Author + information
- Received February 27, 2020
- Revision received April 1, 2020
- Accepted April 1, 2020
- Published online June 10, 2020.
- Marat Fudim, MD, MHSa,b,
- Richard L. Boortz-Marx, MDc,
- Arun Ganesh, MDc,
- Adam D. DeVore, MD, MHSa,b,
- Chetan B. Patel, MDa,
- Joseph G. Rogers, MDa,b,
- Aubrie Coburn, MSa,
- Inneke Johnson, PhDa,
- Amanda Paul, MSa,
- Brian J. Coyne, MEda,
- Sunil V. Rao, MDa,b,
- J. Antonio Gutierrez, MD, MHSa,
- Todd L. Kiefer, MDa,
- David F. Kong, MDa,b,
- Cynthia L. Green, PhDb,d,
- W. Schuyler Jones, MDa,b,
- G. Michael Felker, MD, MHSa,b,
- Adrian F. Hernandez, MD, MHSa,b and
- Manesh R. Patel, MDa,b,∗ ()
- aDivision of Cardiology, Department of Medicine
- bDuke Clinical Research Institute
- cDivision of Pain Medicine, Department of Anesthesiology
- dDepartment of Biostatistics and Bioinformatics;, Duke University School of Medicine, Durham, North Carolina
- ↵∗Address for correspondence:
Dr. Manesh Patel, Duke University Hospital, 2301 Erwin Road, Durham, North Carolina 27710.
Objectives We hypothesized that splanchnic nerve blockade (SNB) would attenuate increased exercise-induced cardiac filling pressures in patients with chronic HF.
Background Chronic heart failure (HF) is characterized by limited exercise capacity driven in part by an excessive elevation of cardiac filling pressures.
Methods This is a prospective, open-label, single-arm interventional study in chronic HF patients. Eligible patients had a wedge pressure ≥15 mm Hg at rest or ≥25 mm Hg with exercise on baseline right heart catheterization. Patients underwent cardiopulmonary exercise testing with invasive hemodynamic assessment, followed by percutaneous SNB with ropivacaine.
Results Nineteen patients were enrolled, 15 of whom underwent SNB. The average age was 58 ± 13 years, 7 (47%) patients were women and 6 (40%) were black. Left ventricular ejection fraction was ≤35% in 14 (93%) patients. No procedural complications were encountered. SNB reduced mean pulmonary arterial pressure at peak exercise from 54.1 ± 14.4 (pre-SNB) to 45.8 ± 17.7 mm Hg (p < 0.001) (post-SNB). Similarly, SNB reduced exercise-induced wedge pressure from 34.8 ± 10.0 (pre-SNB) to 25.1 ± 10.7 mm Hg (p < 0.001) (post-SNB). The cardiac index changed with peak exercise from 3.4 ± 1.2 (pre-SNB) to 3.8 ± 1.1 l/min/m2 (p = 0.011) (post-SNB). After SNB, patients exercised for approximately the same duration at a greater workload (33 ± 24 W vs. 50 ± 30 W; p = 0.019) and peak oxygen consumption VO2 (9.1 ± 2.5 vs. 9.8 ± 2.7 ml/kg/min; p = 0.053).
Conclusions SNB reduced resting and exercise-induced pulmonary arterial and wedge pressure with favorable effects on cardiac output and exercise capacity. Continued efforts to investigate short- and long-term effects of SNB in chronic HF are warranted. Clinical Trials Registration (Abdominal Nerve Blockade in Chronic Heart Failure; NCT03453151).
Dr. Fudim has received grants from the American Heart Association Grant (17MCPRP33460225), the National Institutes of Health (NIH) (T32 grant 5T32HL007101), the Mario Family Award, and the Translating Duke Health Award; and has received personal fees from Coridea, AxonTherapies, Daxor, Edwards Lifesciences, and Galvani. Dr. DeVore has received grants from the American Heart Association, Amgen, Bayer, IntraCellular Therapies, Lutipold Pharmaceuticals, the National Heart, Lung, and Blood Institute (NHLBI), Novartis, and Patient Centered Outcomes Research Institute; and has received personal fees from Amgen, AstraZeneca, Bayer, InnaMed, LivaNova, Mardil Medical, Novartis, Procyrion, scPharmaceuticals, Zoll, and Abbott. Dr. Gutierrez has received personal fees from Amgen and Janssen Therapeutics. Dr. Jones has received grants from the Agency for Healthcare Research and Quality, AstraZeneca, American Heart Association, Bristol-Myers Squibb, the Doris Duke Charitable Foundation, Patient Centered Outcomes Research Institute; and has received personal fees from the American College of Radiology and Daiichi Sankyo. Dr. Felker has received grants from the NHLBI, the American Heart Association, Amgen, Merck, Cytokinetics, and Roche Diagnostics; and has received personal fees from Novartis, Amgen, Bristol-Myers Squibb, Cytokinetics, Medtronic, Cardionomic, Relypsa, V-Wave, Myokardia, Innolife, EBR Systems, Arena, Abbott, Sphingotec, Roche Diagnostics, Alnylam, LivaNova, Windtree Therapeutics, Rocket Pharma, and SC Pharma. Dr. Hernandez has received grants from AstraZeneca, GlaxoSmithKline, Merck, and Novartis; and has received personal fees from AstraZeneca, Bayer, Boehringer Ingelheim, Boston Scientific, Merck, Novartis, and Pfizer. Dr. M.R. Patel has received grants from HeartFlow, Bayer, Janssen, and the NHLBI; and has been on advisory boards for HeartFlow, Bayer, and Janssen. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Heart Failure author instructions page.
- Received February 27, 2020.
- Revision received April 1, 2020.
- Accepted April 1, 2020.
This article requires a subscription or purchase to view the full text. If you are a subscriber or member, click Login or the Subscribe link (top menu above) to access this article.