Splanchnic Nerve Block Mediated Changes in Stressed Blood Volume in Heart Failure.
congestion
heart failure
splanchnic nerve block
stressed blood volume
sympathetic nervous system
Journal
JACC. Heart failure
ISSN: 2213-1787
Titre abrégé: JACC Heart Fail
Pays: United States
ID NLM: 101598241
Informations de publication
Date de publication:
04 2021
04 2021
Historique:
received:
10
09
2020
revised:
30
11
2020
accepted:
21
12
2020
pubmed:
15
3
2021
medline:
26
10
2021
entrez:
14
3
2021
Statut:
ppublish
Résumé
The authors estimated changes of stressed blood volume (SBV) induced by splanchnic nerve block (SNB) in patients with either decompensated or ambulatory heart failure with reduced ejection fraction (HFrEF). The splanchnic vascular capacity is a major determinant of the SBV, which in turn determines cardiac filling pressures and may be modifiable through SNB. We analyzed data from 2 prospective, single-arm clinical studies in decompensated HFrEF (splanchnic HF-1; resting hemodynamics) and ambulatory heart failure (splanchnic HF-2; exercise hemodynamics). Patients underwent invasive hemodynamics and short-term SNB with local anesthetics. SBV was simulated using heart rate, cardiac output, central venous pressure, pulmonary capillary wedge pressure, systolic and diastolic systemic arterial and pulmonary artery pressures, and left ventricular ejection fraction. SBV is presented as ml/70 kg body weight. Mean left ventricular ejection fraction was 21 ± 11%. In patients with decompensated HFrEF (n = 11), the mean estimated SBV was 3,073 ± 251 ml/70 kg. At 30 min post-SNB, the estimated SBV decreased by 10% to 2,754 ± 386 ml/70 kg (p = 0.003). In ambulatory HFrEF (n = 14) patients, the mean estimated SBV was 2,664 ± 488 ml/70 kg and increased to 3,243 ± 444 ml/70 kg (p < 0.001) at peak exercise. The resting estimated SBV was lower in ambulatory patients with HFrEF than in decompensated HFrEF (p = 0.019). In ambulatory patients with HFrEF, post-SNB, the resting estimated SBV decreased by 532 ± 264 ml/70 kg (p < 0.001). Post-SNB, with exercise, there was no decrease of estimated SBV out of proportion to baseline effects (p = 0.661). The estimated SBV is higher in decompensated than in ambulatory heart failure. SNB reduced the estimated SBV in decompensated and ambulatory heart failure. The reduction in estimated SBV was maintained throughout exercise. (Splanchnic Nerve Anesthesia in Heart Failure, NCT02669407; Abdominal Nerve Blockade in Chronic Heart Failure, NCT03453151).
Sections du résumé
OBJECTIVES
The authors estimated changes of stressed blood volume (SBV) induced by splanchnic nerve block (SNB) in patients with either decompensated or ambulatory heart failure with reduced ejection fraction (HFrEF).
BACKGROUND
The splanchnic vascular capacity is a major determinant of the SBV, which in turn determines cardiac filling pressures and may be modifiable through SNB.
METHODS
We analyzed data from 2 prospective, single-arm clinical studies in decompensated HFrEF (splanchnic HF-1; resting hemodynamics) and ambulatory heart failure (splanchnic HF-2; exercise hemodynamics). Patients underwent invasive hemodynamics and short-term SNB with local anesthetics. SBV was simulated using heart rate, cardiac output, central venous pressure, pulmonary capillary wedge pressure, systolic and diastolic systemic arterial and pulmonary artery pressures, and left ventricular ejection fraction. SBV is presented as ml/70 kg body weight.
RESULTS
Mean left ventricular ejection fraction was 21 ± 11%. In patients with decompensated HFrEF (n = 11), the mean estimated SBV was 3,073 ± 251 ml/70 kg. At 30 min post-SNB, the estimated SBV decreased by 10% to 2,754 ± 386 ml/70 kg (p = 0.003). In ambulatory HFrEF (n = 14) patients, the mean estimated SBV was 2,664 ± 488 ml/70 kg and increased to 3,243 ± 444 ml/70 kg (p < 0.001) at peak exercise. The resting estimated SBV was lower in ambulatory patients with HFrEF than in decompensated HFrEF (p = 0.019). In ambulatory patients with HFrEF, post-SNB, the resting estimated SBV decreased by 532 ± 264 ml/70 kg (p < 0.001). Post-SNB, with exercise, there was no decrease of estimated SBV out of proportion to baseline effects (p = 0.661).
CONCLUSIONS
The estimated SBV is higher in decompensated than in ambulatory heart failure. SNB reduced the estimated SBV in decompensated and ambulatory heart failure. The reduction in estimated SBV was maintained throughout exercise. (Splanchnic Nerve Anesthesia in Heart Failure, NCT02669407; Abdominal Nerve Blockade in Chronic Heart Failure, NCT03453151).
Identifiants
pubmed: 33714749
pii: S2213-1779(21)00001-9
doi: 10.1016/j.jchf.2020.12.006
pmc: PMC9990498
mid: NIHMS1871217
pii:
doi:
Banques de données
ClinicalTrials.gov
['NCT03453151', 'NCT02669407']
Types de publication
Clinical Trial
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
293-300Subventions
Organisme : NHLBI NIH HHS
ID : T32 HL007101
Pays : United States
Organisme : NHLBI NIH HHS
ID : U01 HL125205
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL128526
Pays : United States
Informations de copyright
Copyright © 2021 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Funding Support and Author Disclosures This study was supported by American Heart Association (AHA) Grant, 17MCPRP33460225 and Translating Duke Health Award. Dr. Fudim has received grants from the American Heart Association (Grant 17MCPRP33460225), National Institutes of Health (NIH) T32 grant 5T32HL007101, Mario Family Award, Translating Duke Health Award; and has received consulting fees from AxonTherapies, Daxor, and Galvani. Dr. M.R. Patel has received research grants from HeartFlow, Bayer, Janssen, and the National Heart, Lung, and Blood Institute (NHLBI); and is on advisory boards for HeartFlow, Bayer, and Janssen. Dr. Borlaug has received research funding from National Institutes of Health (NIH)/National Heart, Lung, and Blood Institute (NHLBI) (R01 HL128526, U01 HL125205), AstraZeneca, Corvia, Medtronic, Mesoblast, GlaxoSmithKline, and TENAX; and is on advisory boards/consults for Merck, Novartis, Lilly, and Novo Nordisk. Dr. DeVore has received research funding through his institution from the American Heart Association, Amgen, AstraZeneca, Bayer, Intra-Cellular Therapies, American Regent, Inc., the NHLBI, Novartis, and PCORI; has received consulting fees from Amgen, AstraZeneca, Bayer, CareDx, InnaMed, LivaNova, Mardil Medical, Novartis, Procyrion, scPharmaceuticals, Story Health, and Zoll; and has received nonfinancial support from Abbott for educational activities. Dr. Lopes has received research grants from Bristol-Myers Squibb and Pfizer; has received personal fees from Bristol-Myers Squibb, Pfizer, Boehringer Ingelheim, and Bayer AG; and has received grants from Amgen Inc., GlaxoSmithKline, Medtronic PLC, and Sanofi Aventis outside the submitted work. Dr. Mentz has received research support and honoraria from Abbott, American Regent, Amgen, AstraZeneca, Bayer, Boehringer Ingelheim/Eli Lilly, Boston Scientific, Cytokinetics, Fast BioMedical, Gilead, Medtronic, Merck, Novartis, Roche, Sanofi, and Vifor. Dr. Felker has received research funding from NHLBI, AHA, Amgen, Cytokinetics, Merck; and has received consulting fees from Novartis, Amgen, Cytokinetics, Bristol-Myers Squibb, Innolife, Medtronic, EBR Systems, Cardionomic, SC Pharma, and Myokardia. Dr. Hernandez has received research funding from AstraZeneca, GlaxoSmithKline, Merck, and Novartis; and has received consulting fees from AstraZeneca, Bayer, Boehringer Ingelheim, Boston Scientific, Merck, Novartis, and Pfizer. Dr. Burkhoff has received institutional grants from Abiomed, Ancora Heart, Tenax Therapeutics, and Fire 1; and has received consulting fees from PVLoops LLC and Axon Therapeutics. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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