Evidence map›Paper›PMID 26831195›Full record

ArticleHypertension (Dallas, Tex. : 1979)2016

Acute Response to Unilateral Unipolar Electrical Carotid Sinus Stimulation in Patients With Resistant Arterial Hypertension.

Karsten Heusser, Jens Tank, Julia Brinkmann, Jan Menne, Jessica Kaufeld, Silvia Linnenweber-Held, Joachim Beige, Mathias Wilhelmi, André Diedrich, Hermann Haller and 1 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
7.6field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Early experience with baroreflex activation therapy from a vascular surgery perspective.Journal of vascular surgery cases and innovative techniques · 2024
    Article
  11. The coming era of neuromodulation therapies: expectations for baroreceptor stimulation.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Article
  12. Device's design and clinical perspectives for resistant hypertension therapy.International journal of cardiology. Cardiovascular risk and prevention · 2024
    Review
  13. Key challenges in exploring the rat as a preclinical neurostimulation model for aortic baroreflex modulation in hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Review
  14. Article
  15. Brain and cardiovascular-related changes are associated with aging, hypertension, and atrial fibrillation.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2022
    Review
  16. Device-Based Therapy for Resistant Hypertension: An Up-to-Date Review.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2022
    Review
  17. Article
  18. Article
  19. Article
  20. Autonomic cardiovascular alterations as therapeutic targets in chronic kidney disease.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2021
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 2 countries.

Karsten HeusserFrom the Institute of Clinical Pharmacology (K.H., J.T., J.B., J.J.), Clinic for Nephrology (J.M., J.K., S.L.-H., H.H.), Division for Cardiothoracic, Transplantation- and Vascular Surgery (M.W.), Hannover Medical School, Hannover, Germany; Department of Nephrology and KfH Renal Unit, Hospital St. Georg, Leipzig, Germany (J.B.); and Division of Clinical Pharmacology, Department of Medicine, Autonomic Dysfunction Service, Vanderbilt University, Nashville, TN (A.D.).
Jens TankFrom the Institute of Clinical Pharmacology (K.H., J.T., J.B., J.J.), Clinic for Nephrology (J.M., J.K., S.L.-H., H.H.), Division for Cardiothoracic, Transplantation- and Vascular Surgery (M.W.), Hannover Medical School, Hannover, Germany; Department of Nephrology and KfH Renal Unit, Hospital St. Georg, Leipzig, Germany (J.B.); and Division of Clinical Pharmacology, Department of Medicine, Autonomic Dysfunction Service, Vanderbilt University, Nashville, TN (A.D.).
Julia BrinkmannFrom the Institute of Clinical Pharmacology (K.H., J.T., J.B., J.J.), Clinic for Nephrology (J.M., J.K., S.L.-H., H.H.), Division for Cardiothoracic, Transplantation- and Vascular Surgery (M.W.), Hannover Medical School, Hannover, Germany; Department of Nephrology and KfH Renal Unit, Hospital St. Georg, Leipzig, Germany (J.B.); and Division of Clinical Pharmacology, Department of Medicine, Autonomic Dysfunction Service, Vanderbilt University, Nashville, TN (A.D.).
Jan MenneFrom the Institute of Clinical Pharmacology (K.H., J.T., J.B., J.J.), Clinic for Nephrology (J.M., J.K., S.L.-H., H.H.), Division for Cardiothoracic, Transplantation- and Vascular Surgery (M.W.), Hannover Medical School, Hannover, Germany; Department of Nephrology and KfH Renal Unit, Hospital St. Georg, Leipzig, Germany (J.B.); and Division of Clinical Pharmacology, Department of Medicine, Autonomic Dysfunction Service, Vanderbilt University, Nashville, TN (A.D.).
Jessica KaufeldFrom the Institute of Clinical Pharmacology (K.H., J.T., J.B., J.J.), Clinic for Nephrology (J.M., J.K., S.L.-H., H.H.), Division for Cardiothoracic, Transplantation- and Vascular Surgery (M.W.), Hannover Medical School, Hannover, Germany; Department of Nephrology and KfH Renal Unit, Hospital St. Georg, Leipzig, Germany (J.B.); and Division of Clinical Pharmacology, Department of Medicine, Autonomic Dysfunction Service, Vanderbilt University, Nashville, TN (A.D.).
Silvia Linnenweber-HeldFrom the Institute of Clinical Pharmacology (K.H., J.T., J.B., J.J.), Clinic for Nephrology (J.M., J.K., S.L.-H., H.H.), Division for Cardiothoracic, Transplantation- and Vascular Surgery (M.W.), Hannover Medical School, Hannover, Germany; Department of Nephrology and KfH Renal Unit, Hospital St. Georg, Leipzig, Germany (J.B.); and Division of Clinical Pharmacology, Department of Medicine, Autonomic Dysfunction Service, Vanderbilt University, Nashville, TN (A.D.).
Joachim BeigeFrom the Institute of Clinical Pharmacology (K.H., J.T., J.B., J.J.), Clinic for Nephrology (J.M., J.K., S.L.-H., H.H.), Division for Cardiothoracic, Transplantation- and Vascular Surgery (M.W.), Hannover Medical School, Hannover, Germany; Department of Nephrology and KfH Renal Unit, Hospital St. Georg, Leipzig, Germany (J.B.); and Division of Clinical Pharmacology, Department of Medicine, Autonomic Dysfunction Service, Vanderbilt University, Nashville, TN (A.D.).
Mathias WilhelmiFrom the Institute of Clinical Pharmacology (K.H., J.T., J.B., J.J.), Clinic for Nephrology (J.M., J.K., S.L.-H., H.H.), Division for Cardiothoracic, Transplantation- and Vascular Surgery (M.W.), Hannover Medical School, Hannover, Germany; Department of Nephrology and KfH Renal Unit, Hospital St. Georg, Leipzig, Germany (J.B.); and Division of Clinical Pharmacology, Department of Medicine, Autonomic Dysfunction Service, Vanderbilt University, Nashville, TN (A.D.).
André DiedrichFrom the Institute of Clinical Pharmacology (K.H., J.T., J.B., J.J.), Clinic for Nephrology (J.M., J.K., S.L.-H., H.H.), Division for Cardiothoracic, Transplantation- and Vascular Surgery (M.W.), Hannover Medical School, Hannover, Germany; Department of Nephrology and KfH Renal Unit, Hospital St. Georg, Leipzig, Germany (J.B.); and Division of Clinical Pharmacology, Department of Medicine, Autonomic Dysfunction Service, Vanderbilt University, Nashville, TN (A.D.).
Hermann HallerFrom the Institute of Clinical Pharmacology (K.H., J.T., J.B., J.J.), Clinic for Nephrology (J.M., J.K., S.L.-H., H.H.), Division for Cardiothoracic, Transplantation- and Vascular Surgery (M.W.), Hannover Medical School, Hannover, Germany; Department of Nephrology and KfH Renal Unit, Hospital St. Georg, Leipzig, Germany (J.B.); and Division of Clinical Pharmacology, Department of Medicine, Autonomic Dysfunction Service, Vanderbilt University, Nashville, TN (A.D.).
Jens JordanFrom the Institute of Clinical Pharmacology (K.H., J.T., J.B., J.J.), Clinic for Nephrology (J.M., J.K., S.L.-H., H.H.), Division for Cardiothoracic, Transplantation- and Vascular Surgery (M.W.), Hannover Medical School, Hannover, Germany; Department of Nephrology and KfH Renal Unit, Hospital St. Georg, Leipzig, Germany (J.B.); and Division of Clinical Pharmacology, Department of Medicine, Autonomic Dysfunction Service, Vanderbilt University, Nashville, TN (A.D.). jordan.jens@mh-hannover.de.
Klinikum St. Georg · DEVanderbilt University · US

Funding

Structural genomics of norepinephrine transportersP01HL056693 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI ROBERTSON, DAVID HERLIE · 1997 to 2016
$30.8M
NHLBI NIH HHS P01 HL056693
6 · The paper itself

Abstract

Bilateral bipolar electric carotid sinus stimulation acutely reduced muscle sympathetic nerve activity (MSNA) and blood pressure (BP) in patients with resistant arterial hypertension but is no longer available. The second-generation device uses a smaller unilateral unipolar disk electrode to reduce invasiveness while saving battery life. We hypothesized that the second-generation device acutely lowers BP and MSNA in treatment-resistant hypertensive patients. Eighteen treatment-resistant hypertensive patients (9 women/9 men; 53±11 years; 33±5 kg/m(2)) on stable medications have been included in the study. We monitored finger and brachial BP, heart rate, and MSNA. Without stimulation, BP was 165±31/91±18 mm Hg, heart rate was 75±17 bpm, and MSNA was 48±14 bursts per minute. Acute stimulation with intensities producing side effects that were tolerable in the short term elicited interindividually variable changes in systolic BP (-16.9±15.0 mm Hg; range, 0.0 to -40.8 mm Hg; P=0.002), heart rate (-3.6±3.6 bpm; P=0.004), and MSNA (-2.0±5.8 bursts per minute; P=0.375). Stimulation intensities had to be lowered in 12 patients to avoid side effects at the expense of efficacy (systolic BP, -6.3±7.0 mm Hg; range, 2.8 to -14.5 mm Hg; P=0.028 and heart rate, -1.5±2.3 bpm; P=0.078; comparison against responses with side effects). Reductions in diastolic BP and MSNA (total activity) were correlated (r(2)=0.329; P=0.025). In our patient cohort, unilateral unipolar electric baroreflex stimulation acutely lowered BP. However, side effects may limit efficacy. The approach should be tested in a controlled comparative study.

Indexed as

Drug ResistanceAntihypertensive AgentsBaroreflexBlood PressureCarotid SinusElectric StimulationFemaleHumansHypertensionMaleMiddle AgedMuscle, Smooth, VascularSympathetic Nervous SystemVasodilationAntihypertensive Agentsautonomic nervous systembaroreflexcarotid sinuselectrodesheart ratehypertensionpressoreceptors

Identifiers

PMID26831195
PMCPMC4773922
OpenAlexW2259828901

What OpenQuestion holds

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LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.