Baroreflex activation therapy in hypertension

Gassler, John P.; Bisognano, John D.

doi:10.1038/jhh.2013.139

Cited by 32 publications

(23 citation statements)

References 18 publications

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“…118 When the pacing generator source is turned on, blood pressure markedly declines over a few seconds. 119 As with renal denervation, initial studies in patients with resistant hypertension were very promising, 120 but the Pivotal Trial failed to meet all the primary efficacy end points.…”

Section: Baroreflex Activation Therapymentioning

confidence: 99%

Management of hypertension in chronic kidney disease

Townsend

Taler

2015

Nat Rev Nephrol

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Hypertension is a common comorbidity in patients with impaired kidney function. The kidney exerts a marked degree of control over blood pressure through various mechanisms, such as by regulating sodium balance and hormone secretion through the activity of the renin-angiotensin system. The kidney is susceptible to injury, and if already damaged can be at risk of further loss of function as a consequence of elevated blood pressure. Once elevated blood pressure is identified, a combination of sensible lifestyle measures, such as sodium restriction and weight loss, with pharmacological intervention to reduce blood pressure will usually achieve blood pressure goals. In this Review, we outline the importance of blood pressure control for patients with chronic kidney disease (CKD), the mechanisms that affect blood pressure control, and the basis for non-drug and drug therapies. We further discuss the rationale for <140 mmHg systolic and <90 mmHg diastolic targets for blood pressure in patients with CKD, with consideration for tighter targets in the setting of proteinuria.

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Section: Baroreflex Activation Therapymentioning

confidence: 99%

Management of hypertension in chronic kidney disease

Townsend

Taler

2015

Nat Rev Nephrol

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“…However, the acute efficacy criterion was not met, since the proportion of patients with a reduction in SBP of at least 10 mmHg at six months was only 8 % greater in the group receiving BAT from the beginning as compared to the group with device implantation but without immediate BAT. The failure to meet the prespecified acute efficacy endpoint was apparently primarily due to a larger and more variable reduction than expected in SBP at six months in the group with inactive implants, and likely reflected the less-than-optimal trial design [4•, 7]. Notwithstanding the issues related to trial design, the results of the Rheos Pivotal Trial further underscored the promise of BAT for the treatment of resistant hypertension, as both the immediate and delayed treatment groups had 12-month BAT-induced reductions in SBP of more than 30 mmHg, with 50 % of patients achieving SBP of less than 140 mmHg.…”

Section: Clinical Trials Of Bat In Resistant Hypertensionmentioning

confidence: 99%

“…The most prevalent serious adverse events (SAE) were either transient or permanent nerve injury. Unfortunately, the failure to achieve this endpoint may have implied not that procedural complications were too frequent, but that the target set for the procedure was overly optimistic [4•, 7]. Indeed, the SAE profile compares favorably with the results from endarterectomy trials involving intervention in the anatomical region.…”

Section: Clinical Trials Of Bat In Resistant Hypertensionmentioning

confidence: 99%

“…In this review, we will briefly discuss the clinical trials using the prototype Rheos system and the second-generation Barostim neo to deliver BAT in patients with resistant hypertension. A more extensive discussion of these clinical trials has been published by others [3, 4•, 5–7]. The primary focus of this review is on the clinical findings and experimental animal studies that have provided insight into the mechanisms that account for the physiological effects of BAT and the relevance of these mechanisms to hypertension therapy.…”

Section: Introductionmentioning

confidence: 99%

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Baroreflex Activation: from Mechanisms to Therapy for Cardiovascular Disease

2014

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Recent technical advances have led to the development of a medical device that can reliably activate the carotid baroreflex with an acceptable degree of safety. Because activation of the sympathetic nervous system plays an important role in the pathogenesis of hypertension and heart failure, the unique ability of this device to chronically suppress central sympathetic outflow in a controlled manner suggests potential value in the treatment of these conditions. This notion is supported by both clinical and experimental animal studies, and the major aim of this article is to elucidate the physiological mechanisms that account for the favorable effects of baroreflex activation therapy in patients with resistant hyper-tension and heart failure. Illumination of the neurohormonal, renal, and cardiac actions of baroreflex activation is likely to provide the means for better identification of those patients that are most likely to respond favorably to this device-based therapy.

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“…13–15,18–20 However, the afferent mechanisms that account for sympathetic overactivity in obesity are incompletely defined. Since increased metabolic rate and impaired respiratory mechanics are prevalent in obesity, 21–24 it is possible that chronic hypoxemia may provide a tonic drive for chemoreflex activation and subsequent sympathoexcitation in obesity.…”

Section: Introductionmentioning

confidence: 99%

Chronic Interactions Between Carotid Baroreceptors and Chemoreceptors in Obesity Hypertension

Lohmeier

Iliescu

Tudorancea³

et al. 2016

Hypertension

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Carotid bodies play a critical role in protecting against hypoxemia and their activation increases sympathetic activity, arterial pressure and ventilation, responses opposed by acute stimulation of the baroreflex. While chemoreceptor hypersensitivity is associated with sympathetically-mediated hypertension, the mechanisms involved and their significance in the pathogenesis of hypertension remains unclear. We investigated the chronic interactions of these reflexes in dogs with sympathetically-mediated, obesity-induced hypertension based on the hypothesis that hypoxemia and tonic activation of carotid chemoreceptors may be associated with obesity. After 5 weeks on a high-fat diet, the animals experienced a 35–40% weight gain, increases in arterial pressure from 106±3 to 123±3 mm Hg and respiratory rate from 8±1 to 12±1 breaths/min along with hypoxemia (PaO2= 81±3 mm Hg) but eucapnia. During 7 days of carotid baroreflex activation by electrical stimulation of the carotid sinus, tachypnea was attenuated and hypertension was abolished before these variables returned to pre-stimulation values during a recovery period. Following subsequent denervation of the carotid sinus region, respiratory rate decreased transiently in association with further sustained reductions in PaO2 (to 65±2 mm Hg) and substantial hypercapnia. Moreover, the severity of hypertension was attenuated from 125±2 to 116±3 mm Hg (45–50% reduction). These findings suggest that hypoxemia may account for sustained stimulation of peripheral chemoreceptors in obesity and that this activation leads to compensatory increases in ventilation and central sympathetic outflow that contributes to neurogenically-mediated hypertension. Furthermore, the excitatory effects of chemoreceptor hyperactivity are abolished by chronic activation of the carotid baroreflex.

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Baroreflex activation therapy in hypertension

Cited by 32 publications

References 18 publications

Management of hypertension in chronic kidney disease

Management of hypertension in chronic kidney disease

Baroreflex Activation: from Mechanisms to Therapy for Cardiovascular Disease

Chronic Interactions Between Carotid Baroreceptors and Chemoreceptors in Obesity Hypertension

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