## 4 Discussion
Two randomized controlled trials, however, showed no significant change of LVM following RSD [25; 26], emphasizing inconsistencies in available data on LVM reduction following BP reduction. Therefore, our results of LVM reduction after RSD in RH patients are well consistent with previous observational studies, but have to be interpreted with caution considering the possibility of operator bias and a small study sample. The time-course of LVM changes, with significant reductions detectable at three months post RSD, are consistent with other settings such as Transcatheter Aortic Valve Implantation (TAVI) implantations, where abrupt changes of myocardial afterload occur in patients with often severe LVH. In patients post TAVI implantations, reductions in LVM have been documented three to six months after valve implantation [27; 28; 29]. The delay may indicate the time-course of myocardial reverse remodeling to take effect. Considering the prognostic importance of BP reduction in patients with RH and the unsolved problem of missing intra-procedural endpoints in RSD, a reliable indicator of RSD treatment success would be of enormous clinical value. In this context, biomarkers could be of additional value at least to indicate treatment success or failure at an early stage. [PERSON] and colleagues have shown promising data using intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) to predict RSD treatment success, showing that 8-12% of patients in their cohort were non-responders [30]. Generally, the results currently available on biomarkers in RSD show a certain disparity of data. Only a limited number of studies investigated the predictive value of biomarker candidates as potential indicators of a successful RSD procedure. Some studies showed a potential predictive value of soluble Fms-like thyroskininase-1 (sFLT-1), ICAM-1, VCAM, while other biomarkers, including Galectin-3, Copeptin, soluble vascular endothelial growth factor receptor 1 (sVEGFR-1), vascular endothelial growth factor -A/-C (VEGF-A/-C), nitric oxide (NO) and soluble vascular adhesion molecule 1 failed to predict BP lowering effects after RSD. sST-2 is a novel biomarker, which has been proven as very valuable for the prediction of clinical endpoints in acute and chronic cardiac conditions independent of classic cardiac biomarkers as Troponin-T. With regards to patients with high BP and RH, the gradual development from hypertension to LVH and further to hypertensive heart disease with diastolic heart failure corresponds to different serum levels of sST-2. Furthermore, sST-2 is an indicator of cardiac congestion. [PERSON] et al. showed in a cohort of 210 patients that the serum sST-2 levels differentiated between different stages of hypertensive heart disease [31]. The serum levels of sST-2 in patients with hypertensive heart failure were higher than in patients with hypertensive heart disease without heart failure, sensitivity and specificity, at 76.5% and 100%, respectively. Furthermore, within 133 patients with arterial hypertension, those with LVH had higher sST2 levels than those without LVH (23.8 \(\pm\) 8.33 ng/mL vs. 14.5 \(\pm\) 4.9 ng/mL, \(p\) < 0.001) [31]. In our cohort, compared to physiological levels described in the literature (the reference range of sST-2 was 5.7-53.5 \(\upmu\)g/L for men and 4.4-42.4 \(\upmu\)g/L for women) [32; 33], high sST-2 levels were observed at baseline. Consistent with observations regarding reverse remodeling of LVH, a steady decrease was observed that reached statistical significance at three months post intervention. Therefore, consistent with data from patients with hypertensive heart failure, the decrease in sST-2 might reflect a cardiac reverse remodeling process and following a reduction of cardiac afterload. This deduction is consistent with similar observations and a comparable timeframe of reverse ventricular remodeling in TAVI patients.