Assessment of PVR and other hemodynamic parameters in HFpEF and HFmrEF patients with new-onset SGLT-2 inhibitor: Comparison of PAP sensor-derived and echo-based approaches

E. Herrmann (Gießen)¹, M. Guckert (Friedberg)², D. Grün (Frankfurt am Main)³, T. Keller (Bad Nauheim)⁴, S. T. Sossalla (Gießen)¹, B. Aßmus (Gießen)^1
1Universitätsklinikum Gießen und Marburg GmbH Medizinische Klinik I - Kardiologie und Angiologie Gießen, Deutschland; ²Technische Hochschule Mittelhessen - University of Applied Sciences Institute of Mathematics, Natural Sciences and Data Processing Friedberg, Deutschland; ³CCB am AGAPLESION BETHANIEN KRANKENHAUS Medizinisches Versorgungszentrum Frankfurt am Main, Deutschland; ⁴Justus-Liebig-Universität Giessen Medizinische Klinik I, Kardiologie Bad Nauheim, Deutschland

Background: Initiation of sodium-glucose cotransporter 2 inhibitor (SGLT-2-I) treatment was shown to reduce pulmonary artery pressure (PAP) in unselected NYHA class III heart failure (HF) patients being monitored with an implanted PAP sensor. Here we investigated whether SGLT-2-I initiation also has an impact on pulmonary vascular resistance (PVR), pulmonary capillary wedge pressure (PCWP), pulmonary arterial capacitance (PAC), and right ventricle to pulmonary artery (RV-PA) coupling in a small, single-center registry of HF patients with preserved or mildly reduced ejection fraction (HFpEF or HFmrEF).

 

Methods: Right heart catheter hemodynamic measurements including PVR, PCWP, and PAC were obtained at the time of sensor implantation, and serial non-invasive echocardiographic assessment of E/E’, RV-PA coupling, and RV cardiac output assessment was carried out at baseline and every 3 months thereafter. To extend the information provided by pure PAP monitoring, by using a combination of echo-derived stroke-volume and sensor-derived PAP and pulse-pressure values, we calculated PVR and PCWP by 3 different methods. The results were then compared using Bland-Altman plots and Spearman’s correlation. A descriptive analysis was performed for 13 patients. 

 

Results: Within our cohort of 13 optimally managed HF patients (mean age 77±4 years, median LVEF 60 [53-60] years, cardiac index 1.9±0.3) during a total of 9 months of PAP monitoring, the diastolic, systolic, and mean PAP remained stable (DPAP diastolic: 1±3, mmHg, p=0.672; DPAP mean: 1±5 mmHg, p=0.690; DPAP systolic 1±7 mmHg, p=0.771) and showed no change following either PAP sensor implantation or SGLT-2-I treatment initiation. There were also no differences in PVR, PCWP, RV-PA coupling, or PAC. We identified a close association between the 3 different techniques of assessing PVR (PVR_New and PVR_{New Tedford} r=0.614, p<0.001; PVR_New and PVR_echo r=0.394, p=0.016; PVR_{New Tedford} and PVR_echo r=0.446, p=0.006), whereas the 2 methods of PCWP calculation did not show any reliable correlation (PCWP_New and PCWP_Echo r=0.180, p=0.332). 

 

Conclusions: No changes in PAP, PVR, PCWP, RV-PA coupling, or PAC were detected in the first 3-month time interval from PAP sensor implantation to SGLT-2-I initiation or from SGLT-2-I onset to the 6-month follow-up. The non-invasive measurement of PVR and PCWP using the resistance/capacitance method, with and without correction by Tedford in cases with elevated PCWP, and the echo-based approach are both feasible. The 3 different techniques for PVR assessment yielded comparable results, whereas the 2 methods for assessing PCWP showed disparate results. Further investigations in larger trials are needed to confirm these findings, including validation by right heart catheterization. 

 

Keywords: heart failure with preserved ejection fraction, SGLT-2 inhibitors, pulmonary artery pressure, RV-PA coupling, pulmonary vascular resistance