## 1 Introduction  
Resistant hypertension (RH), commonly defined as blood pressure (BP) above a treatment goal despite intake of three antihypertensive drugs including a diuretic, is a major clinical burden, affecting 20 to 30% of patients with arterial hypertension [1]. Higher age and obesity are two of the strongest risk factors for uncontrolled hypertension, potentially leading to an increase in the incidence of RH in industrialized countries over time [1]. Re-establishing BP control represents an important goal to lower cardiovascular risk in RH patients.  
Chronic sympathetic overactivation has been identified as a driver of RH [1], with sympathetic nerve activation causing increased sodium reuptake, increased renin release,increased arteriolar vasoconstriction and reduced diuresis of the kidney. Interventional percutaneous renal sympathetic denervation (RSD) has been established as a promising interventional treatment approach [2]. Despite divergent results of the Simplicity HTN-3 trial [3], a series of new high-quality sham-controlled trials with favorable outcome have supported the therapeutic value of this procedure [4; 5; 6]. Furthermore, previous trials also revealed beneficial effects on cardiac reverse remodeling in RH [7]. Successful RSD was able to reverse cardiac hypertrophy and diastolic dysfunction, indicating that RSD has potential implications for cardiac function in hypertensive heart disease, which is a major health burden in this population.  
Novel devices for RSD are providing an operator-independent treatment pattern with multiple electrodes or circumferential ablation effects, resulting in a more predictable outcome of the procedure [4; 6]. Furthermore, adequate patient selection has been a very important lesson from previous trials. With respect to the lack of an intra-procedural success marker in RSD, reliable markers of treatment success or clinical benefit would be of great value to identify potential patients.  
The novel biomarker soluble suppression of tumorigenicity 2 (sST-2) shows promising results for risk stratification in cardiovascular patients. sST-2 belongs to the IL-1 receptor family. It has an influence on immunologic processes with subsequent cardioprotective effects including prevention of myocardial hypertrophy and fibrosis. This indicates a predictive potential in hypertensive heart disease [8]. ST-2 is a protein with two isoforms--a membrane-bound receptor form (ST-2L) and a soluble form (sST-2) secreted by cardiac myocytes exposed to stretch. Interleukin-33 (IL-33) has been identified as the functional ligand of ST-2L. Their interaction is required for the activation of the cellular cascade of events that protect the myocardium from hypertrophy and fibrosis by opposing the effects of angiotensin-II on myocytes. High levels of sST-2 have a detrimental effect due to its action as a decoy receptor by IL-33 neutralization, thus limiting its availability to bind to ST-2L [9]. Therefore, increased sST-2 levels seem to be a predictive indicator for left ventricular (LV) dysfunction. sST2 levels have been shown to be associated with increased systolic blood pressure and structural cardiac alteration including LV hypertrophy and diastolic dysfunction [10]. Therefore, elevated sST-2 levels may reflect hypertensive heart disease in RH and identify patients at risk who might benefit from more aggressive BP lowering interventions such as RSD. In order to investigate a potential application for sST-2 as a predictor of treatment success in RH patients undergoing RSD, serum levels of sST-2 at baseline and during follow up were correlated with clinical variables including arterial blood pressure levels and left ventricular mass (LVM) calculations obtained by echocardiography. We hypothesize sST-2 to reflect relevant clinical outcomes and predict potential success rates of RSD.