JACC. Case reports · 2026
Managing High-Output Heart Failure Secondary to Prostacyclin Analog and Sotatercept Toxicity in Pulmonary Arterial Hypertension.
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Medina-Hernandez Danielle, Patel Priyesh A, Doshi Amar H, Gordley Connor M, Frank Theodore
Аннотация
BACKGROUND: We present a rare case of high-output heart failure (HF) resulting from prostacyclin analogue toxicity following the addition of sotatercept.
CASE SUMMARY: A 36-year-old woman with World Health Organization Group I pulmonary arterial hypertension (PAH), a history of suspected but hemodynamically unconfirmed heart failure with preserved ejection fraction and morbid obesity maintained on treprostinil and sildenafil therapy, developed progressive hypoxia, anasarca and dyspnea 3 months after sotatercept initiation. Serial right heart catheterizations demonstrated a shift from severe precapillary pulmonary hypertension to a high-output state with elevated biventricular filling pressures. The patient required intensive care unit admission for diuresis, vasopressors and continuous renal replacement therapy. Treprostinil discontinuation improved hemodynamics, followed by normalization after sotatercept discontinuation.
DISCUSSION: Severe obesity in association with synergistic vasodilatory effects from sotatercept and treprostinil therapy reduced systemic vascular resistance, increased cardiac output and raised biventricular filling pressures, culminating in high-output HF and unmasking occult diastolic dysfunction.
TAKE-HOME MESSAGE: High-output HF may occur with prostacyclin toxicity after sotatercept initiation, underscoring individualized careful hemodynamic assessment in complex patients with pulmonary arterial hypertension.
CASE SUMMARY: A 36-year-old woman with World Health Organization Group I pulmonary arterial hypertension (PAH), a history of suspected but hemodynamically unconfirmed heart failure with preserved ejection fraction and morbid obesity maintained on treprostinil and sildenafil therapy, developed progressive hypoxia, anasarca and dyspnea 3 months after sotatercept initiation. Serial right heart catheterizations demonstrated a shift from severe precapillary pulmonary hypertension to a high-output state with elevated biventricular filling pressures. The patient required intensive care unit admission for diuresis, vasopressors and continuous renal replacement therapy. Treprostinil discontinuation improved hemodynamics, followed by normalization after sotatercept discontinuation.
DISCUSSION: Severe obesity in association with synergistic vasodilatory effects from sotatercept and treprostinil therapy reduced systemic vascular resistance, increased cardiac output and raised biventricular filling pressures, culminating in high-output HF and unmasking occult diastolic dysfunction.
TAKE-HOME MESSAGE: High-output HF may occur with prostacyclin toxicity after sotatercept initiation, underscoring individualized careful hemodynamic assessment in complex patients with pulmonary arterial hypertension.