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• W2883803480 abstract "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.1 Accordingly, all new biomarkers should be compared with BNP and/or should be characterized by prognostic capability in selected HF populations. Soluble ST2 has recently been 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 peptides.2 Indeed, a prognostic role of ST2 has been suggested in low-risk populations,3 in patients with chronic,4 advanced, and acute2 HF. 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.5 The changes in ST2 in response to an acute haemodynamic event are presently unknown, and specifically it is unknown whether ST2 response to an acute haemodynamic 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 min maximal exercise, probably mirroring acute pulmonary haemodynamic worsening.6 We studied 30 (67 ± 10 years, 28 male) consecutive patients with chronic severe HF (left ventricular ejection fraction 29 ± 9%) who belonged to an HF population regularly followed at our HF unit. Inclusion criteria were peak oxygen uptake (VO2) <12 mL/kg/min, optimized HF therapy, stable clinical conditions, left ventricular ejection fraction (echocardiography) <45%, and capability to perform spirometry and lung diffusion test. The locally appointed ethics committee approved the research protocol (R115/14-CCM), and informed consent was obtained from all patients. Patients underwent a 10 min cycle-ergometer ramp cardiopulmonary exercise test 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 (Sensor Medics 2200, Yorba Linda, CA, USA). DLCO subcomponents, Vcap and DM, were calculated applying the Roughton and Forster method. Soluble ST2 levels were assessed using a highly sensitive sandwich monoclonal immunoassay (Presage® ST2 Assay, Critical Diagnostics, San Diego, CA, USA). BNP was measured using the chemiluminescent microparticle immunoassay on the Architect i2000 analyser (Abbott Diagnostics, Abbott Park, IL, USA). Data confirmed severe exercise limitation, since peak VO2 was 855 ± 224 mL/min, equivalent to 10.8 ± 1.6 mL/kg/min and to 45 ± 8% of the predicted value, VO2 at anaerobic threshold was 8.0 ± 1.4 mL/kg/min, and ventilation/carbon dioxide production relationship slope was 38 ± 10. DLCO, BNP and ST2 at rest and peak exercise are reported in Table 1. BNP (rest–peak +15 ± 16%, P < 0.05), but not ST2 (rest–peak 1 ± 12%), significantly increased at peak exercise, showing that a transitory haemodynamic impairment differently influences ST2 and BNP in severe HF patients. Several previous studies showed the prognostic value of ST2 additive to that of natriuretic peptides in HF patients.5 However, their response to major HF stimuli and/or the time frame of these responses are likely different, but this has not been previously shown. We used exercise as a model of acute haemodynamic stress. Indeed, exercise is associated with a fast and transient increase of pulmonary pressure and fluid, so that it is a live model of acute HF.6 For example, strenuous exercise after saline challenge induces acute pulmonary haemodynamic impairment in normal subjects,7 and, in HF patients, exercise has been associated with extravascular lung fluid increase, as shown by the reduction in alveolar capillary membrane diffusion.6 As a matter of fact, in severe HF patients, exercise is associated with a further transient BNP increase, which allows to directly link haemodynamic impairment, lung fluid increase and BNP increase.6 Indeed, although ST2 has a documented prognostic role in acute HF, it is a marker of myocardial fibrosis and remodelling. In other words, an increase of ST2 should parallel a chronic volume and pressure overload, but not an acute one. Differently, BNP increases in response to both acute and chronic haemodynamic impairment. In conclusion, using a simple but intriguing physiological research model, we showed that exercise-induced heamodynamic impairment is associated with a major increase in BNP but not in ST2, confirming that the causes and/or the time frame of their responses to acute and short-lasting pulmonary pressure increase are different. These results can be seen as the rationale for the additive prognostic role of BNP and ST2 in acute HF. Conflict of interest: none declared." @default.
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• W2883803480 date "2018-07-27" @default.
• W2883803480 modified "2023-10-17" @default.
• W2883803480 title "ST2 and B-type natriuretic peptide kinetics during exercise in severe heart failure" @default.
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• W2883803480 doi "https://doi.org/10.1002/ejhf.1246" @default.
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