Overview

• Congenital defect in which the interatrial septum fails to develop normally, resulting in communication between the atria. Unknown cause; genetic basis suspected. Acquired ASD secondary to atrial rupture reported in dogs with degenerative mitral valve disease.
• Comprises 0.7–3.7% of congenital heart defects in dogs and <10% of congenital heart defects in cats. Significantly higher incidence (37.7%) noted in a more recent study.
• 3 major types of ASD classified based on the location of the defect within the interatrial septum: ostium primum ASD (most apical portion of septum, adjacent to the atrioventricular valves), ostium secundum ASD (central portion of the septum, region of fossa ovalis), and sinus venosus ASD (upper portion of septum, junction of cranial vena cava).
• Secundum ASD with left-to-right shunting is most common (98.7% in one study of dogs and cats).
• Ostium primum ASDs typically large; may be component of atrioventricular (AV) canal defect.
• Sinus venosus ASDs typically located at the junction of the cranial vena cava (less commonly the caudal vena cava) and right atrium. Right pulmonary veins may be directed at the right atrium through the defect. May be associated with anomalous pulmonary venous connections of some or all pulmonary veins.
• Isolated ASDs typically shunt left-to-right. Magnitude of flow dependent on size (ostium) of defect, relative systemic and pulmonary resistance, and relative compliance of the ventricles. Small defects allowing atria to maintain normal differential pressure are termed restrictive. Large defects more likely to cause significant left-to-right shunting and volume overload to the right heart and pulmonary vessels. Development of secondary pulmonary hypertension can lead to reverse (right-to-left) shunting, termed Eisenmenger's physiology. ASDs may occur with concurrent defects; conditions increasing right atrial pressure (i.e., pulmonic stenosis, tricuspid valve dysplasia, tricuspid valve stenosis) can also cause balanced or reverse shunting.

Signalment

• Dog and cat
• Various breeds affected; higher prevalence in boxer and standard poodle
• No sex predisposition

Signs

CBC/Biochemistry/Urinalysis

• Typically normal.
• Polycythemia in some patients with right-to-left shunting.

Imaging

Other

General

• Long-term prognosis for small ASDs is good; treatment is not typically required.
• Large ASDs with hemodynamically significant shunting and right-sided enlargement warrant closure.

Medical Therapy

• Standard treatment of CHF (furosemide, pimobendan, ACE inhibitor).
• Treatment of polycythemia (right-to-left shunting) if clinically indicated.

Surgical Therapy

• Open heart surgery under cardiopulmonary bypass- direct surgical closure using patch graft.
• Pulmonary artery banding as palliative measure to limit left-to-right shunting.

Catheter-Based Therapy

• Amplatzer^® atrial septal occluder (ASO) device delivered percutaneously through the jugular vein for secundum-type defects; requires adequate atrial diameter, ostium diameter, ASD rim tissue, and vessel size for venous access.
• Hybrid procedure involving surgical access to right atrium, transatrial delivery of ASO device, and active device fixation under inflow occlusion reported.

Patient Monitoring

Recheck when decompensation or other clinical signs develop.

Expected Course and Prognosis

• Dependent on defect size and co-existing abnormalities.
• Small, isolated defects unlikely to cause clinical signs.
• Defects >12 mm more likely to cause heart failure.

Abbreviations

• ASD = atrial septal defect
• CHF = congestive heart failure