29 Jan 2026
Impact of guideline-directed medical therapy on long-term outcome after tricuspid TEER
This case has been accredited by EBAC with 1 CME credit
A 79-year-old woman with advanced right heart failure (NYHA III) was referred after repeated hospitalisations for decompensation despite optimal medical therapy. Echocardiography revealed torrential functional tricuspid regurgitation with suitable anatomy for T-TEER. Given her high surgical risk (TRISCORE 7/12) and borderline pulmonary hypertension, how would you treat?
Authors
Learning objectives
- To know the impact of T-TEER on long-term outcome
- To know about interventional strategies in T-TEER: Clover vs. bicuspidalization
- To understand the importance of medical therapy in postprocedural care
Clinical presentation
A 79-year-old female presented in Ulm University heart valve centre with advanced right heart failure symptoms: NYHA class III dyspnea, lower limb edema. She was a healthy elderly woman until 6 months earlier, when she was hospitalised repeatedly for decompensated heart failure in another hospital.
Relevant comorbidities included HFpEF, impaired right ventricular function (TAPSE 17 mm), type 2 diabetes mellitus, chronic kidney disease and arterial hypertension.
Pathological lab values:
eGFR | 39 ml/min/1.73 m² |
NT-proBNP | 2,104 pg/ml |
All other lab values were within normal range, including liver function parameters.
Medication:
Apixaban | 5 mg | 1-0-1 |
Candesartan | 8 mg | 0-0-1 |
Torasemid | 20 mg | 2-1-0 |
Spironolacton | 25 mg | 1-0-0 |
Echocardiographic assessment
Transgastric leaflets
Hemodynamic assessment by right heart catheterisation
- sPAP: 62 mmHg
- mPAP: 33 mmHg
- PVR: 2.8 WU
- PCWP: 16 mmHg
Evaluation for tricuspid intervention
Despite optimal medical therapy, the patient remained symptomatic. Heart Team discussion highlighted borderline pulmonary hypertension (sPAP 62 mmHg) as a potential negative prognostic factor. However, since PVR was < 3 WU, this was not considered a contraindication.
The TRISCORE was 7/12, indicating a 34% predicted mortality for isolated tricuspid surgery. Thus, the patient was deemed inoperable but suitable for percutaneous tricuspid intervention.
The Heart Team further discussed tricuspid anatomy derived from echocardiography as shown above and qualified according to Hausleiter J et al. (JACC 2025) in the feasible anatomy for T-TEER group, according to the following case criteria:
- Torrential functional TR with septolateral coaptation gap ≤ 7 mm
- Regurgitant jets: anteroseptal and posteroseptal
- Leaflet morphology: suitable with identifiable segmentations of posterior and septal leaflets
- No CIED leads present
- Echocardiographic visualisation: adequate
The interventional team decided to perform T-TEER using two TriClip XT devices.
- Clover technique: First device implanted anterior-septal, second posterior-septal, to address both regurgitant jets
- Bicuspidalization technique: Bicuspidalization with two anterior-septal devices (“zipping technique”)
We aimed for a Clover technique in order to reduce the posterior regurgitation jet adequately. However, bicuspidalization also often reduces posterior regurgitation jets due to annular reduction effects of TEER and subsequent reverse remodelling of the right ventricle.
After the first TriClip XT implantation, sufficient TR reduction was achieved with only mild residual TR posterior to the first TEER device.
Despite this adequate TR reduction, we aimed for a second TEER device implantation in Clover technique.
After second TriClip XT implantation, trivial (<I) TR was achieved. 4 days later, the patient was discharged with the following lab values and medication:
Lab values:
| before T-TEER | 4 days after T-TEER |
eGFR | 39 ml/min/1.73 m² | 36 ml/min/1.73 m² |
NT-proBNP | 2,104 pg/ml | 1,536 pg/ml |
Medication:
Apixaban | 5 mg | 1-0-1 |
Candesartan | 16 mg | 0-0-1 (uptitrated) |
Torasemid | 20 mg | 2-1-0 |
Spironolacton | 25 mg | 1-0-0 |
Follow-Up
2 months after T-TEER
After discharge, the patient’s symptoms (both edema and dyspnea) improved rapidly and diuretics were reduced immediately and terminated within the first month.
After 2 months, the patient experienced recurrence of mild dyspnea at exertion (NYHA II) and mild edema. Tricuspid regurgitation was now moderate and NT-proBNP increased.
Modifications of the diuretics immediately and during short-term follow-up after tricuspid interventions should be done with caution and only if clinically indicated, since alterations of the fluid status might impact on TR result.
TTE 2 months after T-TEER
Lab values:
| before T-TEER | discharge after T-TEER | 2 months after T-TEER |
eGFR | 39 ml/min/1.73 m² | 36 ml/min/1.73 m² | 40 ml/min/1.73 m² |
NT-proBNP | 2,104 pg/ml | 1,536 pg/ml | 4,287 pg/ml |
Medication:
Apixaban | 5 mg | 1-0-1 | 1-0-1 |
Candesartan | 16 mg | 0-0-1 | 0-0-1 |
Spironolacton | 25 mg | 1-0-0 | 1-0-0 |
Torasemid | 20 mg | 2-1-0 | (was terminated)
|
We recommended starting with initial dose of Torasemid 20 mg 2-1-0 and continuing for the next months up to 1 year.
2 years after T-TEER
The patient presented with only mild dyspnea (NYHA II) and no edema. She had good quality of life. In the meantime, approximately 1 year after T-TEER, Torasemid was halved as suggested.
TTE 2 years after T-TEER
Excellent long-term TR result was achieved with mild TR. TAPSE improved to 19 mm, but left ventricular function slightly decreased (LVEF from 58% to 53%).
Lab values:
| before T-TEER | Discharge after T-TEER | 2 months after T-TEER | 2 years after T-TEER |
eGFR | 39 ml/min/m2 | 36 ml/min/m2 | 40 ml/min/m2 | 42 ml/min/m2 |
NT-proBNP | 2,104 pg/ml | 1,536 pg/ml | 4,287 pg/ml | 921 pg/ml |
Medication:
|
| before T-TEER | After discharge | 2 months after T-TEER | 2 years after T-TEER |
Apixaban | 5 mg | 1-0-1 | 1-0-1 | 1-0-1 | 1-0-1 |
Candesartan | 16 mg | 0-0-1 | 0-0-1 | 0-0-1 | 0-0-1 |
Spironolacton | 25 mg | 1-0-0 | 1-0-0 | 1-0-0 | 1-0-0 |
Torasemid | 20 mg | 2-1-0 | (terminated) | 2-1-0 | 1-0-0 |
Empagliflozin | 10 mg |
|
|
| 1-0-0 |
We recommended adding SGLT2-inhibitor for HFpEF with NYHA II.
3 years after T-TEER
In the long-term follow-up, after T-TEER symptoms further improved. The patient had no relevant dyspnea (NYHA I) and no edema. Torasemid was further reduced.
TTE 3 years after T-TEER:
Echocardiographic assessment demonstrated trivial TR (<I), recovered LVEF to 58% and preserved right ventricular function were observed.
Conclusion
- Both Clover and bicuspidalization techniques are feasible for T-TEER with multiple devices
- Diuretic management in the early post-interventional period is crucial to maintain durable TR reduction. Premature withdrawal may result in functional recurrence
- Continuous optimisation of guideline-directed medical therapy (GDMT) is essential for long-term outcome and prognosis
Supported through a restricted educational grant from Abbott Germany
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1 comment
In general, the valvular pathologies are difficult to treat and the medical treatment and some kind of interventional procedure to reduce the severity of the regurgitation are complementary to each other rather than mutually exclusive. Medical treatment should therefore be continued during the initial months after T-TEER and should only be tried to taper down of taper off later on when the patient tolerates.