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Hypertension is highly prevalent and one of the most frequent chronic diseases worldwide.1 Prognoses for the next decades suggest that up to 50% of the adult population will be diagnosed as hypertensives using the standard guideline definitions of hypertension.1 Approximately 5–20% of all patients with high blood pressure are resistant to drug treatment,2 defined as blood pressure uncontrolled (>140/90 mm Hg; >130–139/80–85 mm Hg in patients with diabetes mellitus; >130/80 mm Hg in chronic kidney disease), despite the use of at least three antihypertensive agents of different classes, including a diuretic, at maximum or highest tolerated doses.3 Attention should be paid to differentiate between true resistance and pseudo-resistance, which is probably related to poor medication adherence, situational evoked blood pressure elevation (white coat hypertension), or suboptimal drug combination.4 In approximately 20% of all patients suffering from resistant hypertension, a secondary, potentially reversible cause can be found, which should be excluded systematically in all such individuals.2 ,4 Current non-invasive therapeutic strategies are mainly based on lifestyle interventions and pharmacological treatment.3 There is a mass of evidence indicating the profound effect of the sympathetic nervous system on all phenotypes of hypertension, which is consequently a relevant target for new therapeutic strategies.5 ,6 This article evaluates the treatment of resistant hypertension by catheter based renal sympathetic denervation.
Aetiology of resistant hypertension
The aetiology of resistant arterial hypertension is multifactorial. Relevant clinical features associated with uncontrolled hypertension are male sex, advanced age, obesity, high salt consumption, diabetes mellitus, chronic kidney disease, high systolic blood pressure (SBP), and left ventricular hypertrophy.2 Reasons for an inadequate reduction of blood pressure can be suboptimal combinations or underuse of antihypertensive drugs. Several drug interactions can contribute to increases of blood pressure or reduced effects of antihypertensive medications by sodium retention, extracellular volume expansion, and direct or indirect …
Contributors SE, CU, MB and FM have substantially contributed to the interpretation of data and drafting of the article. All authors have approved the final version of the manuscript to be published.
Competing interests In compliance with EBAC/EACCME guidelines, all authors participating in Education in Heart have disclosed potential conflicts of interest that might cause a bias in the article. The institution has received scientific support from Medtronic/Ardian. MB and FM were investigators of the Symplicity HTN1 and HTN 2 trials. CU, MB and FM have received speaker honorarium and consultancy from Medtronic/Ardian. CU, MB and FM are supported by Deutsche Forschungsgemeinschaft (KFO 196). SE and FM is supported by Deutsche Hochdruckliga.
Provenance and peer review Commissioned; internally peer reviewed.