Navigating multiple valvular heart disease in a patient with heart failure

Clinical presentation (December 2024)

An 82-year-old male (BMI of 23.7 kg/m² - BSA 1.75) with arterial hypertension, type 2 diabetes mellitus, previous smoking habit, and occasional alcohol consumption, presented with increased shortness of breath, NYHA class III, and a history of frequent hospital admissions related to heart failure.

Physical examination

Vital signs were within normal range: blood pressure was 140/80 mmHg; heart rate was 86 beats/min; respiratory rate was 15 breaths/min; and oxygen saturation was 98 % on oxygen therapy via nasal cannula at 2 L/min. 

The cardiac examination revealed an irregular cardiac activity, with a systolic murmur (4/6L) over all auscultation areas, radiating to the carotids. Signs of fluid overload were present: bilateral crackles on chest auscultation with bilateral lower limb edema and estimated jugular venous pressure. 

No relevant neurological alterations.

Initial work-up

EKG: atrial fibrillation with paced ventricular rhythm at rate 50 bpm.

Lab tests: 
 

• Hemoglobin: 11,4 g/dl
• White blood cell count: 4,9 x 109/L
• Platelets: 124 x 109/L
• Creatinine: 1.16 mg/dl
• Alanine aminotransferase: 87 U/L
• Alkaline phosphatase: 75 U/L
• Total bilirubin: 1 µmol/L
• NT-ProBNP: 3456 ng/L

Chest x-ray: mild bilateral pleural effusion with hilar-perihilar congestion; no evidence of parenchymal consolidation.

Transthoracic echocardiogram at hospital admission (Figure 1):

• Left ventricle: normal dimensions with global hypokinesia without segmental wall motion abnormalities resulting in a moderate reduction of the biplane ejection fraction (LVEF 35 %). 
• Right ventricle: normal size, global and longitudinal systolic function (TAPSE 22 - S’ TDI 10 cm/sec). 
• Severe left and right atrial volume dilation (LAVi 68 ml/m² - RAVi 73 ml/m²)
• Severe aortic stenosis with mild aortic regurgitation 
   
  1. Anatomy: tricuspid valve
  2. Etiology: calcific degeneration
  3. Severity: G med 20 mmHg; AVA 0.78 cm²; AVAi 0.65 cm²/m²; DVI 0.22; SVi: 30 mL/m²
  4. Hemodynamic phenotype: classic low-flow low-gradient AS
  5. Cardiac damage staging: stage 3
• Severe tricuspid regurgitation (TR)
• Systolic PAP (sys-PAP) 55 mmHg
• Dilated IVC (22 mm), collapsible

Powered by Quiz Maker 

Based on the clinical presentation and initial diagnostic work-up, the patient was diagnosed with acute decompensated heart failure due to multiple valvular heart diseases (VHD). Treatment with intravenous furosemide 120 mg was started^1,2.

The diagnostic work-up of our patient continued with coronary angiography, which showed no significant coronary artery disease (Figure 2). The cardiac computed tomography was performed to complete the diagnostic work-up of severe AS (aortic valve calcium score » 2000 HU, Figure 2) and to proceed with Transcatheter Aortic Valve Implantation (TAVI) procedural planning³ (Figure 2).

Given the acute decompensated heart failure due to multiple severe VHD, the patient was discussed in the Heart Team weekly meeting. The final decision was to proceed first with TAVI and reassess the severity of tricuspid regurgitation at strict follow-up.

 The patient was then discharged in stable NYHA class II. Dapagliflozin 10 mg OD was also started during the hospitalisation.

TAVI procedure (Feb. 2025) - Figure 3

Transfemoral TAVI with Navitor 29 mm bioprosthesis (Abbott Structural Heart, St Paul, MN, USA)
 

• No procedural complications
• Normal valve gradient with trivial perivalvular leak (Gmax/mean 10/6 mmHg, V max 1,6 cm/sec, DVI > 0.60)
• Residual severe tricuspid regurgitation with Sys-PAP 45 mmHg. 
• The patient was discharged on day 3 after the procedure in NYHA class II. The first follow-up was planned after 45 days to reassess the TR severity.

Clinical follow-up (April 2025)

The patient remained clinically stable, even though mild lower limb edema with elevated BNP levels in blood tests persisted. At follow-up TT echocardiogram, significant improvement of LVEF (35 % → 50 %) was observed. Normal valve function with stable trivial perivalvular leak (Grad. max/mean 10/4 mmHg) was described. Residual severe TR (VC 8 mm - TR EROA 41 mm²) with Sys-PAP 50 mmHg was reported.

Powered by Quiz Maker 

To assess the suitability for Tricuspid Transcatheter Edge-to-Edge Repair (T-TEER), a TEE was performed (March 2025) (Figure 4):

• Normal RV size and function (TAPSE 23 mm, S’ TDI 14 cm/sec, FAC 47 %, RVFWLS -30 %). 
• Persistent severe secondary atrial functional TR (RAVi 78 ml/m², tenting height < 9 mm, tricuspid annulus 27 mm/m²):  
  • Anatomy: 4 leaflets morphology (Type III)
  • Jet localisation: central jet with a greater jet component between the septal/anterior leaflet
  • Coaptation gap 6-7 mm
  • Pacemaker lead positioned at the posterior commissure, thus not significantly contributing to the underlying mechanism of the TR etiology. 
  • Optimal echocardiographic view for leaflet visualisation
• Elevated sys-PAP (estimated 50 mmHg)

According to all these features, the anatomy was deemed feasible for T-TEER⁴.

T-TEER procedure (May 2025) - Figure 5

The Heart Team confirmed the indication for T-TEER.

Edge-to-edge repair was then performed:
 

• Implantation of a single TriClip XTW (Abbott Structural Heart, St Paul, MN, USA) between the anterior and septal leaflets
• Procedural success without complications 

Post-procedural echocardiogram: residual mild TR.

Clinical follow-up (June 2025)

• Asymptomatic at rest (no angina or palpitations), with significant improvement in dyspnea. 
• Hemodynamically stable (HR 52 bpm, BP 140/90 mmHg)
• TT echocardiography (Figure 6): 

• LVEF 55 %
• TAVI bioprosthesis (Navitor 29 mm): well-positioned with normal function (Max/mean gradient 8/4 mmHg), no significant intra- or paravalvular leaks
• TriClip: stable position of the clip between anterior and septal leaflets, with mild residual TR (anterograde gradient 1–2 mmHg)
• No pericardial effusion

Acute decompensated heart failure (AHF) is often due to valvular heart disease (VHD) and can be triggered by acute hemodynamic stress or the deterioration of valve function. Clinical presentation may vary from chronic heart failure to acute decompensated heart failure and cardiogenic shock. Assessing the severity of VHD may be difficult because of the rapid variation in loading conditions, concomitant destabilisation of the associated comorbidities, and the presence of multiple VHD^1,5.

Multiple VHD (i.e. the combination of stenotic or regurgitant lesions occurring on ≥ 2 cardiac valves) is common but understudied, and its diagnosis is complicated by hemodynamic interactions that affect standard assessment methods. Yet, there is only limited data in the literature and current guidelines to support and guide clinical decision-making⁶.

Patients with multiple VHD should be followed in specialized Heart Valve Clinics, with the use of multimodality imaging strongly recommended to confirm the diagnosis and overcome the limitations of isolated echocardiographic assessment^6,7.

Therapeutic management strategy in multiple VHD should be individualised by a multidisciplinary Heart Team, considering the single valve severity, individual patient risk, the natural history of each valvular lesion if left untreated, and prosthesis-related morbidity. Intervention is indicated in the presence of symptoms or ventricular dysfunction, starting with the most distal valve suitable for percutaneous treatment⁶.

None