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Systemic hypertension in the elderly
Published in Wilbert S. Aronow, Jerome L. Fleg, Michael W. Rich, Tresch and Aronow’s Cardiovascular Disease in the Elderly, 2019
Wilbert S. Aronow, William H. Frishman
The Symplicity HTN-3 study randomized 535 patients with treatment-resistant hypertension to renal sympathetic denervation using a Medtronic Symplicity catheter system or to a sham-control arm (148,149). At 6-month follow-up, the primary endpoint of the change in office systolic BP at 6 months was not significantly different between both treated groups (148). The 1-year follow-up data from this study support no further decrease in office or ambulatory BP (149).
Experimental perturbations to investigate cardiovascular physiology
Published in Neil Herring, David J. Paterson, Levick's Introduction to Cardiovascular Physiology, 2018
Neil Herring, David J. Paterson
Surgical training often makes use of animal models as an educational tool, but the development of new techniques and the implantation of novel prostheses and devices often occurs in animal models before implementation in man. In terms of cardiovascular physiology, several recent developments stand out in this regard as being developed initially in animal models. This includes renal sympathetic denervation (see Chapter 18.4). However, with percutaneous radiofrequency ablation within the renal artery in man, there is no operative end point to establish that it has been successful. In rodent animal models, the approach to denervation is often via a flank incision and lesioning performed on the epivascular surface of the renal arteries where the neural plexus resides. Electrical stimulation of the vessel distal to the lesions failing to produce a rise in blood pressure (BP) is then used as an end point for the procedure to ensure successful denervation. Other examples include stellectomy as a treatment for ventricular arrhythmias (see Chapter 5, Section 5.11), and carotid body denervation as a treatment for hypertension (see Chapter 18, Section 18.4). Implantation of a variety of neural stimulators targeting the cervical vagus nerve, thoracic spinal cord, dorsal root ganglia and deep brain nuclei has also been studied both in animal models and in man. How such stimulators interfere with reflex neural integration and how stimulators should be programmed in terms of frequency, intensity and pulse width to achieve therapeutic outcomes remains poorly understood.
Renal sympathetic denervation attenuates left ventricle hypertrophy in spontaneously hypertensive rats by suppressing the Raf/MEK/ERK signaling pathway
Published in Clinical and Experimental Hypertension, 2021
Bing Xiao, Fan Liu, Ye-Hui Jin, Ya-Qiong Jin, Li Wang, Jing-Chao Lu, Xiu-Chun Yang
Accumulating evidence has shown that hypertension is a kind of systemic disease caused by multiple risk factors, including genetic and environmental factors, or their interactions, having great associations with the high prevalence and mortality of cerebrovascular events (1,2). Left ventricle hypertrophy (LVH), one of the most important target organ damages in hypertension, has been well recognized as an independent risk factor for cardiovascular morbidity and fatality, and continuous myocardial hypertrophy may eventually result in heart failure, malignant arrhythmia or even sudden death (3,4). Thus, how to delay or even reverse the progression of LVH is a major issue in the research and development of new strategies for the prevention and treatment of myocardial diseases (5). Recent studies have indicated that renal sympathetic denervation (RSD) can efficiently decrease blood pressure (6,7). Mechanistically, RSD can specifically block the renal sympathetic nerves, i.e., the renal sympathetic afferent nerve-hypothalamus-renal sympathetic efferent nerve circuit decreases the activity of sympathetic nerves, thus decreasing blood pressure (8,9). In addition to the decrease in blood pressure, Krum H et al. also observed improved LVH and heart function after RSD (10). However, although the roles of RSD in decreasing blood pressure and suppressing sympathetic pressure have been clarified, the potential mechanism affecting LVH remains to be elucidated in further studies.
The randomised Oslo study of renal denervation vs. Antihypertensive drug adjustments: efficacy and safety through 7 years of follow-up
Published in Blood Pressure, 2021
Ola Undrum Bergland, Camilla Lund Søraas, Anne Cecilie K. Larstorp, Lene V. Halvorsen, Ulla Hjørnholm, Pavel Hoffman, Aud Høieggen, Fadl Elmula M. Fadl Elmula
Over the last decade, renal sympathetic denervation (RDN) has emerged as a treatment option for arterial hypertension, even showing promising results in patients who are seemingly treatment-resistant [1]. A few published trials showed promising results of RDN with modest blood pressure (BP)-lowering effect in selected individuals [2]. After the initial proof-of-concept studies Symplicity HTN-1 and HTN-2 sparked great interest in invasive treatment of hypertension, the sham-controlled Symplicity HTN-3 caused some controversy after it failed to demonstrate RDN superiority in reducing daytime ABPM 6 months after the procedure [3,4]. The more recent proof-of-concept-trials SPYRAL HTN-ON-MED and SPYRAL HTN OFF-MED showed promising results, however, with modest effect comparable to that achieved by a single antihypertensive drug [5–7]. As with all novel treatment methods, efficacy and safety of RDN need close follow-up in regard to any potential complications of both short- and long-term. A previously published meta-analysis revealed RDN as a safe procedure up to 6 months, while more recently published data from a large cohort suggests that the reduction in office- and ambulatory-BP is sustained up to 3 years without any deterioration in renal function [8–10]. Follow-up data on outcomes and safety beyond 3 years are lacking [11]. In this study, we aimed to describe long-term follow-up data of the participants in the randomised Oslo RDN study after 3 and 7 years to assess both efficacy and safety of renal denervation, providing additional knowledge of RDN compared to optimised drug treatment.
Effect of exercise and physical activity on blood pressure in adults with resistant hypertension: a protocol for a systematic review
Published in Physical Therapy Reviews, 2020
Suranga Dassanayake, Gisela Sole, Gerard Wilkins, Margot Skinner
RHT is defined as ‘blood pressure of a hypertensive patient which remains above the goal despite the concurrent use of three different classes of antihypertensive agents administered in maximum or maximally tolerated doses and appropriate frequency or achieve target blood pressure levels by ≥4 antihypertensive agents’ (page e511) and (page e54) [5, 8]. The main section of the definition first published in the Scientific Statement of the American Heart Association (AHA), in 2008 (page e511) has remained unchanged in the updated definition in the 2018 Scientific Statement of the AHA (page e54). The new definition specifically now also includes the antihypertensive agents, long acting calcium channel blockers (CCB), angiotensin converting enzyme [ACE] inhibitor or angiotensin receptor blocker [ARB] and diuretics, all of which are commonly used for the current management of HT [8]. RHT has a higher risk of end organ damage, (damage in heart, brain, kidneys and eyes, the major organs which are supplied by the circulatory system), cardiovascular disease (CVD) risk and mortality compared to HT [9, 18, 19]. The most widely used treatment for RHT is antihypertensive medications, but noncompliance has been identified as one of the main causes of treatment resistance [8, 20]. An alternative management approach, a surgical procedure involving renal sympathetic denervation, has been found to have limited success [21, 22].