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Clinical Variables Associated with Pre-Fontan Aortopulmonary Collateral Burden
David E Segar1,2, Amy Y Pan2,3, Daniel I McLennan1,2
1Division of Cardiology, Department of Pediatrics, Herma Heart Institute, Medical College of Wisconsin, Children's Wisconsin, 9000 West Wisconsin Avenue, Milwaukee, WI, 53226, USA.
Aortopulmonary collaterals (APCs) are universally increased in single ventricle congenital heart disease (CHD) patients with Glenn circulation. Smaller pulmonary artery size is linked to higher APC burden, though other factors likely contribute.
Area of Science:
- Cardiology
- Pediatric Cardiology
- Congenital Heart Disease Research
Background:
- Aortopulmonary collaterals (APCs) are common in single ventricle congenital heart disease (CHD).
- The degree of APC development varies significantly among patients.
- Understanding factors influencing APC burden is crucial for managing single ventricle physiology.
Purpose of the Study:
- To investigate the association between APC burden and non-invasive clinical variables in patients with single ventricle CHD.
- To identify predictors of increased APC flow in patients with Glenn circulation.
Main Methods:
- Retrospective single-center study of 29 patients with single ventricle CHD and prior Glenn palliation.
- Cardiac magnetic resonance (CMR) imaging used to quantify APC flow (normalized to aortic and pulmonary vein flow).
- Univariate, multivariable, and Classification and Regression Tree (CART) analyses performed.
Main Results:
- All patients exhibited increased APC flow, with significant variability (APC/QAo range: 11.9-44.4%).
- Pulmonary artery size (Nakata index) was the sole variable associated with APC flow on multivariable analysis (p < 0.020).
- CART analysis identified smaller pulmonary artery size as the most significant factor inversely related to APC burden.
Conclusions:
- APC flow is universally elevated but highly variable in single ventricle CHD with Glenn circulation.
- Reduced pulmonary artery size is a key predictor of increased APC burden.
- APC pathogenesis is likely multifactorial, necessitating further research into contributing factors.
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