ST2 and B-type natriuretic peptide kinetics during exercise in severe heart failure
In chronic heart failure (HF), risk stratification is one of the most challenging issues, with a plethora of biomarkers available for this purpose. The key role is played by B-type natriuretic peptide (BNP) and/or its amino-terminal fragment NT-proBNP. Accordingly, all new biomarkers must be compared with BNP and/or must be characterized by prognostic capability in selected HF populations. Soluble ST2 has been recently introduced among the new biomarkers. The presence of high levels of ST2 is related to the severity of HF and to an increased risk of complications, such as arrhythmias, acute decompensation, and death, independently of natriuretic peptide. Indeed, a prognostic role of ST2 has been suggested in low-risk populations, in patients with chronic , advanced, and acute heart failure. Regardless, at present, the most defined role of ST2 is to provide a prognostic value additive to that of NT-proBNP within a multiparametric prognostic approach. The changes in ST2 in response to an acute hemodynamic event are presently unknown, and specifically it is unknown whether an ST2 response to an acute hemodynamic event has the same magnitude and time frame of that reported for BNP. Indeed, in patients with severe HF, BNP increases even during a 10-minute maximal exercise, probably mirroring acute pulmonary hemodynamic worsening. We studied 30 (67±10 years, 28M) consecutive patients with chronic severe HF. Patients underwent a 10-minute cycle-ergometer ramp cardiopulmonary exercise test (CPET) protocol. Immediately before exercise and at peak exercise, venous blood was sampled for BNP and ST2 determination. At the same time, lung diffusion (DLCO) and its two components membrane diffusion (DM) and capillary volume (Vcap) were measured. DLCO was measured by the single-breath constant expiratory flow technique. We showed, using a simple but intriguing physiological research model, that exercise-induced hemodynamic impairment is associated with a major increase of BNP but not of ST2, confirming that the causes and/or the time frame of their responses to acute and short-lasting pulmonary pressure increase are different.