Valvular Heart Disease — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mr Nguyen, 78 years old, Vietnamese-born retired farmer. ^[1]

Presenting complaint: Three months of exertional central chest tightness (walking 50 metres on flat ground, relieved by rest) and two episodes of near-syncope while walking uphill. No orthopnoea or paroxysmal nocturnal dyspnoea. Increasing fatigue. ^[1]

Past history:

• Hypertension (15 years)
• Type 2 diabetes (HbA1c 64 mmol/mol)
• Stage 3a CKD (eGFR 48, baseline creatinine 130)
• Permanent atrial fibrillation (diagnosed 4 years ago)
• Dyslipidaemia
• Mild ascending aortic dilatation on prior imaging (39 mm)
• No prior cardiac surgery or PCI ^[1]

Current medications:

• Perindopril 5 mg OD
• Amlodipine 10 mg OD
• Metformin 1 g BD
• Gliclazide 80 mg OD
• Atorvastatin 40 mg ON
• Apixaban 5 mg BD ^[1]

Examination findings (trainee elicits):

• Comfortable at rest at 45 degrees, no distress. Malar flush absent.
• Pulse: 74, irregularly irregular, slow-rising and small volume. BP 145/85 (narrow pulse pressure).
• JVP: not elevated.
• Apex: 5th intercostal space, mid-clavicular line, sustained and non-displaced (pressure overload).
• Auscultation: ejection systolic murmur at the upper right sternal edge radiating to the carotids, late-peaking, grade 4/6 with a palpable thrill; soft S2 with paradoxical splitting; no diastolic murmur; separate soft pansystolic murmur at the apex (functional MR) and a softer pansystolic murmur at the lower left sternal edge louder on inspiration (functional TR).
• Lungs: clear. No peripheral oedema. No hepatic enlargement. ^[1]

Investigations:

• ECG: AF, HR 74, normal QRS duration (96 ms), no prior infarct, LV voltage criteria for hypertrophy.
• Echo: aortic valve area 0.7 cm², mean gradient 52 mmHg, peak velocity 4.8 m/s; LVEF 55%; moderate functional MR and TR; LV end-diastolic diameter 56 mm; mild ascending aortic dilatation (39 mm); estimated RVSP 38 mmHg.
• Bloods: Hb 132, eGFR 48, HbA1c 64, normal LFTs, normal TFTs. ^[1]

Candidate's structured presentation (model)

Opening statement: ^[1]

"Mr Nguyen is a 78-year-old Vietnamese-born retired farmer who presents with a 3-month history of exertional chest tightness and two episodes of near-syncope, on a background of hypertension, type 2 diabetes, stage 3a CKD, and permanent atrial fibrillation. ^[1]

His main problems are:

1. Severe symptomatic aortic stenosis — valve area 0.7 cm², mean gradient 52 mmHg, peak velocity 4.8 m/s, preserved EF 55%. This is Stage D and is the primary problem requiring valve intervention.
2. Moderate functional mitral and tricuspid regurgitation — secondary to the AS afterload and atrial dilatation; expected to improve after AVR.
3. Permanent atrial fibrillation, appropriately anticoagulated with apixaban.
4. Stage 3a CKD and type 2 diabetes — influence procedural contrast and perioperative management.
5. Mild ascending aortic dilatation to 39 mm — below surgical threshold, needs surveillance.
6. Frailty and reduced functional reserve — favour TAVI over SAVR.
7. Social: lives with his wife, limited English, daughter is his primary support and interpreter." ^[1]

Investigation summary: ^[1]

"His echocardiogram confirms severe calcific aortic stenosis with preserved left ventricular function, and moderate functional MR and TR that reflect the afterload and remodelling from the AS rather than primary leaflet disease. The mild ascending aortic dilatation is below the threshold for intervention. His ECG shows atrial fibrillation with a normal QRS duration, which is relevant because a pre-existing conduction abnormality would raise his pacing risk after TAVI." ^[1]

Management plan: ^[1]

1. Confirm severity and plan the intervention:

   • CT aortogram with annular sizing for TAVI planning; assess iliofemoral access.
   • Coronary angiography (or CT coronary angiography) to exclude concurrent CAD requiring PCI or CABG.
   • Frailty and surgical risk assessment (STS score, clinical heart team judgement). ^[1]

2. Intervention — refer to the heart team; recommend TAVI based on his age (78), frailty, CKD and diabetes. PARTNER 3 (PMID 30973341) showed TAVI was non-inferior to SAVR in low-risk patients, and CoreValve High Risk (PMID 24097881) showed self-expanding TAVI was superior to SAVR in high-risk patients — he sits where TAVI is favoured. The functional MR and TR are expected to improve once the AS is relieved (afterload reduction). ^[1]

3. Comorbidity optimisation: minimise contrast peri-procedurally for his CKD; continue perindopril; optimise diabetes (consider SGLT2i for cardiovascular and renal benefit); continue apixaban for AF (it remains appropriate after bioprosthetic TAVI — DOACs are contraindicated only in mechanical valves). Stop amlodipine if it adds to polypharmacy without clear benefit. ^[1]

4. Peri-procedural anticoagulation: interrupt apixaban ~48 hours pre-TAVI, resume once haemostasis secure; add antiplatelet per local protocol with attention to bleeding risk. ^[1]

5. Follow-up and surveillance: baseline post-TAVI echo; ECG monitoring for conduction disease (self-expanding valve ~15–20% pacemaker risk; check for new LBBB); surveillance echo at 30 days, 12 months, then annually; ascending aorta surveillance annually; endocarditis prophylaxis education. ^[1]

6. Communication and shared decision-making: trained interpreter; explain SAVR vs TAVI trade-offs; clarify his values at 78; involve his daughter appropriately; advance care planning. ^[1]

Examiner discussion questions

Q: "Why not just watch him and treat his symptoms medically?" ^[1]

"Symptomatic severe aortic stenosis carries a median survival of around 2 to 5 years without intervention, with a high risk of sudden death. No medical therapy — including statins, which the SEAS and ASTRONOMER trials showed do not slow AS progression — improves survival once the valve is severely stenotic and the patient is symptomatic. AVR is the only disease-modifying treatment. The RECOVERY trial (PMID 31733181) reinforced that intervention should not be delayed. Waiting would expose him to progressive heart failure and sudden death." ^[1]

Q: "How would you decide between a balloon-expandable and a self-expanding TAVI valve?" ^[1]

"Both have class I support. Balloon-expandable valves (Sapien, used in PARTNER 3) have a lower pacemaker rate (~6%) and are deployed quickly. Self-expanding valves (Evolut/CoreValve, used in the CoreValve High Risk trial) have a lower gradient, a larger effective orifice area (relevant if he has a small annulus or risk of patient-prosthesis mismatch), and may have better outcomes in anatomies with low coronary ostia — but a higher pacemaker rate (~15–20%). The choice depends on his CT anatomy (annulus size, sinus of Valsalva dimensions, coronary heights, calcification pattern), his baseline conduction (a pre-existing RBBB pushes me toward balloon-expandable to limit pacing risk), and the operator's expertise." ^[1]

Q: "What happens to his functional MR after TAVI?" ^[1]

"Functional MR in severe AS is driven by the high LV afterload and the resulting LV and mitral annular remodelling. Once the AS is relieved, the afterload falls acutely and the LV remodels over weeks to months, so the functional MR usually improves — often substantially. I would not address the MR at the time of TAVI unless it is severe and clearly independent of the AS. I would reassess it on the 30-day and 6-month post-TAVI echoes; if it remains severe and symptomatic, I would then consider transcatheter edge-to-edge repair." ^[1]

Q: "He has CKD. Does that change your contrast strategy?" ^[1]

"Yes. Contrast-induced AKI is a real risk around the CT angiogram and the TAVI procedure itself. I would use a contrast-minimisation strategy: lowest possible contrast volume, iso-osmolar or low-osmolar contrast, pre-procedural hydration with normal saline, hold nephrotoxins, and monitor renal function closely for 48 hours. If his eGFR is borderline for contrast CT, I might use non-contrast CT for access and annular planning where feasible. The TAVI procedure itself can often be done with very low contrast once the anatomy is mapped." ^[1]

Q: "Does he need endocarditis prophylaxis before the TAVI, and afterwards?" ^[1]

"Before the TAVI procedure, he is managed per the procedural protocol with antibiotics for the device implantation (a surgical-style prophylaxis). After TAVI, under ACC/AHA guidance he falls into the high-risk group for which dental prophylaxis is recommended — prosthetic material used for valve repair or TAVI qualifies. Before dental procedures involving gingival manipulation, he should receive amoxicillin 2 g orally (or clindamycin 600 mg if penicillin-allergic) 30–60 minutes beforehand. The NICE position in the UK is more restrictive — no routine prophylaxis — but the ANZ and ESC default is to offer it for high-risk patients like him." ^[1]