Serum soluble ST2 and interleukin-33 levels in patients with pulmonary arterial hypertension.

Pulmonary arterial hypertension (PAH) is a rare disease characterized by a dramatic, progressive rise of pulmonary vascular resistance (PVR), leading to elevated pulmonary artery pressures, right ventricular (RV) overload, and, eventually, failure. Current evaluation of PAH is based on invasive hemodynamics (RHC), exercise capacity, echocardiography, and N-terminal pro brain natriuretic peptide (NT-proBNP) levels [1]; although published survival data support a strong clinical role for cardiac magnetic resonance imaging (CMR) of the RV, this technique is still underused [2]. Much research is currently focusing on the exploration of candidate soluble biomarkers of RV dysfunction and prognosis. Soluble ST2 (sST2) is a member of the interleukin 1-receptor family, which increases in response to acute and chronic cardiomyocyte strain [3]; its circulating levels rise in chronic and acutely decompensated heart failure, and the extent of their elevation seems to be especially related to the presence and severity of RV compromise [4,5]. The circulating ligand of sST2, interleukin 33 (IL-33), probably plays a role in several inflammatory states. The aimof the present studywas to assess peripheral serumlevels of sST2 and IL-33 in a group of patients with PAH of different etiology and severity compared with healthy controls, and to explore their possible relation with clinical features and with parameters of RV remodeling and failure as measured by CMR.