Temporary hemodynamic improvement after splanchnic nerve block
Splanchnic nerve block for acute heart failureNews - May 26, 2018
//Presented at ESC Heart Failure 2018 by Marat Fudim (Durham, US)//
Introduction and methods
Heart failure (HF) decompensation is a congestion problem. According to the current paradigm, congestion is due to external volume gain. However, fluid overload is insufficient to explain all of decompensation. A new paradigm says that congestion is due to volume redistribution.
The rationale stems from the observation that the splanchnic compartment is the main site of blood storage; 40% of total blood volume is located there. This area is densely innervated by the autonomic nervous system, and a small increase in vasomotor tone results in large fluid shifts.
Increase in sympathetic tone and of splanchnic vascular tone lead to volume redistribution into the thoracic compartment. As this process can be simulated by stimulation of the splanchnic nerve. It is hypothesized that splanchnic nerve block can serve as treatment in heart failure, as it should result in volume redistribution in to the abdominal compartment.
This hypothesis was tested in the current proof of concept study. Bilateral splanchnic nerve block at level T11-L1, with fluoroscopic guidance was performed on day 0, while the patient was lying on the stomach. Safety was evaluated up to 48 hours after the intervention. The primary endpoint was improvement in invasive hemodynamics. 7 Patients of at least 18 years old with a known history of HF, who were hospitalized for HF, and with NYHA class III/IV were included in this small study, of whom 5 underwent the procedure. Exclusion criteria were SBP <90 mmHg, severe fixed pulmonary hypertension, use of oral anticoagulation or DAPT, spine deformity or wedge pressure ≤15 mmHg (or ≤12 mmHg on inotropes).
- Mean pulmonary arterial pressure (MPAP) dropped significantly within 15 minutes (baseline MPAP: 46 mmHg, 95%CI: 40-52, at 30 minutes: 37 mmHg, 95%CI: 31-43, P<0.01). At 90 minutes the effect was slightly attenuated (MPAP: 41, 95%CI: 36-47, P=0.02.
- Pulmonary capillary wedge pressure (PCWP) was reduced as compared with baseline (mean PCWP: 28 (95%CI: 21-36), at 30 minutes: 21 (95%CI: 14-28) and at 90 minutes: 24 (95%CI: 17-31).
- No safety issues were noted.
- Cardiac index showed a peak effect at 30 minutes (2.54 L/min/m2, 95%CI: 2.17-2.91) as compared with baseline (1.92 L/min/m2, 95%CI: 1.55-2.29, P<0.01). At 90 minutes, the effect (CI: 1.98 L/min/m2, 95%CI: 1.62-2.35, P=0.65) no longer differed significantly from baseline.
- Mean arterial pressure also showed a peak effect at 30 minutes (72 mmHg, 95%CI: 59-84, P<0.01) as compared with baseline (89 mmHg, 95%CI: 77-102), with an attenuated effect at 90 minutes (MAP: 80, P=0.01).
- The 6-minute walking test was non-significantly increased by 31.2 meters (P=0.11), and an immediate improvement in shortness of breath (Likert scale) was observed.
- Serum levels of epinephrine, norepinephrine and NT-proBNP levels and pulse wave velocity were not significantly modified after the intervention.
This small first-in-man proof of concept study had reassuring initial results. No procedural complications occurred, when applying splanchnic nerve block, and improved hemodynamics were observed, as well as improved patient symptoms and physiologic markers. A drawback of this study is that the number of patients was limited, thus larger, placebo-controlled studies are needed.
Discussant J.G.F. Cleland (Glasgow, UK) thought this concept reflects a good idea. However, he noted that these patients did not have acute HF. One cannot do an intervention in AHF patients while lying face down. Thus, these patients likely had decompensated chronic HF.
While the data look credible, the effect of the intervention lasts only 90 minutes. How is it possible to give a prolonged splanchnic block? Many questions remain to be answered to know how this might work in practice. Dr. Cleland said this was an interesting, fantastic concept, and well-executed, and the results make him wonder what the next step will be.
Our reporting is based on the information provided at the ESC Heart Failure 2018 congress