Sotatercept Blunts Ventilatory Drive to Carbon Dioxide with Improved Exertional Dyspnea in Pulmonary Arterial Hypertension

Patients with pulmonary arterial hypertension(PAH) have right heart failure with limited cardiac output(CO) reserve. This results in dead space, with ventilatory inefficiency characterized by inappropriate elevation in ventilation(V_E) relative to carbon dioxide production(VCO₂). Beyond dead space, patients with PAH also have augmented chemosensitive ventilatory drive to carbon dioxide (CO₂) driven in part by sympathetic overactivation, further exacerbating ventilatory inefficiency [1–3]. In contrast to vasodilators, sotatercept does not increase CO [4]. Despite this, exercise tolerance improves which we have demonstrated to be due to combined central, hematologic and peripheral benefits. The present secondary analysis was performed to evaluate effects on ventilatory response.