faints, particularly with exertion.
• Breathing is laboured or your dog coughs.
• The abdomen may enlarge because of fluid accumulation.
• Your dog may be weak and reluctant to move.

With some right-to-left shunts, mucous membranes may look blue from insufficient oxygen. A murmur is the sound of abnormal blood flow heard through a stethoscope. Even severe stenosis may cause no symptoms before a serious arrhythmia.

Reversed PDA usually lacks the characteristic continuous murmur. A congenital vascular ring compressing the oesophagus can cause food regurgitation.

Complications and consequences

Heart failure and other complications

Stenosis can thicken the muscle wall of the ventricle working against it. Blood supply to this muscle may become inadequate. This can predispose to life-threatening ventricular arrhythmias and sudden death. SAS also increases the risk of bacterial aortic valve infection.

Untreated, significant PDA often leads to left-sided failure within the first 1–2 years. Left-sided failure can cause fluid accumulation in the lungs. Right-sided failure may cause abdominal or chest cavity fluid. Increasing pulmonary artery pressure can reverse shunt direction. A right-to-left shunt can increase red blood cell numbers.

Food regurgitated because of oesophageal compression can enter the airway and cause pneumonia.

Outlook varies by defect

A dog with a mild defect may have a normal lifespan. A small VSD generally does not affect welfare or lifespan. Severe valve dysplasia combined with heart failure can have a poor outlook. Early PDA closure before symptoms is associated with an excellent outlook.

In the 520-patient PDA study, estimated median total lifespan without another congenital defect was 12 years after closure and 2 years without closure. Other concurrent defects can worsen the outlook. Long-term prognosis for right-to-left PDA is guarded to poor.

Among 456 dogs undergoing PDA closure, 2.6% died within the first 3 days. Cardiac symptoms before closure are associated with a poorer long-term outlook. Severe mitral regurgitation within 24 hours after closure is also associated with shorter survival.

Diagnosis at the vet

A murmur is not a final diagnosis

Your vet listens to the heart and assesses circulatory findings. Murmur intensity, location and timing in the cardiac cycle help guide investigation. PDA usually causes a continuous, machinery-like murmur. Listening alone cannot always distinguish an innocent murmur from disease.

A puppy's physiological murmur may disappear by about 6 months. A loud, continuous or diastolic murmur needs further investigation. SAS can worsen during growth even if no murmur is audible in a young puppy. Excluding SAS may therefore require assessment at around 1 year too.

Ultrasound, ECG and chest X-rays

Ultrasound reveals cardiac structure, size and contraction. Doppler-measured flow velocity helps assess stenosis severity. Examination also looks for concurrent structural defects. Ultrasound helps determine whether monitoring is sufficient or intervention is needed.

X-rays assess heart size and possible lung fluid. An electrocardiogram, or ECG, assesses electrical activity and arrhythmias. Holter monitoring records rhythm for at least 24 hours. It can detect intermittent arrhythmias missed during a short appointment.

An aortic arch compressing the oesophagus is investigated with X-rays and CT if needed for surgical planning.

Treatment

Treatment follows anatomy and severity

Your vet chooses monitoring, medication or corrective intervention according to the defect's significance. A small septal opening with little circulatory effect generally needs no treatment. Mild aortic stenosis may also be monitored without medication. More severe stenosis or an arrhythmia may need cardiac medication. Medication for stenosis can reduce heart muscle oxygen demand and wall stress.

Closing a patent ductus arteriosus

Closure of a usual left-to-right PDA is generally recommended soon after diagnosis. A device introduced through a blood vessel can close it. Alternatively, the vessel can be tied off during chest surgery. Surgical closure may be more suitable than a catheter procedure for a small dog. Existing heart failure is treated before anaesthesia.

A right-to-left PDA is generally not closed because closure can worsen circulation. Treatment instead targets pulmonary artery pressure and excessive red blood cell numbers. Shunt direction is therefore established before planning intervention.

Balloon treatment of stenosis and other cardiac care

Balloon valvuloplasty can be performed for moderate or severe pulmonary valve stenosis. This is a minimally invasive way to widen the narrowed valve. An abnormal coronary artery course can change procedural safety and selection. Suspicion may require CT or coronary angiography.

SAS generally responds less well to conventional balloon dilation than pulmonary valve stenosis. Medication may include a beta-blocker and an antiarrhythmic if needed. Severe valve dysplasia and resulting failure are generally treated medically. In right-sided failure, abdominal fluid can be drained if needed.

A vascular ring compressing the oesophagus can be released surgically.

Follow-up after intervention

After catheter PDA closure, dogs often go home the next day. Any removable stitches are generally taken out after 7–10 days. Keep the wound and dressings clean and dry. Heart ultrasound is usually repeated 1–3 months after closure. Long-term monitoring is particularly needed if cardiac changes remain or your dog takes heart medication.

Enlarged heart structures may decrease in size during prolonged follow-up after PDA closure. Among 456 PDA patients, 2.4% needed another procedure to close a residual shunt.

Prevention

Dogs with inherited heart disease should not be used for breeding. Breeding decisions also consider relatives' cardiac health. In some breed health programmes requiring cardiac screening, the required report must be valid at mating.

In one official cardiac screening scheme, the usual minimum age for auscultation is 12 months. Breed-specific programmes within it may set a different limit. A comprehensive official congenital heart defect report can also be issued before 12 months.

Under this scheme, a report excluding congenital heart disease generally needs no renewal if issued at 12 months or older.

Important for dog owners

Record breathing changes, tiring and any fainting episodes. Agree an individual exercise plan if your dog has stenosis or exertional symptoms. Ask which structure is abnormal and how strongly it strains circulation.

Suspected disease is investigated in puppyhood: examination of a symptomatic puppy is not delayed because of a breeding report's age threshold. Under the scheme above, a congenital heart disease report issued before 12 months with a result of "Not detected" or "Inconclusive" is valid for 12 months. "Inconclusive" means follow-up is needed to resolve the assessment.

Frequently asked questions

Is a puppy's heart murmur always dangerous?

A puppy can have an innocent physiological murmur without a structural defect. It usually disappears by about 6 months. Listening alone cannot always distinguish an innocent sound from disease, so ultrasound is performed if needed.

Can a congenital defect be discovered only in adulthood?

A small defect may cause no symptoms and be found later. PDA has been diagnosed even in a 12.4-year-old dog. SAS can also worsen during growth, so a normal early listening examination does not definitively exclude it.

Can a congenital heart defect be cured?

For some defects, corrective intervention can remove the abnormality straining circulation. A usual PDA can be closed with a catheter device or surgery. Moderate or severe pulmonary valve stenosis can often be eased by balloon valvuloplasty, but the same treatment does not suit every defect.

Can a dog live normally with a heart defect?

A mild defect may remain symptom-free without shortening lifespan. A small VSD generally needs no treatment. Nevertheless, ultrasound findings determine the outlook according to type and severity, and a significant PDA should be closed early.

Can a dog be bred after heart defect treatment?

Breeding from dogs with inherited heart disease is not recommended. Inheritance is known or suspected in many congenital defects. Treatment success and breeding suitability are therefore assessed separately, considering the dog's results, disease within the breed and close relatives' health records.