## 4 Discussion  
Hypertensive heart disease, characterized by structural alterations like atrial enlargement, left ventricular hypertrophy (LVH) and functional abnormalities like diastolic dysfunction, is a key feature of organ damage in longstanding RH. The presence of LVH is associated with cardiovascular endpoints [12] and an increase in cardiovascular risk independent of in-office or out-of-office BP [13]. Conversely, successful BP reduction in hypertension is associated with a regression of LVH, whereas large meta-analyses have shown this effect to vary significantly between antihypertensive drug regimens [14,15]. Furthermore, if left ventricular reverse remodeling with a reduction in LVM can be achieved in the course of antihypertensive treatment, this is also associated with a reduction in cardiovascular endpoints [12]. With regards to RSD, a multitude of sham controlled clinical trials have been conducted to underscore the potential of RSD to improve blood pressure control in hypertensive patients. These include different technical approaches with second-generation catheters, allowing multisite ablations within the renal arteries using radiofrequency energy [4,5], intravascular ultrasound [6,16] and other techniques [17]. Consistent with these results, our study cohort showed a consistent reduction in mean office systolic BP, reaching  
Figure 4: Pearson’s correlation of baseline SST-2 (SST2) with SBP three months after RSD revealed no significant correlation. Figure 3: Pearson’s correlation of baseline sST-2 levels with SBP one month after RSD revealed a significant correlation. ** marks statistical significance. the level of statistical significance at three months. According to the 2018 ESC guidelines for management of arterial hypertension [18], only patients with RH had been selected for RSD treatment within the study, which results in a somewhat selective patient cohort. Consistent with previous studies on RSD, higher initial SBP and DBP values were associated with a better therapy response. Similar effects were observed in patients undergoing renal angioplasty [19] and conventional antihypertensive drug treatment [20]. In most previous or ongoing renal denervation studies, the presence of RH with a systolic blood pressure of 160 mmHg or more despite the administration of three or more antihypertensive drugs including a diuretic was required as an inclusion criteria. Due to the small sample size in our cohort, the trend towards DBP reduction did not reach the level of statistical significance. Given the current evidence supporting the fundamental role of LVH for cardiovascular risk in patients with RH, expectations were high that RSD might also be able to achieve LVH regression on top of improved BP control. Several clinical trials have detected a relevant reduction of the LVM post RSD using TTE [7] and magnetic resonance imaging [21]. [PERSON] et al. reported a reduction in the LVM index at six months, showing that the effect of LVH regression was independent of BP reduction [22]. Due to the heterogeneity of trials, meta-analyses may add more reliable data for a prediction of the potential effect of RSD on LVH [23; 24]. [PERSON] et al. analyzed 14 observational studies (11 uncontrolled, 3 controlled) and 2 randomized controlled trials investigating LV structural changes after RSD with different follow-up intervals [24]. The authors found that observational studies using TTE reported an average reduction in the LVM index of \(-13.88\) g/m\({}^{2}\) (the 95% confidence interval CI ranging from \(-19.94\) to \(-7.82\) g/m\({}^{2}\)) at 6 months and \(-16.67\) g/m\({}^{2}\) at 12 months (95% CI \(-25.38\) to \(-7.97\) g/m\({}^{2}\)). In trials using MRI, the effect was smaller, with a mean LVM index reduction of \(-5.18\)g/m\({}^{2}\) at 6 months and \(-3.00\) g/m\({}^{2}\) (95% CI \(-11.38\) to \(5.38\) g/m\({}^{2}\)) at 12 months.