Key result
Pulmonary vasodilators improve oxygen consumption at anaerobic threshold by ~1.1 mL/min/kg in Fontan patients.
Why the study?
The effect of pulmonary vasodilator therapy on exercise capacity and hemodynamic parameters in patients with Fontan circulation remains unclear.
Does pulmonary vasodilator therapy improve exercise capacity and hemodynamic parameters in patients with Fontan circulation?
Meta-Analysis (n=667)
Does pulmonary vasodilator therapy improve exercise capacity and hemodynamic parameters in patients with Fontan circulation?
This meta-analysis demonstrates that pulmonary vasodilator therapy significantly improves submaximal exercise capacity (VO2 AT and Ve/VCO2 slope) and invasive pulmonary hemodynamics in patients with Fontan circulation, though peak VO2 was not significantly changed.
Answers are grounded in this paper and cite their sources.
Supports consideration of pulmonary vasodilators to improve submaximal exercise capacity in Fontan patients; extends hemodynamic data to CPET parameters.
BACKGROUND AND OBJECTIVES: The effect of pulmonary vasodilator therapy on patients with Fontan circulation remains unclear. This study aims to assess its impact on exercise capacity and hemodynamic parameters in this population. METHODS: We searched PubMed, Embase, and the Cochrane Library for relevant studies up to November 2023. Pooled outcomes were used to evaluate the efficacy of pulmonary vasodilators in Fontan patients. RESULTS: A total of 18 studies with 667 patients were included. Exercise capacity was assessed in 14 studies (526 patients). Pulmonary vasodilator therapy improved oxygen consumption anaerobic threshold (VO₂AT; MD, 1.12 mL/min/kg; 95% CI, 0.35 to 1.89; p=0.004) and Ve/VCO₂ slope (MD, -1.14; 95% CI, -1.97 to -0.31; p=0.007) during exercise. No significant differences were found among drug classes regarding peak oxygen consumption, Ve/VCO₂, or VO₂AT. Invasive hemodynamics were evaluated in 6 studies (126 patients). Pulmonary vasodilators significantly reduced mean pulmonary arterial pressure (MD, -2.28 mmHg; p=0.02), pulmonary vascular resistance (MD, -0.91 WU*m²; p=0.01), and improved pulmonary flow (MD, 0.46 L/min/m²; p=0.02). CONCLUSIONS: Pulmonary vasodilator therapy appears beneficial for exercise capacity and pulmonary hemodynamics in Fontan patients. More randomized controlled trials are needed to confirm these findings.
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Cho et al. (2025) conducted a meta-analysis in Fontan circulation (n=667). Pulmonary vasodilator therapy (PDE5 inhibitors, ERAs, prostacyclin analogs) vs. Control group (in 8 RCTs) or pre-treatment baseline (in 10 non-randomized before-after studies) was evaluated on Oxygen consumption at anaerobic threshold (VO2AT) (MD 1.12 mL/min/kg, 95% CI 0.35 to 1.89, p=0.004). Pulmonary vasodilator therapy improved oxygen consumption at anaerobic threshold (MD 1.12 mL/min/kg; p=0.004) and Ve/VCO2 slope (MD -1.14; p=0.007) in Fontan patients.
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