Explore the vast range of titles available.

The initiation of sodium–glucose cotransporter 2 (SGLT2) inhibitor treatment was shown to reduce pulmonary artery pressure (PAP) in New York Heart Association (NYHA) class III heart failure (HF) patients with an implanted PAP sensor. We aimed to investigate the impact of SGLT2-I initiation on pulmonary vascular resistance (PVR), pulmonary capillary wedge pressure (PCWP), pulmonary arterial capacitance (PAC), and right ventricle (RV) to PA (RV-PA) coupling in a pilot cohort of HF with preserved/mildly reduced ejection fraction (HFpEF/HFmrEF) patients and whether PVR and PCWP can be serially calculated non-invasively using PAP sensor data during follow-up. Methods: Right heart catheterization parameters (PVR, PCWP, and PAC) were obtained at sensor implantation and echocardiographic assessments (E/E’, RV-PA coupling, and RV cardiac output) were made at baseline and every 3 months. SGLT2 inhibition was initiated after 3 months of telemedical care. Three methods for calculating PVR and PCWP were compared using Bland–Altman plots and Spearman’s correlation. Results: In 13 HF patients (mean age 77 ± 4 years), there were no significant changes in PAP, PVR, PCWP, RV-PA coupling, or PAC over 9 months (all p-values > 0.05), including after SGLT2-I initiation. PVR values were closely correlated across the three methods (PVRNew and PVRNew Tedford (r = 0.614, p < 0.001), PVREcho and PVRNew Tedford (r = 0.446, p = 0.006), and PVREcho and PVRNew (r = 0.394, p = 0.016)), but PCWP methods lacked reliable association (PCWPEcho and PCWPNew (r = 0.180, p = 0.332). Conclusions: No changes in cardiopulmonary hemodynamics were detected after hemodynamic telemonitoring either prior to or following SGLT2-I initiation. Different PVR assessment methods yielded comparable results, whereas PCWP methods were not associated with each other. Further investigations with larger cohorts including repeated right heart catheterization are planned.

Background/Objectives: Patients with New York Heart Association (NYHA) class III heart failure (HF) suffer from frequent hospitalizations. Non-invasive pulmonary artery pressure (PAP) sensor-guided HF care has been shown to reduce hospitalizations. However, it is unknown whether the PAP changes prior to hospitalization differ between clinical right, left or global cardiac decompensation. Methods: Sensor-derived PAP data and HF hospitalization records from 41 patients with NYHA class III HF were classified retrospectively into predominantly left, right or global decompensation. Linear mixed-effect regression models were used for statistical evaluations of the PAP in selected hospitalizations for which admission was at least 28 days after the last admission and 14 days after the last hospital discharge and with readings in between. Results: During 24.4 months of follow-up, 127 hospitalizations in 38 patients were evaluated. The global cardiac decompensation (n = 13) had the highest PAP before hospitalization, followed by left-sided (n = 20) decompensation. Patients with right-sided decompensation (n = 9) had comparable PAP values before hospitalization to the cohort without any cardiac decompensation (n = 85). The diastolic PAP showed a significant increase of 0.035 mmHg/day (p = 0.0097) in left-sided decompensation and of 0.13 mmHg/day (p < 0.0001) in global cardiac decompensation, whereas no significant change in the diastolic PAP occurred prior to the right-sided decompensation. The baseline right ventricular function and right ventricle–pulmonary arterial coupling (TAPSE/PASP ratio) were impaired in patients with subsequent global cardiac decompensation. Conclusion: PAP telemonitoring-guided therapy can reliably detect early signs of left and global cardiac decompensation but may be limited in detecting right-sided cardiac congestion. The routine assessment of RV–PA coupling may improve the detection of global cardiac decompensation, as severe impairments could indicate impending deterioration. In contrast, monitoring the RV contractility may aid in identifying isolated right-sided congestion and imminent decompensation.

Aim Chronic heart failure (HF) is a frequent comorbidity in elderly patients undergoing major non-cardiac surgery with increasing prevalence. This trial aims to evaluate a new interdisciplinary, multimodal and individually optimised treatment strategy in patients with established or at risk for HF throughout the entire perioperative period. Methods The PeriOP-CARE HF trial is a prospective, multicentre, randomised, controlled and interventional trial. The primary hypothesis is that an interdisciplinary, intersectoral and standardised approach to the preoperative evaluation, optimisation and perioperative management of patients aged ≥ 65 years undergoing non-cardiac surgery with intermediate or high surgical risk and preoperative N-terminal pro-brain natriuretic peptide levels ≥ 450 pg/mL, will reduce postoperative morbidity. The preoperative evaluation includes clinical evaluations by anaesthesiologists and cardiologists, electrocardiography and echocardiography, as well as a discussion of these findings by a perioperative management team, where all involved specialities, including the speciality surgeon, will decide the perioperative treatment strategy for each patient. Intraoperative strategies include individualised haemodynamic optimisation. The interdisciplinary team and specialised HF nurses will screen patients for HF-related postoperative complications. The primary end point will be a composite morbidity end point, comprising any rehospitalisation, acute kidney injury, suspected or proven bacterial infection requiring treatment and acute decompensated HF at postoperative day 90. Conclusion The new treatment form can potentially reduce the morbidity burden after major non-cardiac surgery in patients with known or unknown HF. If the PeriOP-CARE HF trial yields positive results, the treatment of patients with HF undergoing major non-cardiac surgery could be considerably improved. Trial Registration clinicaltrials.gov: NCT06381427, registered April 24, 2024.