Management of Uncontrollable Hypertension With a Carotid Sinus Stimulation Device
2007; Lippincott Williams & Wilkins; Volume: 50; Issue: 5 Linguagem: Inglês
10.1161/hypertensionaha.107.099416
ISSN1524-4563
AutoresMarkus G. Mohaupt, Jürg Schmidli, Friedrich C. Luft,
Tópico(s)Migraine and Headache Studies
ResumoHomeHypertensionVol. 50, No. 5Management of Uncontrollable Hypertension With a Carotid Sinus Stimulation Device Free AccessCase ReportPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessCase ReportPDF/EPUBManagement of Uncontrollable Hypertension With a Carotid Sinus Stimulation Device Markus G. Mohaupt, Jürg Schmidli and Friedrich C. Luft Markus G. MohauptMarkus G. Mohaupt From the Division of Hypertension, Departments of Nephrology/Hypertension (M.G.M.) and Cardiovascular Surgery (J.S.), University of Berne, Berne, Switzerland; and the Medical Faculty of the Charité (F.C.L.), Experimental and Clinical Research Center, HELIOS Klinikum Berlin-Buch, Berlin, Germany. , Jürg SchmidliJürg Schmidli From the Division of Hypertension, Departments of Nephrology/Hypertension (M.G.M.) and Cardiovascular Surgery (J.S.), University of Berne, Berne, Switzerland; and the Medical Faculty of the Charité (F.C.L.), Experimental and Clinical Research Center, HELIOS Klinikum Berlin-Buch, Berlin, Germany. and Friedrich C. LuftFriedrich C. Luft From the Division of Hypertension, Departments of Nephrology/Hypertension (M.G.M.) and Cardiovascular Surgery (J.S.), University of Berne, Berne, Switzerland; and the Medical Faculty of the Charité (F.C.L.), Experimental and Clinical Research Center, HELIOS Klinikum Berlin-Buch, Berlin, Germany. Originally published24 Sep 2007https://doi.org/10.1161/HYPERTENSIONAHA.107.099416Hypertension. 2007;50:825–828Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: September 24, 2007: Previous Version 1 Hypertensive crisis is a serious condition that results in target-organ damage, such as stroke, heart attack, or renal failure, if left untreated.1 Causes of acute increases in blood pressure in patients with primary essential hypertension include medication noncompliance and poorly controlled chronic hypertension. Treatment of a hypertensive crisis should be tailored to each individual based on the extent of target-organ injury and comorbid conditions. Prompt and rapid reduction of blood pressure under continuous surveillance is essential. We encountered a patient with target-organ damage and poor response to accepted antihypertensive regimens. Many terms are used to describe this degree of hypertension; the term "uncontrollable" will be used here. After an 8-drug regimen was not successful, we elected a radical, controversial, but novel therapy. Only long-term clinical trials, perhaps above-and-beyond the trial in which we currently participate, will be necessary to answer the hypothesis that a device-based treatment can triumph over tablets alone.The PatientA 58-year-old woman with known primary hypertension for 40 years was referred to our clinic because of difficult-to-control "resistant or uncontrollable" hypertension. She did not have diabetes or known renal disease. However, she did have modest proteinuria at ≈500 mg/d. Her left ventricle wall thickness was moderately enlarged by echocardiography. Five or more different concomitantly prescribed medications failed to result in adequate blood pressure control. She had been diagnosed earlier with accelerated (malignant) hypertension on the basis of severe headaches, retinal hemorrhages, and macular edema. Secondary causes of hypertension were sought but not identified. Her medication consisted of furosemide, minoxidil, atenolol, metolazone irbesartan, amiloride, and glyceryl trinitrate. Amlodipine was added; however, an outpatient visit disclosed a blood pressure of 240/140 mm Hg (these and subsequent values are in the presented supine position). The drug doses were commensurate with the maximum-recommended doses given in the package inserts. Therefore, the patient was offered participation in the Device-Based Therapy of Hypertension Trial. This multicenter study is currently being conducted at 9 clinical centers in Switzerland, the Netherlands, Germany, Poland, and Latvia.After written, informed consent was obtained following due approval from the ethics committee (internal review board), a device for stimulation of both carotid sinuses simultaneously was operatively placed in the patient under general anesthesia. Briefly, both carotid sinuses were surgically exposed and electrodes (Figure 1A) were placed around the carotid adventitial surface bilaterally. The electrode placement was tested in terms of adequate blood pressure and heart rate reductions after stimulation. The leads were subcutaneously tunneled and connected to the implantable stimulation device that was then placed in a subclavian subcutaneous position on the anterior chest wall as shown in the roentgenogram (Figure 1B). The patient recovered uneventfully and left the hospital. Download figureDownload PowerPointFigure 1. A, Electrode system that is implanted on both carotid sinuses is shown. The adventia is stimulated directly. Pacing electrodes and suture pads of the electrodes are prepared to accommodate placement close to the carotid bifurcation. B, Chest roentgenogram after implantation showing the electrodes in place and the stimulator that is somewhat larger than a conventional pacemaker.According to the protocol, the device was not to be activated until 1 month postoperatively. One week after discharge, the patient presented with headache and a supine blood pressure of 260/160 mm Hg. She was admitted to the hospital, and the ethics committee was consulted to request premature activation of the device. After due approval, the blood pressure was monitored semiautomatically (Dynamap), and electrical baroreflex activation was initiated on both carotid sinuses simultaneously with incremental voltages as indicated (Figure 2). The stimulation was constantly kept on a continuous square-wave pattern at a frequency of 100 Hz and a pulse width of 480 μs; no burst-like or further complex configurations were activated. Blood pressure progressively decreased with increasing stimulation. Systolic blood pressure fell more than diastolic blood pressure, whereas heart rate decreased from 125 to 100 bpm. To verify that the device activation was causal for the blood pressure responses, the stimulation was intermittently interrupted, which resulted in a prompt increase in blood pressure to 200/160 mm Hg. The device was then restarted, and blood pressure again decreased. During further "on-off" testing, the average decrease in systolic blood pressure was 19±7 mm Hg, and diastolic blood pressure decreased by 14±7 mm Hg. Complete control of blood pressure was achieved only with activation of the device and the entire palette of blood pressure medications. When the patient was noncompliant to the medication regimen, blood pressure increased in spite of the device. However, with the device and continued medications, the patient's 24-hour blood pressure control was improved by 22 mm Hg systolic, 9 mm Hg diastolic, and 13 mm Hg mean blood pressure, respectively, at the 3-month inspection. The resting heart rate had decreased by 13 bpm at that time. Download figureDownload PowerPointFigure 2. Dinamap blood pressure measurements of the patient during a hypertensive crisis are shown. Systolic blood pressure decreased >45 mm Hg, and diastolic blood pressure decreased 50 mm Hg. Thereafter, the device was shut off, and blood pressure increased over 4 hours. Continuation of the stimulus resulted in blood pressure decreases to the previous stimulation values. Voltage is indicated on the x axis. The stimulation was bilateral with on a continuous square-wave pattern at a frequency of 100 Hz and a pulse width of 480 μs.DiscussionInterestingly, attempts to lower blood pressure by means of carotid sinus afferent stimulation is not new.2 A rich literature from the 1960s and 1970s reflects the investigation into therapeutic modulation of the carotid baroreflex in the treatment of refractory hypertension and angina pectoris.3–9 These early reports were enthusiastic and clearly showed the potential use of the technique. However, technical difficulties made the approach unattractive. For instance, the transistor had not even been introduced, printed circuits were rudimentary, chip technology was inconceivable, the electrode technology of the time was unreliable, and battery capacity was insufficient. These technical problems have been overcome, and the surgical implantation technique is now fully established.10Those of us who grew up with systems analysis in terms of blood pressure regulation recall the teachings of Guyton et al.11 They emphasized that 3 main factors are extremely important in blood pressure regulation, namely: (1) control of pressure by autonomic reflexes, (2) control of arterial pressure by changes in body fluid volumes and electrolytes, and (3) control of arterial pressure by the renin-angiotensin-aldosterone mechanism. Guyton et al11 stated that, "The autonomic mechanisms seem to play their most significant role in short-term regulation of arterial pressure from second-to-second, minute-to-minute, and hour-to-hour, while other factors seem to play the primary role in long-term regulation of arterial pressure." Nevertheless, the authors go on to state, "However, the nervous mechanisms can affect the long-term also, as will be pointed out." The systems analysis of the Guytonians reveals 2 startling conclusions: changes in total peripheral resistance, per se, play essentially no role in the long-term regulation of arterial pressure, and it is impossible to change the arterial pressure chronically from its status quo level without either altering the function of the kidneys in some way to change their output of water and electrolytes or changing the intake of water and electrolytes. As an aside, the current introduction and "buzz word" of systems biology would have bemused Guyton; he surely would have studied this report carefully as well.Guyton et al11 returned to neurogenic hypertension later in their presentation. They pointed out the importance of nervous stimuli to the kidney that can cause the necessary tendency for water and salt retention. In his Cannon lecture, DiBona12 discussed the important role of the renal sympathetic nerves to regulate various aspects of overall renal function and blood pressure regulation. DiBona12 described the renal nerves as "self-regulatory agencies, which operate to preserve the constancy of the fluid matrix." More insight into devices and blood pressure regulation can be gained by examining the results of animal investigations.Lohmeier et al13 chronically implanted electrodes around both carotid sinuses and used the same device reported here to activate the carotid baroreflex in conscious dogs. Control values for mean blood pressure and heart rate were 93 mm Hg and 64 bpm, respectively. After control measurements, the carotid baroreflex was activated bilaterally for 7 days at a level that produced a prompt and substantial reduction in mean blood pressure to 75 mg for 7 days. When one considers the fact that drugs do not generally reduce blood pressure in nonhypertensive animals or humans, the results are impressive indeed. During prolonged baroreflex activation, heart rate decreased in parallel with blood pressure. Lohmeier et al13 also reported ≈35% reduction in plasma norepinephrine concentrations. After baroreflex activation was discontinued, hemodynamic measures and plasma levels of norepinephrine returned to control levels.Lohmeier et al14 next studied a model involving chronic angiotensin (Ang) II infusion in the dog. The animals were exposed to the same carotid stimulation protocol that decreased blood pressure by ≈20 mm Hg for a week without Ang II. However, with Ang II at an infusion rate (5 ng/kg per minute) and a mean blood pressure of 129 mm Hg, the carotid stimulation protocol decreased blood pressure by only ≈5 mm Hg. Thus, long-term baroreflex-medicated reductions in arterial blood pressure are markedly attenuated but not totally eliminated by chronic Ang II infusions. Conceivably, the actions of Ang II could have been central, because the peptide could have crossed the blood-brain barrier and influenced relevant brain regions.15 The clinical implications of these data are uncertain and will have to be tested.Lohmeier et al16 next investigated the effects of renal innervation. The teachings of Guyton et al11 and the detailed studies of DiBona12 would make this notion an obvious hypothesis. Thus, 6 dogs underwent bilateral carotid baroreflex electrical activation for 7 days before and after bilateral renal denervation. Before renal denervation, control values for mean blood pressure and plasma norepinephrine concentration were 95 mm Hg and 96 pg/mL, respectively. During day 1 of carotid sinus stimulation, mean blood pressure decreased 13 mm Hg, and there was modest sodium retention. Daily sodium balance was subsequently restored, but reductions in mean blood pressure were sustained throughout the 7 days of baroreflex activation. Activation of the baroreflex was associated with decreases in plasma norepinephrine concentration and plasma renin activity. All of the values returned to control levels during a 7-day recovery period. Two weeks after renal denervation, control values for mean blood pressure, plasma norepinephrine concentration, plasma renin activity, and sodium excretion were similar to those measured when the renal nerves were intact. Moreover, after renal denervation, all of the responses to activation of the baroreflex were not different than those observed before renal denervation. Astonishingly, the renal nerves were not an obligate requirement for achieving long-term reductions in arterial pressure during prolonged activation of the baroreflex. Nonetheless, sympathetic innervation involves not only the kidneys but also all areas of the body. Conceivably, reduction in sympathetic tone to nonrenal areas was more important than most nephrologists would care to admit. Because circulating norepinephrine is a composite of total body release, clearance, and metabolism, its reduction is a further clue as to the significance of reduced sympathetic nerve activity to nonrenal areas. "Smart money" was lost on this one! The clinical implications are, at the moment, not interpretable, but will require novel studies along "translational" lines in animals and humans.Lohmeier et al17 have also studied a dog model of obesity-related hypertension. After 4 weeks of a high-fat diet, the dogs gained weight from 25 to 39 kg. Their mean blood pressure increased from 97 to 110 mm Hg; their heart rates increased from 67 to 91 bpm and plasma norepinephrine concentration from 141 to 280 pg/mL. Plasma glucose and insulin concentrations were elevated, but increases in plasma renin activity during the initial weeks of the high-fat diet were not sustained. During week 5, baroreflex activation resulted in sustained reductions in mean blood pressure, heart rate, and plasma norepinephrine concentration; at the end of week 5, these values were 87 mm Hg, 77 bpm and 166 pg/mL, respectively. These suppressed values returned to week-4 levels during a 7-day recovery period after baroreflex activation. There were no changes in plasma glucose or insulin concentrations or plasma renin activity during prolonged carotid sinus stimulation. The findings indicate that baroreflex activation can chronically suppress the sympathoexcitation associated with obesity and abolish the attendant hypertension while having no effect on hyperinsulinemia or hyperglycemia.These careful animal studies allow several important conclusions. Carotid sinus stimulation for a week lowers blood pressure reproducibly whereas decreasing norepinephrine levels. When the stimulation is discontinued, the basal state is reestablished. Ang II, at least when infused chronically, interferes with baroreflex activation-mediated blood pressure reduction. The renal nerves are not the prime mediators of the long-term effects of baroreflex activation, whereas circulating norepinephrine might be. A model of obesity-induced hypertension in the dog is amenable to baroreflex activation. Again, reduction in circulating norepinephrine levels is a prominent feature in this model.The carotid sinus stimulator was first investigated in a proof-of-concept study.18 The Device-Based Therapy of Hypertension Trial was then initiated as a multicenter clinical trial of electrical carotid sinus stimulation in patients with uncontrollable or poorly controlled hypertension.19 In our department, these patients are invariably minoxidil treatment failures. In addition, although carefully considered as a prerequisite of study inclusion, patient compliance is an ongoing concern in uncontrollable hypertension. The objective means to improve therapy adherence, as has been demonstrated for electronic drug monitors.20 Device-based blood pressure control could provide an advantage, because device programming is independent of patient behavior. The device does not forget.There are numerous unanswered questions that this study and subsequent investigations must answer. Does this device effectively lower blood pressure in humans long term? If so, by what mechanism does the baroreflex activation work? We could imagine that sympathetic tone is diminished. However, because renal nerve activity was apparently not a prerequisite, nerve traffic to the kidney may not be the only mechanism. Renal denervation reduced renal nerve traffic to 0 in the study by Lohmeier et al.16 For this reason, muscle sympathetic nerve activity should and can be readily measured in humans. The notion underscores the possible importance of nonrenal sympathetically regulated areas. We plan such measurements in device-treated patients. However, in patients with autonomic failure and with autosomal-dominant hypertension with brachydactyly, muscle sympathetic nerve activity was actually reduced, although baroreflex blood pressure buffering was almost absent.21 In any event, some answers will be forthcoming to a variety of fascinating clinical questions regarding the baroreflex. Perhaps the pioneers in device-related antihypertensive strategies will be vindicated at long last.2–9PerspectivesFinally, what does device-related medicine mean for most of our patients? The data regarding Life After the Multicenter Automatic Defibrillator Implantation Trial suggest, at least to the senior author, that the chances of exiting this life without a "lump on the chest" are slim. The cost-effectiveness of internal cardiac defibrillators appears to be given if we compare the quality-adjusted life years with the disability-adjusted life years.22 We are possibly being too restrictive in our thinking about carotid sinus stimulators. Persons with severe vascular injury and target-organ damage represent the cohort that we would like to protect from such an outcome in the first place. Conceivably, device-related blood pressure treatment could be introduced much earlier in the treatment chain. Failure of nocturnal "dipping" could be an example of an early indication.DisclosuresM.G.M., J.S., and F.C.L. participate in the Device-Based Therapy of Hypertension Trial, which manufactures this device. The manufacturer had no input into this presentation and did not provide sanction or approval. F.C.L. is an advisor to Novartis, Boehringer-Ingelheim, and Cadbury, all of whom have nothing to do with this project.FootnotesCorrespondence to Friedrich C. Luft, Experimental and Clinical Research Center, Lindenberger Weg 80, 13125 Berlin, Germany. E-mail [email protected] References 1 Calhoun DA, Oparil S. Treatment of hypertensive crisis. N Engl J Med. 1990; 323: 1177–1183.CrossrefMedlineGoogle Scholar2 Warner HR. The frequency-dependent nature of blood pressure regulation by the carotid sinus studied with an electric analog. Circ Res. 1958; 6: 35–40.CrossrefMedlineGoogle Scholar3 Bilgutay AM, Lillehei CW. Treatment of hypertension with an implantable electronic device. JAMA. 1965; 191: 649–653.CrossrefMedlineGoogle Scholar4 Agishi T, Temples J, Peirce EC. Electrical stimulation of the carotid sinus nerve as an experimental treatment of hypertension. J Surg Res. 1969; 9: 305–309.CrossrefMedlineGoogle Scholar5 Schwartz SI, Griffith LCS. Chronic carotid sinus nerve stimulation in the treatment of essential hypertension. Am J Surg. 1967; 114: 5–15.CrossrefMedlineGoogle Scholar6 Braunwald NS, Epstein SE, Braunwald E. Carotid sinus nerve stimulation for the treatment of intractable angina pectoris: surgical technic. Ann Surg. 1970; 172: 810–816.Google Scholar7 Parsonnet V, Rothfeld EL, Raman KV, Myers GH. Electrical stimulation of the carotid sinus nerve. Surg Clin North Am. 1969; 49: 589–596.CrossrefMedlineGoogle Scholar8 Reich T, Tuckman J, Lyon AF, Jacobson JH II. The effects of radio frequency carotid sinus nerve stimulators in severe hypertension. Surg Forum. 1967; 18: 174–176.Google Scholar9 Brest AN, Wiener L, Bachrach B. Bilateral carotid sinus nerve stimulation in the treatment of hypertension. Am J Cardiol. 1972; 29: 821–825.CrossrefMedlineGoogle Scholar10 Tordoir JHM, Scheffers I, Schmidli J, Savolainen H, Liebeskind U, Hansky B, Herold U, Irwin E, Kroon AA, de Leeuw P, Peters TK, Kieval R, Cody R. An implantable carotid sinus baroreflex activating system: surgical technique and short-term outcome from a multicenter feasibility trial for the treatment of resistant hypertension. Eur J Vasc Endovasc Surg. 2007; 33: 414–421.CrossrefMedlineGoogle Scholar11 Guyton AC, Coleman TG, Granger HJ. Circulation: overall regulation. Annu Rev Physiol. 1972; 34: 13–41.CrossrefMedlineGoogle Scholar12 DiBona GF. Physiology in perspective: the wisdom of the body. Neural control of the kidney. Am J Physiol Regul Integr Comp Physiol. 2005; 289: R633–R641.CrossrefMedlineGoogle Scholar13 Lohmeier TE, Irwin ED, Rossing MA, Serdar DJ, Kieval RS. Prolonged activation of the baroreflex produces sustained hypotension. Hypertension. 2004; 43: 306–311.LinkGoogle Scholar14 Lohmeier TE, Dwyer TM, Hildebrandt DA, Irwin ED, Rossing MA, Serdar DJ, Kieval RS. Influence of prolonged baroreflex activation on arterial pressure in angiotensin hypertension. Hypertension. 2005; 46: 1194–2000.LinkGoogle Scholar15 Dibona GF. Central angiotensin modulation of baroreflex control of renal sympathetic nerve activity in the rat: influence of dietary sodium intake. Acta Physiol Scand. 2003; 177: 285–289.CrossrefMedlineGoogle Scholar16 Lohmeier TE, Hildebrandt DA, Dwyer TM, Barrett AM, Irwin ED, Rossing MA, Kieval RS. Renal denervation does not abolish sustained baroreflex-mediated reductions in arterial pressure. Hypertension. 2007; 49: 373–379.LinkGoogle Scholar17 Lohmeier TE, Dwyer TM, Irwin ED, Rossing MA, Kieval RS. Prolonged activation of the baroreflex abolishes obesity-induced hypertension. Hypertension. 2007; 49: 1307–1314.LinkGoogle Scholar18 Schmidli J, Savolainen H, Eckstein F, Irwin E, Peters TK, Martin R, Kieval R, Cody R, Carrel T. Acute device-based blood pressure reduction: electrical activation of the carotid baroreflex in patients undergoing elective carotid surgery. Vascular. 2007; 15: 63–69.CrossrefMedlineGoogle Scholar19 Sica DA, Lohmeier TE. Baroreflex activation for the treatment of hypertension: principles and practice. Expert Rev Med Devices. 2006; 3: 595–601.CrossrefMedlineGoogle Scholar20 Burnier M, Schneider MP, Chiolero A, Stubi CL, Brunner HR. Electronic compliance monitoring in resistant hypertension: the basis for rational therapeutic decisions. J Hypertens. 2001; 19: 335–341.CrossrefMedlineGoogle Scholar21 Jordan J, Toka HR, Heusser K, Toka O, Shannon JR, Tank J, Diedrich A, Stabroth C, Stoffels M, Naraghi R, Oelkers W, Schuster H, Schobel HP, Haller H, Luft FC. Severely impaired baroreflex-buffering in patients with monogenic hypertension and neurovascular contact. Circulation. 2000; 102: 2611–2618.CrossrefMedlineGoogle Scholar22 Sanders GD, Hlatky MA, Owens DK. Cost-effectiveness of implantable cardioverter-defibrillators. N Engl J Med. 2005; 353: 1471–1480.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Cavalcante G, Brognara F, Oliveira L, Lataro R, Durand M, Oliveira A, Nóbrega A, Salgado H and Sabino J (2021) Benefits of pharmacological and electrical cholinergic stimulation in hypertension and heart failure, Acta Physiologica, 10.1111/apha.13663, 232:3, Online publication date: 1-Jul-2021. Huo L, Gao Y, Zhang D, Wang S, Han Y, Men H, Yang Z, Qin X, Wang R, Kong D, Bai H, Zhang H, Zhang W and Jia Z (2021) Piezo2 channel in nodose ganglia neurons is essential in controlling hypertension in a pathway regulated directly by Nedd4-2, Pharmacological Research, 10.1016/j.phrs.2020.105391, 164, (105391), Online publication date: 1-Feb-2021. Stavrakis S, Kulkarni K, Singh J, Katritsis D and Armoundas A (2020) Autonomic Modulation of Cardiac Arrhythmias, JACC: Clinical Electrophysiology, 10.1016/j.jacep.2020.02.014, 6:5, (467-483), Online publication date: 1-May-2020. Sohinki D and Stavrakis S (2020) New approaches for treating atrial fibrillation: Focus on autonomic modulation, Trends in Cardiovascular Medicine, 10.1016/j.tcm.2019.10.009, 30:7, (433-439), Online publication date: 1-Oct-2020. Gierthmuehlen M and Plachta D (2015) Effect of selective vagal nerve stimulation on blood pressure, heart rate and respiratory rate in rats under metoprolol medication, Hypertension Research, 10.1038/hr.2015.122, 39:2, (79-87), Online publication date: 1-Feb-2016. Thomas P and Dasgupta I (2014) The role of the kidney and the sympathetic nervous system in hypertension, Pediatric Nephrology, 10.1007/s00467-014-2789-4, 30:4, (549-560), Online publication date: 1-Apr-2015. Seravalle G and Grassi G (2015) Carotid Baroreceptor Stimulation in Resistant Hypertension and Heart Failure, High Blood Pressure & Cardiovascular Prevention, 10.1007/s40292-015-0083-6, 22:3, (233-239), Online publication date: 1-Sep-2015. Chobanyan-Jürgens K and Jordan J (2015) Electrical Carotid Sinus Stimulation: Chances and Challenges in the Management of Treatment Resistant Arterial Hypertension, Current Hypertension Reports, 10.1007/s11906-015-0587-4, 17:9, Online publication date: 1-Sep-2015. Victor R (2015) Carotid baroreflex activation therapy for resistant hypertension, Nature Reviews Cardiology, 10.1038/nrcardio.2015.96, 12:8, (451-463), Online publication date: 1-Aug-2015. Frishman W and Glicklich D (2014) The Role of Nonpharmacologic Device Interventions in the Management of Drug-Resistant Hypertension, Current Atherosclerosis Reports, 10.1007/s11883-014-0405-5, 16:5, Online publication date: 1-May-2014. Townsend R (2014) Interventional management in hypertension, Current Opinion in Nephrology and Hypertension, 10.1097/MNH.0000000000000046, 23:5, (444-448), Online publication date: 1-Sep-2014. Jordan J (2014) CrossTalk opposing view: Which technique for controlling resistant hypertension? Carotid sinus stimulation, The Journal of Physiology, 10.1113/jphysiol.2013.268078, 592:18, (3933-3935), Online publication date: 15-Sep-2014. Schmidli J, S. von Allmen R and G. Mohaupt M (2014) Electrical carotid baroreceptor stimulationInterventionelle kardiovaskuläre Therapie bei Bluthochdruck, Wiener Medizinische Wochenschrift, 10.1007/s10354-014-0329-2, 164:23-24, (508-514), Online publication date: 1-Dec-2014. Fiala J, Bingger P, Ruh D, Foerster K, Heilmann C, Beyersdorf F, Zappe H and Seifert A (2012) An implantable optical blood pressure sensor based on pulse transit time, Biomedical Microdevices, 10.1007/s10544-012-9689-9, 15:1, (73-81), Online publication date: 1-Feb-2013. Jordan J, Mann J and Luft F (2013) Research needs in the area of device-related treatments for hypertension, Kidney International, 10.1038/ki.2013.56, 84:2, (250-255), Online publication date: 1-Aug-2013. Campese V (2013) Interventional hypertension, Journal of Hypertension, 10.1097/HJH.0b013e328364d3f1, 31:11, (2118-2122), Online publication date: 1-Nov-2013. Jordan J, Heusser K, Brinkmann J and Tank J (2012) Electrical carotid sinus stimulation in treatment resistant arterial hypertension, Autonomic Neuroscience, 10.1016/j.autneu.2012.10.009, 172:1-2, (31-36), Online publication date: 1-Dec-2012. Parati G and Esler M (2012) The human sympathetic nervous system: its relevance in hypertension and heart failure, European Heart Journal, 10.1093/eurheartj/ehs041, 33:9, (1058-1066), Online publication date: 1-May-2012. Peter D, Alemu Y, Xenos M, Weisberg O, Avneri I, Eshkol M, Oren T, Elazar M, Assaf Y and Bluestein D (2012) Fluid Structure Interaction With Contact Surface Methodology for Evaluation of Endovascular Carotid Implants for Drug-Resistant Hypertension Treatment, Journal of Biomechanical Engineering, 10.1115/1.4006339, 134:4, Online publication date: 1-Apr-2012. Esler M (2012) Harnessing the Autonomic Nervous System for Therapeutic Intervention Primer on the Autonomic Nervous System, 10.1016/B978-0-12-386525-0.00137-2, (649-652), . Daulatzai M (2012) Dysfunctional Nucleus Tractus Solitarius: Its Crucial Role in Promoting Neuropathogentic Cascade of Alzheimer's Dementia—A Novel Hypothesis, Neurochemical Research, 10.1007/s11064-011-0680-2, 37:4, (846-868), Online publication date: 1-Apr-2012. Victor R (2012) Systemic Hypertension Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 10.1016/B978-1-4377-0398-6.00045-7, (935-954), . Tousoulis D, Androulakis E, Papageorgiou N and Stefanadis C (2012) Novel therapeutic strategies in the management of arterial hypertension, Pharmacology & Therapeutics, 10.1016/j.pharmthera.2012.05.004, 135:2, (168-175), Online publication date: 1-Aug-2012. Papademetriou V, Doumas M, Faselis C, Tsioufis C, Douma S, Gkaliagkousi E and Zamboulis C (2011) Carotid Baroreceptor Stimulation for the Treatment of Resistant Hypertension, International Journal of Hypertension, 10.4061/2011/964394, 2011, (1-5), . Ng M, Sica D and Frishman W (2011) Rheos, Cardiology in Review, 10.1097/CRD.0b013e3181f87921, 19:2, (52-57), Online publication date: 1-Mar-2011. Joyner M, Charkoudian N, Curry T, Eisenach J and Wehrwein E (2011) What we talk about when we talk with medical students, Advances in Physiology Education, 10.1152/advan.00058.2010, 35:1, (16-21), Online publication date: 1-Mar-2011. Seca L, Silva J, Oliveira H, Costa M and Leitão-Marques A (2011) Normalização da pressão arterial em hipertenso grave após angioplastia carotídea bilateral, Revista Portuguesa de Cardiologia, 10.1016/S0870-2551(11)70006-3, 30:7-8, (675-677), Online publication date: 1-Jul-2011. Esler M (2011) The sympathetic nervous system through the ages: from Thomas Willis to resistant hypertension, Experimental Physiology, 10.1113/expphysiol.2011.052332, 96:7, (611-622), Online publication date: 1-Jul-2011. Martin E and Victor R (2010) Premise, Promise, and Potential Limitations of Invasive Devices to Treat Hypertension, Current Cardiology Reports, 10.1007/s11886-010-0156-z, 13:1, (86-92), Online publication date: 1-Feb-2011. Seca L, Silva J, Oliveira H, Costa M and Leitão-Marques A (2011) Blood pressure control after bilateral carotid angioplasty in a patient with severe hypertension, Revista Portuguesa de Cardiologia (English Edition), 10.1016/S2174-2049(11)70006-X, 30:7-8, (675-677), Online publication date: 1-Jul-2011. Heusser K, Tank J, Engeli S, Diedrich A, Menne J, Eckert S, Peters T, Sweep F, Haller H, Pichlmaier A, Luft F and Jordan J (2010) Carotid Baroreceptor Stimulation, Sympathetic Activity, Baroreflex Function, and Blood Pressure in Hypertensive Patients, Hypertension, 55:3, (619-626), Online publication date: 1-Mar-2010.Mancia G, Parati G and Zanchetti A (2010) Electrical Carotid Baroreceptor Stimulation in Resistant Hypertension, Hypertension, 55:3, (607-609), Online publication date: 1-Mar-2010. Grassi G, Quarti-Trevano F, Brambilla G and Seravalle G (2014) Blood pressure control in resistant hypertension: new therapeutic options, Expert Review of Cardiovascular Therapy, 10.1586/erc.10.138, 8:11, (1579-1585), Online publication date: 1-Nov-2010. Fiala J, Bingger P, Foerster K, Heilmann C, Beyersdorf F, Zappe H and Seifert A (2010) Implantable sensor for blood pressure determination via pulse transit time 2010 Ninth IEEE Sensors Conference (SENSORS 2010), 10.1109/ICSENS.2010.5690619, 978-1-4244-8170-5, (1226-1229) Lohmeier T, Iliescu R, Dwyer T, Irwin E, Cates A and Rossing M (2010) Sustained suppression of sympathetic activity and arterial pressure during chronic activation of the carotid baroreflex, American Journal of Physiology-Heart and Circulatory Physiology, 10.1152/ajpheart.00372.2010, 299:2, (H402-H409), Online publication date: 1-Aug-2010. Cogiamanian F, Brunoni A, Boggio P, Fregni F, Ciocca M and Priori A (2010) Non-invasive brain stimulation for the management of arterial hypertension, Medical Hypotheses, 10.1016/j.mehy.2009.08.037, 74:2, (332-336), Online publication date: 1-Feb-2010. Esler M, Lambert E and Schlaich M (2010) Point: Chronic Activation of the Sympathetic Nervous System is the Dominant Contributor to Systemic Hypertension, Journal of Applied Physiology, 10.1152/japplphysiol.00182.2010, 109:6, (1996-1998), Online publication date: 1-Dec-2010. Scheffers I, Kroon A and de Leeuw P (2010) Carotid Baroreflex Activation: Past, Present, and Future, Current Hypertension Reports, 10.1007/s11906-009-0087-5, 12:2, (61-66), Online publication date: 1-Apr-2010. Esler M (2010) The 2009 Carl Ludwig Lecture: pathophysiology of the human sympathetic nervous system in cardiovascular diseases: the transition from mechanisms to medical management, Journal of Applied Physiology, 10.1152/japplphysiol.00832.2009, 108:2, (227-237), Online publication date: 1-Feb-2010. DeLoach S and Mohler E (2010) Atherosclerotic Risk Factors Rutherford's Vascular Surgery, 10.1016/B978-1-4160-5223-4.00029-9, (451-460), . (2010) Comments on Point:Counterpoint: The dominant contributor to systemic hypertension: Chronic activation of the sympathetic nervous system vs. Activation of the intrarenal renin-angiotensin system, Journal of Applied Physiology, 10.1152/japplphysiol.01160.2010, 109:6, (2003-2014), Online publication date: 1-Dec-2010. Wustmann K, Kucera J, Scheffers I, Mohaupt M, Kroon A, de Leeuw P, Schmidli J, Allemann Y and Delacrétaz E (2009) Effects of Chronic Baroreceptor Stimulation on the Autonomic Cardiovascular Regulation in Patients With Drug-Resistant Arterial Hypertension, Hypertension, 54:3, (530-536), Online publication date: 1-Sep-2009. Trindade Jr. A, Moreira E, Silva G and Krieger E (2009) Evidence that blood pressure remains under the control of arterial baroreceptors in renal hypertensive rats, Brazilian Journal of Medical and Biological Research, 10.1590/S0100-879X2009001000013, 42:10, (954-957), Online publication date: 1-Oct-2009. Durand M, Fazan Jr. R, Salgado M and Salgado H (2009) Acute and chronic electrical activation of baroreceptor afferents in awake and anesthetized subjects, Brazilian Journal of Medical and Biological Research, 10.1590/S0100-879X2009000100009, 42:1, (53-60), Online publication date: 1-Jan-2009. Zhang G and Zhang W (2009) Heart rate, lifespan, and mortality risk, Ageing Research Reviews, 10.1016/j.arr.2008.10.001, 8:1, (52-60), Online publication date: 1-Jan-2009. Doumas M, Guo D and Papademetriou V (2009) Carotid baroreceptor stimulation as a therapeutic target in hypertension and other cardiovascular conditions, Expert Opinion on Therapeutic Targets, 10.1517/14728220902780185, 13:4, (413-425), Online publication date: 1-Apr-2009. Textor S (2009) What Price For Blood Pressure Control?, The Journal of Clinical Hypertension, 10.1111/j.1751-7176.2009.00193.x, 11:10, (537-539), Online publication date: 1-Oct-2009. Mastracci T and Greenberg R (2009) Neuromodulation and Hypertension Neuromodulation, 10.1016/B978-0-12-374248-3.00071-9, (845-854), . Kawada T, Shimizu S, Yamamoto H, Shishido T, Kamiya A, Miyamoto T, Sunagawa K and Sugimachi M (2009) Servo-Controlled Hind-Limb Electrical Stimulation for Short-Term Arterial Pressure Control, Circulation Journal, 10.1253/circj.CJ-08-1058, 73:5, (851-859), . Joyner M, Charkoudian N and Wallin B (2008) A sympathetic view of the sympathetic nervous system and human blood pressure regulation, Experimental Physiology, 10.1113/expphysiol.2007.039545, 93:6, (715-724), Online publication date: 1-Jun-2008. Weerakkody Y and Sorrentino S (2011) Carotid pacemaker Radiopaedia.org, 10.53347/rID-14865 November 2007Vol 50, Issue 5 Advertisement Article InformationMetrics https://doi.org/10.1161/HYPERTENSIONAHA.107.099416PMID: 17893424 Manuscript receivedAugust 7, 2007Manuscript acceptedSeptember 6, 2007Originally publishedSeptember 24, 2007Manuscript revisedAugust 21, 2007 PDF download Advertisement SubjectsClinical StudiesDevelopmental BiologyGeneticsHypertensionPacemaker
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