Clin Res Cardiol (2022). https://doi.org/10.1007/s00392-022-02002-5

Impact of preoperative exercise haemodynamics in patients with severe tricuspid valve regurgitation undergoing valve surgery
A. Rieth1, C. Hellner1, M. Schönburg2, S. Kriechbaum1, T. Keller3, J. Sperzel1, U. Fischer-Rasokat1, C. W. Hamm4
1Abteilung für Kardiologie, Kerckhoff Klinik GmbH, Bad Nauheim; 2Abteilung für Herzchirurgie, Kerckhoff Klinik GmbH, Bad Nauheim; 3Franz-Groedel-Institut (FGI), Justus-Liebig-Universität Giessen, Bad Nauheim; 4Medizinische Klinik I - Kardiologie und Angiologie, Universitätsklinikum Gießen und Marburg GmbH, Gießen;
Background:
Isolated tricuspid valve surgery (TVS) is considered to be a high-risk procedure in patients with severe tricuspid valve regurgitation (TR). Risk factors for in-hospital mortality include severe right ventricular (RV) dysfunction and severe pulmonary hypertension; however, thresholds for these have not been defined. RV dysfunction may manifest as the inability of the RV to generate pressure during exercise. The primary objective of the present study was to explore associations between preoperative pulmonary haemodynamics (rest / exercise) and in-hospital mortality after TVS.

Methods:
Between July 2010 and May 2018, 56 patients with symptomatic severe TR underwent comprehensive haemodynamic evaluation by right heart catheterization at rest and during exercise or volume challenge (VC; i.e. passive leg raise), if not able to use a bicycle ergometer, before TVS. In-hospital mortality was the primary outcome, and multiple haemodynamic parameters as well as echocardiographic parameters were compared between survivors and nonsurvivors.

Results:
Patients had a median age of 74 years (IQR 69-76), 54% of the patients were female, and 73% presented with symptoms of heart failure according to NYHA class III. Mean tricuspid annular systolic excursion (TAPSE) was 16 mm, mean RV end-diastolic diameter (RVEDD) 47 mm, and median LV ejection fraction 58%. The median NT-proBNP serum level was 1590 pg/ml (IQR 831-3924), and echocardiography revealed that 100% had severe TR (grade III of III). Using the recently proposed scale of I-V, grade III was present in 71%, IV in 20%, and V in 9%. TR was judged as primary in 11 patients. Fifty patients were able to use the bicycle ergometer, and 6 were only able to perform a VC. For statistical evaluation, VC was defined as comparable to 0 watt workload (no-load). Isolated TVS was performed in 36 patients, whereas 20 underwent combined surgery.
The primary outcome of in-hospital death was met by 6 patients (10.7%). Compared with those alive at hospital discharge, the nonsurvivors had 1) a lower increase (delta) in systolic pulmonary artery pressure (sPAP) during exercise or VC (median 9 vs. 14 mmHg, p=0.03); 2) a lower maximum mean PAP (median 28 vs. 38 mmHg, p=0.002); and 3) a lower workload (0 vs 25 W, p=0.01). None of the resting haemodynamic parameters were significantly different between survivors and nonsurvivors, and this was also the case for TAPSE and RVEDD.

Conclusions:
In our cohort of patients with severe TR undergoing TVS, in-hospital mortality was similar to previously reported rates. Echocardiographic parameters of RV function and remodelling were not different between survivors and nonsurvivors, which was also true of haemodynamic resting parameters of pulmonary vasculopathy. Only the ability to perform exercise with workload and the consecutive rise in pulmonary artery pressures were different. Frailty and the incapability of the RV to generate pressure may be significant risk factors for TVS. 

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