Splanchnic Nerve Block for Acute Heart Failure

acute heart failure ◼ congestion ◼ splanchnic nerve block T he abdominal vascular compartment is the main storage of intravascular blood volume, and decreased abdominal vascular capacitance has been proposed as a major contributor to the complex pathophysiology of heart failure (HF) in animals and humans.1,2 In HF, as a result of a neurohormonal imbalance, the vascular capacitance (storage space) is decreased and acute sympathetic nerve activation can result in acute volume redistribution 3 from the abdominal compartment to the thoracic compartment (heart and lungs), which increases intracardiac pressures and precipitates HF symptoms (Figure A).The sympathetic nervous system controls the splanchnic compartment via branches from the sympathetic thoracic ganglia (T6 through T11). 4 We have identified the splanchnic nerves as a potential target for treating HF.Patients were enrolled in an approved protocol (ClinicalTrials.gov:NCT02669407) from April to November 2017 at Duke University Medical Center.The protocol was approved by the Institutional Review Board, and all patients provided written informed consent.To qualify for enrollment, patients had to be admitted for acute HF with New York Heart Association class III/IV symptoms.Patients were required to have a pulmonary capillary wedge pressure >15 mm Hg (>12 mm Hg if on inotropes).Before and immediately after the splanchnic nerve block (SNB), all patients were tested for catecholamine levels and N-terminal pro-B-type natriuretic peptide levels, transthoracic echocardiogram, aortic pulse wave velocity (SphygmoCor, AtCor Medical), 6-minute walk test, and Likert shortness of breath questionnaires.After the baseline evaluation, all patients underwent a right heart catheterization (via the internal jugular vein) in the supine position, followed by bilateral SNB (15 mL of 1% lidocaine on each side), at the level of T11-T12, in the prone position using fluoroscopic guidance (Figure B).Expected duration of sympatholytic effects were ≤90 minutes.All pressures were recorded in the supine position.Statistical methods included paired t tests or Wilcoxon rank sum tests.Repeated measures analyses (0, 15, 30, 45, 60, 75, and 90 minutes) with a mixed-effects model were used to compare pulmonary arterial mean, pulmonary capillary wedge pressure, cardiac index, and systemic vascular resistance.Tukey's method was used to adjust for multiple pairwise comparisons of each postprocedure time point to baseline.Five patients underwent the SNB.The average age was 56 years, 4/5 patients were male, and ischemic cardiomyopathy was observed in 2 cases.All patients had acute advanced systolic HF with a left ventricular ejection fraction of ≤20% as assessed by transthoracic echocardiogram.No procedural or hemodynamic complications were observed for 48 hours.Bilateral SNB resulted in a temporary reduction of intracardiac pressures such as mean pulmonary arterial pressures and pulmonary capillary wedge pressure (Figure C).