Abstract
Soluble ST2 (sST2) is upregulated in response to myocardial stress and may serve as biomarker in adults with pulmonary hypertension (PH). This prospective cohort study investigated sST2 levels and its association with echocardiographic and hemodynamic measures, and adverse clinical outcomes in adults with PH of different etiologies. sST2 was measured during the diagnostic right heart catheterization for PH, in adult patients enrolled between May 2012 and October 2016. PH due to left heart failure was excluded. The association between sST2 and a primary endpoint composed of death or lung transplantation and a secondary composite endpoint including death, lung transplantation or heart failure, was investigated using Cox regression with adjustment for NT-proBNP. In total 104 patients were included (median age was 59 years, 66% woman, 51% pulmonary arterial hypertension). Median sST2 was 28 [IQR 20–46] ng/mL. Higher sST2 was associated with worse right ventricular dysfunction and higher mean pulmonary and right atrial pressures. Median follow-up was 3.3 [IQR 2.3–4.6] years. The primary and secondary endpoint occurred in 33 (31.7%) and 43 (41.3%) patients, respectively. sST2 was significantly associated with both endpoints (HR per 2-fold higher value 1.53, 95%CI 1.12–2.07, p = 0.007 and 1.45, 95%CI 1.10–1.90, p = 0.008, respectively). However, after adjustment for NT-proBNP, both associations did not reach statistical significance. In conclusions, higher sST2 levels are associated with more severe PH and right ventricular dysfunction and yields prognostic value in adults with PH, although not independently of NT-proBNP.
Highlights
The soluble form of suppression of tumorigenicity-2 is a member of the interleukin-1 receptor family. sST2 is known for its release induced by myocardial strain and stress [1], and for its involvement in type 2 immune responses [2]
Of the 106 patients who were originally included in this cohort of adults with pulmonary hypertension (PH), sST2 was measured in 104 patients
REVIEWMedian sST2 level was 27.9 (IQR 19.6–44.9) ng/mL. sST2 levels according to the different subgroups of PH are shown in Figure 1. sST2 levels differed significantly between PH subgroups and we7reofth14e lowest in chronic thromboembolic pulmonary hypertension (CTEPH) patients
Summary
The soluble form of suppression of tumorigenicity-2 (sST2) is a member of the interleukin-1 receptor family. sST2 is known for its release induced by myocardial strain and stress [1], and for its involvement in type 2 immune responses [2]. Right ventricular dysfunction is one of the major problems in patients with pulmonary hypertension (PH). Elevated pulmonary arterial pressures caused by an increased pulmonary vascular resistance can lead to progressive right ventricular failure over time [5], contributing to a very poor prognosis in these patients [6,7]. A previous study showed that the circulating ligand of sST2, interleukin-33, may play a role in the vascular remodeling of the pulmonary endothelium in idiopathic pulmonary arterial hypertension (iPAH) [9]. Levels of sST2 have been correlated with right ventricular dysfunction in pulmonary arterial hypertension (PAH) patients [10]. As sST2 may reflect both cardiac as well as pulmonary vascular remodeling, sST2 could be a valuable biomarker to monitor deterioration in patients with PH
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