Systemic-to-pulmonary collateral flow in patients with palliated univentricular heart physiology: measurement using cardiovascular magnetic resonance 4D velocity acquisition
- Equal contributors
1 Division of Imaging Sciences and Biomedical Engineering, King’s College London. NIHR Biomedical Research Centre at Guy’s & St Thomas’ NHS Foundation Trust, 4th Floor Lambeth Wing, St. Thomas Hospital, SE1 7EH, London, UK
2 Department of Congenital Heart Diseases, Evelina Children’s Hospital, Guy’s & St Thomas’ NHS Foundation Trust, Westminster Bridge Road, London, UK
3 Department of Congenital Heart Disease and Paediatric Cardiology, Deutsches Herzzentrum Berlin, Unit of Cardiovascular Imaging, Berlin, Germany
4 Radiology Department, Pontificia Universidad Católica de Chile, Santiago de Chile, Chile
5 Department of Pediatric Cardiology, Charité Universitaetsmedizin Berlin, Berlin, Germany
Journal of Cardiovascular Magnetic Resonance 2012, 14:25 doi:10.1186/1532-429X-14-25Published: 27 April 2012
Systemic-to-pulmonary collateral flow (SPCF) may constitute a risk factor for increased morbidity and mortality in patients with single-ventricle physiology (SV). However, clinical research is limited by the complexity of multi-vessel two-dimensional (2D) cardiovascular magnetic resonance (CMR) flow measurements. We sought to validate four-dimensional (4D) velocity acquisition sequence for concise quantification of SPCF and flow distribution in patients with SV.
29 patients with SV physiology prospectively underwent CMR (1.5 T) (n = 14 bidirectional cavopulmonary connection [BCPC], age 2.9 ± 1.3 years; and n = 15 Fontan, 14.4 ± 5.9 years) and 20 healthy volunteers (age, 28.7 ± 13.1 years) served as controls. A single whole-heart 4D velocity acquisition and five 2D flow acquisitions were performed in the aorta, superior/inferior caval veins, right/left pulmonary arteries to serve as gold-standard. The five 2D velocity acquisition measurements were compared with 4D velocity acquisition for validation of individual vessel flow quantification and time efficiency. The SPCF was calculated by evaluating the disparity between systemic (aortic minus caval vein flows) and pulmonary flows (arterial and venour return). The pulmonary right to left and the systemic lower to upper body flow distribution were also calculated.
The comparison between 4D velocity and 2D flow acquisitions showed good Bland-Altman agreement for all individual vessels (mean bias, 0.05±0.24 l/min/m2), calculated SPCF (−0.02±0.18 l/min/m2) and significantly shorter 4D velocity acquisition-time (12:34 min/17:28 min,p < 0.01). 4D velocity acquisition in patients versus controls revealed (1) good agreement between systemic versus pulmonary estimator for SPFC; (2) significant SPCF in patients (BCPC 0.79±0.45 l/min/m2; Fontan 0.62±0.82 l/min/m2) and not in controls (0.01 + 0.16 l/min/m2), (3) inverse relation of right/left pulmonary artery perfusion and right/left SPCF (Pearson = −0.47,p = 0.01) and (4) upper to lower body flow distribution trend related to the weight (r = 0.742, p < 0.001) similar to the controls.
4D velocity acquisition is reliable, operator-independent and more time-efficient than 2D flow acquisition to quantify SPCF. There is considerable SPCF in BCPC and Fontan patients. SPCF was more pronounced towards the respective lung with less pulmonary arterial flow suggesting more collateral flow where less anterograde branch pulmonary artery perfusion.