Increased muscle sympathetic nerve activity (MSNA) is associated with poor prognosis in patients with different stages of chronic heart failure. The improving effect of interventional mitral regurgitation therapy on increased MSNA in patients with chronic heart failure has been previously shown. In current practice, >80% of patients undergoing interventional repair suffer from functional tricuspid regurgitation (FTR) due to right ventricle dilation and annulus dilation following with coaptation gap. MSNA in patients with symptomatic FTR has not been evaluated yet, and the effect of interventional tricuspid valve repair (ITVR) on MSNA is unknown. 

We prospectively included 30 patients with ≥severe FTR, who underwent ITVR. All patients underwent comprehensive echocardiography inclusively blood tests before and 12 months after the procedure.

MSNA was determined by microneurography, and continuous non-invasive blood pressure was done for the assessment of arterial baroreflex gain. Microneurography was performed as described previously; a tungsten needle (200 µm) was introduced into the nervus peroneus longus close to the caput fibuli to record multiunit postganglionic sympathetic activity. There are two MSNA-defining parameters - burst frequency (burst/min) and burst incidence (burst/beats). The baroreflex gain is a parameter for the severity of arterial sympathoexcitation, which is calculated as the ratio between burst incidence and mean value of continuous diastolic blood pressure.

30 patients (76.4 ± 6.9 years, 46.66% female) with highly symptomatic (100 % NYHA functional class > II) FTR (severe TR: 43.33%, massive TR: 26.66%, torrential TR 30%; effective regurgitant orifice area 0.63 ± 0.7cm, vena contracta width 0.9 ± 0.3 cm, regurgitant volume 76.5 ± 11.6 ml/beat) were prospectively included. Echocardiographically determined left ventricular function (LVEF) was 55.5 ± 11.3%, serum level of NT pro-BNP was 2659.3 ± 2214.3pg/dl. There was no relevant mitral regurgitation at baseline (MR ≤ moderate). 

At baseline, we found a significantly increased MSNA (121.41 ± 23.4 burst/min, 143.4 ± 16.4 bursts/beats, average value about 60 burst/min), and impaired sympathetic baroreflex gain (2.3± 0.4 bursts/mmHg). MSNA was found to be significantly correlated with the serum level of NT pro-BNP (r=0.79, p=0.001), and there was no relevant correlation with renal function at baseline (r=0.1, p=0.3). 

In all patients, interventions were successful with a TR reduction to TR<severe or at least one grade TR reduction without any major intervention related complication. 

At FU, we found sustained TR reduction (85% TR<severe) and improved functional capacity (82% NYHA <III). Left ventricular function (LVEF: 55.5 ± 11.3% to 56.3 ± 12.3%, p=0.8) and the severity of MR (≤moderate) stayed unchanged. MSNA (121.41 ± 23.4 burst/min to 77.2±13.3 burst/min, p=0.001; 143.4 ± 16.4 burst/beats to 98.32 ± 24.3 burst/beats p=0.04) and baroreflex gain (2.3 ± 045 burst/mmHg to 4.3 ± 2.1 burst/mmHg, p=0.04) were found to be significantly improved at FU.

To the best of our knowledge, this is the first study to show increased MSNA as well as decreased arterial baroreflex function in patients with FTR. MSNA correlated well with levels of NT-pro BNP but was independent of renal function. Additionally, ITVR improves MSNA and baroreflex gain, which might be accounted for a pathomechanism of postinterventional clinical improvements