Quantification of systemic-to-pulmonary artery collateral flow: challenges and opportunities.

Abnormal vascular connections between systemic arteries and the pulmonary vascular bed—systemic-to-pulmonary collateral (SPC) vessels—manifest in patients with a variety of congenital and acquired heart disease. These vessels, which originate from branches off the brachiocephalic arteries, chest wall arteries, and the descending aorta, vary markedly in size, number, course, and distribution. Although the precise mechanisms that lead to development of SPCs are incompletely understood, hypoxemia, diminished global or regional pulmonary blood flow, and nonpulsatile flow in the pulmonary arteries are some of the commonly cited contributors.1 Indeed, SPCs are frequently encountered in patients with cardiac anomalies that include 1 of these abnormalities such as severe forms of tetralogy of Fallot and functional single ventricle (FSV). In the latter group, the clinical importance of SPCs and their optimal management have been topics of intense debate for 2 decades.2–6