https://doi.org/10.1007/s00392-025-02625-4
1Bremer Institut für Herz- und Kreislaufforschung (BIHKF) Bremen, Deutschland; 2Universitätsklinikum Schleswig-Holstein Medizinische Klinik II / Kardiologie, Angiologie, Intensivmedizin Lübeck, Deutschland
Background: Transcatheter edge-to-edge repair (T-TEER) for severe tricuspid regurgitation (TR) emerged as a novel treatment option for patients not amenable for surgery. However, knowledge regarding independent risk factors for worse prognosis is rarely available.
Objective: The study sought to investigate the impact of invasively derived cardiac power efficiency (CPE) on 1-year outcome in patients with severe symptomatic TR undergoing T-TEER.
Methods: Consecutive patients with severe TR who underwent T-TEER between 08/2020 to 05/2024 were included and followed prospectively. Baseline clinical and invasive hemodynamic variables, changes in echocardiographic parameters and New York Heart Association (NYHA) functional class, periprocedural and in-hospital major adverse events were assessed. Primary endpoint was defined as all-cause mortality at 12 ± 9 months after T-TEER. A multivariable Cox proportional-hazards regression analysis was performed to identify independent risk factors for all-cause mortality. CPE was calculated as: (cardiac power output (CPO) / body surface area) / pulmonary capillary wedge pressure = W × mmHg/m².
CPO is calculated as: (cardiac output × mean arterial pressure) / 451 = W. Receiver operator characteristic (ROC) analysis was used to determine discriminative capacity of CPE. The prognostic value of CPE threshold was tested using Kaplan-Meier analysis.
Results: 147 patients (mean age 81 ± 5.9 years, 55 % women) at high operative risk (LogEuro-Score 13 %; 8 %-23 %) underwent T-TEER for severe TR. Primary endpoint occurred in 37 patients (28 %). ROC curve analysis demonstrated that CPE was associated with an area under the curve of 0.67 (95 % confidence interval [CI] 0.57-0.77). CPE threshold of 0.023 W × mmHg/m² (from ROC curve analysis) was associated with 84 % sensitivity and 48 % specificity for all-cause mortality. Survival was significantly higher in the CPE > 0.023 W × mmHg/m² group compared to those with CPE ≤ 0.023 W × mmHg/m² (12 % vs. 39 %; log-rank p < 0.001). In Cox regression analysis CPE threshold of 0.023 W × mmHg/m² was an independent predictor for all-cause mortality (Hazard ratio 3.55; 95 % CI 1.2-10.5; p < 0.022).
Conclusions: CPE is associated with mortality among patients undergoing T-TEER for severe TR.
Therefore, this hemodynamic predictor might be useful in risk stratification of T-TEER candidates with severe TR.