Aortopulmonary Collaterals in Single-Ventricle Congenital Heart Disease

Abstract

Broadly defined, aortopulmonary collateral blood vessels (APCs) arise from the systemic arteries and supply blood to the pulmonary circulation. In the setting of acquired and congenital pulmonary and cardiac disease, the number and caliber of these vessels can increase and lead to a significant systemic-to-pulmonary shunt. APCs typically arise from the descending aorta, subclavian artery branches, and bronchial and intercostal arteries. Unlike normal bronchial arteries, they often supply flow to the terminal respiratory unit and do not necessarily travel in close proximity to the bronchial tree. Prominent APCs are associated with a variety of congenital heart diseases but are more prevalent with cyanotic lesions, particularly tetralogy of Fallot with pulmonary valve atresia. APCs are also commonly found in patients with single-ventricle heart disease, and their extent may fluctuate with successive surgical procedures.1–4 The impact and assessment of APCs in patients with a functionally single ventricle is the focus of the discussion that follows. Article see p 219 From a physiological standpoint, APCs may have both beneficial and adverse consequences. The principal advantageous effect of APCs is to improve systemic arterial oxygen saturation by increasing pulmonary blood flow leading to a higher “mixed” saturation in the ventricle. In addition, APCs may potentially inhibit the development of pulmonary arteriovenous malformations in patients with a bidirectional Glenn shunt by providing a route for hepatic venous blood to reach the lungs. Among the negative effects of APC flow is that it can compete with and limit the more effective, lower saturated blood flow to the lungs from the pulmonary arteries. Also of concern is that all APC flow returns to the single ventricle and thereby results in an additional volume load. Because these patients are at risk for the development of systolic and diastolic heart failure and atrioventricular valve regurgitation, any increased work …