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Collaterals in congenital heart disease: when and how to treat?
Alexander Van De Bruaene1, Werner Budts1
1Congenital and Structural Cardiology, University Hospitals Leuven, and Department of Cardiovascular Sciences, Catholic University Leuven, Leuven, Belgium.
Insights
Collateral circulation in adults with congenital heart disease and heart failure can impact hemodynamics and oxygen levels. This article offers a practical guide for assessing these collaterals to aid clinical decisions.
Area of Science:
- Cardiology
- Vascular Biology
- Congenital Heart Disease
Background:
- Collateral circulation is common in patients with congenital heart defects, potentially affecting hemodynamics and causing systemic arterial desaturation.
- Therapeutic management of collaterals in adult congenital heart disease patients with heart failure is under-reported.
- Systemic venous anomalies, including collaterals, occur in 20-40% of patients post-Glenn or Fontan procedure.
Purpose of the Study:
- To provide a pragmatic approach for assessing collateral circulation in adult congenital heart disease patients experiencing heart failure.
- To offer a practical tool for clinical decision-making regarding the management of these collaterals.
- To highlight key types of collateral circulation: systemic venous-to-venous, systemic venous-to-pulmonary venous, and pulmonary arteriovenous malformations.
Main Methods:
- Review and synthesis of existing literature on collateral circulation in congenital heart disease and heart failure.
- Focus on hemodynamic principles and clinical implications of different collateral types.
- Discussion of potential etiological factors for collateral formation, including angiogenesis and embryological remnants.
Main Results:
- Collateral circulation can significantly alter cardiovascular hemodynamics and lead to systemic arterial desaturation.
- Potential causes of collateral formation include reduced effective pulmonary blood flow, increased oxygen demand, and pressure gradients between caval and atrial systems.
- Systemic venous anomalies are frequent, particularly after Glenn or Fontan procedures.
Conclusions:
- A systematic assessment of collateral circulation, considering hemodynamics and clinical impact, is crucial for managing heart failure in adults with congenital heart disease.
- Understanding the types and causes of collateral formation can guide therapeutic strategies.
- Further research is needed to elucidate the precise mechanisms of collateral development (angiogenesis vs. embryological channels).
Abstract:
The development of collateral circulation is not that rare in patients with congenital heart defects. These collaterals can affect cardiovascular hemodynamics and cause systemic arterial desaturation, which arises the question whether these should be closed. To date, few if any reports have been published on the therapeutic management of collaterals in adult patients with congenital heart disease in heart failure (HF). The focus of this article is to provide a pragmatic approach in the assessment of collateral circulation of the patient with HF. By considering the underlying hemodynamics and overall effects of the collateral circulation, we aim to provide a practical tool useful in clinical decision making. The paper highlights mainly the systemic venous to systemic venous collaterals, systemic venous to pulmonary venous (or pulmonary venous atrium) collaterals, and pulmonary arterio-venous malformations. Systemic venous anomalies are frequent and reported in 20% to 40% of patients who underwent Glenn or Fontan procedure. A reduction in effective pulmonary blood flow, coupled with increasing oxygen demands with growth, as well as a pressure difference between the higher pressure caval venous system and lower pressure atria (so called decompressing collaterals) are potential causes of collateral formation. Whether angiogenesis de novo or reappearance of embryological venous channels is responsible for collateral formation remains to be elucidated.
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