Atrial Septal Defect (ASD) Overview

Atrial Septal Defect (ASD)

• Description: An abnormal opening between the atria, allowing higher-pressure left atrial blood to flow into the lower-pressure right atrium. Three types exist:
  • Ostium primum: Opening at the lower septum, potentially associated with mitral valve issues.
  • Ostium secundum: Opening near the septum's center.
  • Sinus venosus: Opening near the superior vena cava/right atrium junction, possibly linked to partial anomalous pulmonary venous connection.
• Pathophysiology: Left atrial pressure exceeds right atrial pressure, causing high oxygenated blood flow into the right heart. The low pressure difference creates a high flow rate due to low pulmonary vascular resistance and right atrial distensibility. This right heart volume overload is usually well tolerated. Right atrial and ventricular enlargement is common but heart failure is infrequent initially. Pulmonary vascular changes are rare until later in life if uncorrected.
• Clinical Manifestations: Symptoms can be absent. Spontaneous closure is more common in younger patients and those with smaller defects. Heart failure is more likely in late diagnosis as pulmonary artery pressure builds up. A characteristic murmur is present. Risk of atrial dysrhythmias, pulmonary vascular issues, and later emboli formation.
• Surgical Closure: Patch closure (pericardial or Dacron) is for moderate to large defects, often before school age. Sinus venosus defects require patch placement redirecting anomalous pulmonary venous return to the left atrium. ASD 1 might need mitral valve repair/replacement.
• Transcatheter Closure: Common for ASD 2 closure with devices like Amplatzer septal occluders. Outpatient procedure for smaller, appropriately sized defects. Risk of reintervention might be higher with transcatheter closure compared to surgery. Aspirin for 6 months post-procedure.
• Prognosis: Excellent outcomes with both surgical and transcatheter closure. Data suggest possible similar or better procedural success rates with surgery.

Ventricular Septal Defect (VSD)

• Description: An abnormal opening between the ventricles, often classified as membranous (80%) or muscular. Size varies from small to complete absence of the septum. Frequently associated with other heart conditions like pulmonic stenosis, great vessel transposition, patent ductus arteriosus, atrial defects, and aortic coarctation. A significant portion (20-60%) spontaneously close. Spontaneous closure is most common in the first year of life in children with small to moderate defects.
• Pathophysiology: Higher left ventricular pressure leads to left-to-right blood flow into the pulmonary artery. Increased blood volume promotes pulmonary vascular resistance. Increased right ventricular pressure (due to shunting and resistance) causes muscular hypertrophy. Right atrium may also enlarge.
• Clinical Manifestations: Heart failure is common. Characteristic murmur is present.
• Surgical Treatment:
  • Palliative: Pulmonary artery banding to reduce pulmonary blood flow in infants with severe VSDs or complex anatomy. Complete repair is preferred when possible.
  • Complete Repair: Small defects are sutured; large ones use a Dacron patch. Cardiopulmonary bypass is utilized during both. Repair is often accessed through right atrium/tricuspid valve. Post-surgery, potential complications include residual VSD and conduction disturbances.
• Transcatheter Closure: Common for muscular, postoperative, or fenestrated VSDs. Device closure carries more risks than for ASDs, with a notable, but low, complication of complete atrioventricular block requiring pacemaker insertion.
• Prognosis: Risk varies on defect type, other associated conditions, and closure method. Single membranous defects have a lower mortality.