Clin Res Cardiol (2023). https://doi.org/10.1007/s00392-023-02180-w

The effect of SGLT-2 inhibitors on sympathetic nerve activity in patients with chronic heart failure
C. Öztürk1, L. Nagel1, G. Nickenig1, M. Weber1, C. Hammerstingl2, M. U. Becher3
1Medizinische Klinik und Poliklinik II, Universitätsklinikum Bonn, Bonn; 2Innere Medizin/Kardiologie, Eduardus-Krankenhaus, Köln; 3Klinik für Kardiologie und internistische Intensivmedizin, Städt. Klinikum Solingen gGmbH, Solingen;

Background:

The improving and prognostic relevant effect of SGLT-2 inhibitors in patients with chronic heart failure has been previously shown. In this study, we aimed to evaluate the effect of SGLT-2 inhibitors on sympathetic nerve activity in patients with chronic heart failure. 

 

Methods:

We prospectively included 30 patients with chronic heart failure (LVEF< 50%). All patients underwent microneurography, comprehensive echocardiography inclusively blood tests before and 12 months after the start with a SGLT-2 inhibitor.

Microneurography was performed to assess sympathetic nerve activity as described previously; after local disinfection, a tungsten needle (200 µm) was introduced into the nervus peroneus longus close to the caput fibuli to record multiunit postganglionic sympathetic activity. Burst frequency (burst/min) and burst incidence (burst/beats) were generated from recorded data as MSNA-defining parameters.

 

Results:

30 patients (69.4 ± 12.3 years, 32 % female) with chronic heart failure (LVEF: 41.26 ± 8.32 %) without any relevant valvular disease or cardiac decompensation were prospectively included. Medical heart failure therapy was comparable between groups at baseline and at follow-up. 

At baseline, we found a significantly increased MSNA (101.3 ± 13.8 burst/min, 111.5 ± 8.9 bursts/beats, average value about 60 burst/min). 

Left ventricular function (LVEF: 46.23 ± 13.4%, p=0.05) was found to be significantly increased at follow-up. Correspondingly, we found improved MSNA (101.3 ± 13.8 burst/min to 87.8 ±18.2 burst/min, p=0.003; 111.5 ± 8.9 burst/beats to 91.1 ± 17.7 burst/beats p=0.05) at follow-up.

We documented no major events (mortality or hospitalization due to cardiac decompensation) during the follow-up.

 

Conclusion:

Sympathetic nerve activity was found to be significantly decreased under therapy with SGLT-2 inhibitor in patients with chronic heart failure in addition to improving effect on left ventricular function. 


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