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Impact of Atrial Fibrillation on Fontan Circulation: Fontan Computational Model
Koichi Sughimoto1, Tetsuya Ueda2, Takashi Fujiwara3
1Department of Cardiovascular Surgery, Chiba Kaihin Municipal Hospital, Chiba, Japan; Graduate School of Engineering, Chiba University, Chiba, Japan.
Insights
Atrial fibrillation significantly reduces cardiac output in Fontan circulation. Dobutamine offers limited hemodynamic improvement, particularly during atrial fibrillation, underscoring the importance of maintaining sinus rhythm in these patients.
Area of Science:
- Cardiology
- Pediatric Cardiology
- Computational Biology
Background:
- Patients with Fontan circulation are susceptible to heart failure and atrial fibrillation.
- The hemodynamic effects of inotropic agents like dobutamine in Fontan circulation, especially with atrial fibrillation, are not well understood.
Purpose of the Study:
- To investigate the efficacy of dobutamine therapy in improving hemodynamics in Fontan circulation models with and without atrial fibrillation.
Main Methods:
- Utilized lumped computational models simulating biventricular, atriopulmonary connection, and extracardiac total cavopulmonary connection Fontan circulations.
- Introduced atrial fibrillation conditions including irregular ventricular contraction and time-varying elastance.
- Administered varying doses of dobutamine by adjusting ventricular elastance, heart rate, and peripheral resistance.
Main Results:
- Atrial fibrillation reduced cardiac output by 22.5%–25.8% across all models.
- Dobutamine (10 μg·kg⁻¹·min⁻¹) increased cardiac output by 32.3% in biventricular models but only 9.1%–9.2% in Fontan models under sinus rhythm.
- In atrial fibrillation, dobutamine's effect on cardiac output was significantly blunted in Fontan circulations (11.8%–11.9% increase) compared to biventricular models (32.3% increase).
Conclusions:
- Atrial fibrillation markedly decreases cardiac output in Fontan circulation, with dobutamine showing limited benefit.
- Maintaining sinus rhythm is crucial for optimizing cardiac function in patients with Fontan circulation.
Background:
Patients with Fontan circulation may have heart failure resulting in atrial fibrillation during the late phase. Inotropic effects to ameliorate hemodynamics on the Fontan circulation are not well understood, especially when in atrial fibrillation. This study was performed to determine whether dobutamine therapy in patients with Fontan circulation has limited effects on improving hemodynamics.
Methods:
Lumped computational models (sinus and atrial fibrillation) were used, including biventricular, atriopulmonary connection, and extracardiac total cavopulmonary connection Fontan models. The condition of atrial fibrillation including lack of atrial beat, irregular ventricular contraction, and time-varying elastance for the ventricle was introduced. A different dose of dobutamine was given by varying the elastance of the ventricle, heart rate, and peripheral resistance.
Results:
In all models, the cardiac output decreased by 22.5% to 25.8% in atrial fibrillation. At 10 μg · kg-1 · min-1 dobutamine in sinus rhythm, the cardiac output increased by 32.3% in the biventricular model but by only 9.2% (P < .001) and 9.1% (P < .001) in the atriopulmonary connection and total cavopulmonary connection Fontan models, respectively. At 10 μg · kg-1 · min-1 dobutamine in atrial fibrillation, the percent increase in the cardiac output in the Fontan circulation (11.8% increase in atriopulmonary connection, P < .001; and 11.9% increase in total cavopulmonary connection, P < .001) was significantly less than that in the biventricular circulation (32.3% increase).
Conclusions:
In the Fontan circulation, atrial fibrillation itself reduced the cardiac output by approximately 25%, and dobutamine had a limited effect on increasing the cardiac output, especially when in atrial fibrillation. Maintaining sinus rhythm in patients with Fontan circulation is very important.

