Valvular Heart Disease — Written Clinical Reasoning

SAQ 1 — Integrated Management (20 marks, 30 minutes)

Prompt: Outline your integrated assessment and management plan for this patient, including the diagnostic work-up, the intervention decision and its justification, comorbidity optimisation, and follow-up. Justify each decision with reference to evidence. [1]

Model Answer

Problem list (4 marks):

1. Severe symptomatic calcific aortic stenosis (Stage D, mean gradient >40 mmHg, AVA 0.7 cm²) — the primary problem requiring intervention
2. Moderate functional MR and TR — likely secondary to the AS-related afterload and LA/LV remodelling; expected to improve after AVR
3. Permanent AF on appropriate anticoagulation (apixaban)
4. CKD stage 3a (eGFR 48) and type 2 diabetes — influence procedural contrast and perioperative management
5. Mild ascending aortic dilatation (39 mm) — below surgical threshold but needs surveillance
6. Frailty / functional assessment pending — influences SAVR vs TAVI
7. Polypharmacy and comorbidity (hypertension, dyslipidaemia) [1]

Diagnostic work-up to confirm severity and plan intervention (4 marks): [1]

• Confirm severe AS on current echo (already established: AVA 0.7 cm², mean gradient 52 mmHg, peak velocity 4.8 m/s). The echo shows severe AS with preserved EF — no need for dobutamine stress echo (reserved for low-flow low-gradient AS).
• Assess surgical risk and anatomy: STS-predicted mortality; frailty assessment; CT aortogram and annulus sizing for TAVI planning; assess femoral access and iliofemoral vessels.
• Coronary angiography (or CT coronary angiography if TAVI route likely) to exclude concurrent coronary artery disease that might require PCI (around TAVI) or CABG (with SAVR).
• TOE only if MR severity or mechanism is uncertain and would change management; otherwise TTE is sufficient.
• Baseline bloods, ECG (already in AF — note baseline conduction for pacing risk post-TAVI), and pulmonary function if SAVR is contemplated. [1]

Intervention decision — TAVI vs SAVR (6 marks): [1]

Refer to the heart team. Recommend transfemoral TAVI based on:

• Age (78 years) — the durability uncertainty of TAVI over 15+ years is less relevant.
• Frailty and comorbidity (CKD, diabetes, hypertension) — raise surgical risk.
• The evidence: PARTNER 3 (balloon-expandable, PMID 30973341) showed TAVI was non-inferior (1-year superior) to SAVR in low-risk patients; CoreValve US High Risk (self-expanding, PMID 24097881) showed TAVI superior to SAVR in high-risk patients. An intermediate-risk 78-year-old with frailty and CKD sits where TAVI is favoured.
• Aortic annulus and femoral access are the deciding anatomical factors (pending CT). [1]

SAVR would be preferred if: concomitant significant CAD needing CABG; unfavourable TAVI anatomy (bicuspid with heavy calcification, annulus unsuitable, hostile femoral access); or the patient's life expectancy exceeds ~15 years and valve durability is a priority. Neither applies strongly here. [1]

The mild ascending aortic dilatation (39 mm) is below the threshold for intervention (≥5.5 cm, or ≥5.0 cm with risk factors) and will be surveilled. [1]

Comorbidity optimisation (4 marks): [1]

• AF/anticoagulation: he is appropriately anticoagulated on apixaban for non-valvular AF. After TAVI, anticoagulation continues for AF; the valve team will manage peri-procedural interruption (typically stop apixaban ~48 h pre-procedure, resume once haemostasis secure). Note: apixaban is fine for native-valve AF, but DOACs are never used in mechanical valves (he will receive a bioprosthetic TAVI valve, so apixaban remains appropriate).
• CKD: minimise contrast during CT and TAVI; pre-procedural hydration; consider the contrast-sparing protocol. eGFR 48 is acceptable for TAVI but raises the risk of contrast-induced AKI.
• Diabetes: optimise glycaemic control peri-procedurally; SGLT2i has cardiovascular and renal benefit and should be continued (hold on the morning of procedure per local protocol). Consider switching gliclazide if hypoglycaemia risk.
• Blood pressure: continue perindopril; stop amlodipine if it adds to polypharmacy without clear benefit; control hypertension to reduce afterload and aortic growth.
• Prophylaxis: amoxicillin 2 g PO before dental procedures is NOT needed routinely after TAVI for native dental work in many regions — but ACC/AHA classifies prosthetic material used for valve repair/TAVI as a high-risk condition warranting dental prophylaxis; clarify with local protocol. [1]

Communication, follow-up and surveillance (2 marks): [1]

• Shared decision-making: explain SAVR vs TAVI (recovery time ~1 week vs 4–6 weeks; pacemaker risk ~15–20% for self-expanding, ~6% balloon-expandable; durability uncertainty at >8 years); clarify goals of care given frailty; involve family.
• Post-TAVI: baseline echo; ECG monitoring for conduction disease (a new LBBB or high-degree block may need pacemaker); surveillance echo at 30 days, 12 months, then annually.
• Ascending aorta surveillance echo/CT annually.
• Endocarditis prophylaxis education and good oral hygiene.
• Advance care planning appropriate given age and comorbidity. [1]

SAQ 2 — Prosthetic Valve Complication (20 marks, 30 minutes)

Prompt: A 59-year-old woman with a mechanical mitral valve (placed 6 years ago for rheumatic MS) presents with progressive exertional dyspnoea and fatigue over 2 months, with haemoglobin 92 g/L, MCV 102 fL, reticulocytes 180 × 10⁹/L, LDH 760 U/L, haptoglobin undetectable, INR in range, and stable valve gradients on TTE. Outline your differential diagnosis, key investigations, and management. [1]

Model Answer

Differential diagnosis of anaemia in a prosthetic valve patient (5 marks): [1]

1. Prosthetic valve-related haemolysis — most likely given the haemolytic picture (raised LDH, undetectable haptoglobin, reticulocytosis, dark urine). Causes: paravalvular leak (most common), pannus, dehiscence, or (rarely) structural valve deterioration. The mechanical mitral valve is particularly prone because of high closing forces and turbulent flow.
2. Infective endocarditis — the key differential: can cause both haemolysis and anaemia; fever, new murmur, emboli would support it. Must be actively excluded.
3. Prosthetic valve thrombosis — less likely with stable gradients and INR in range, but partially obstructive thrombus or pannus can present subacutely.
4. Non-valvular causes: iron deficiency (GI loss), B12/folate deficiency, haematological malignancy, CKD — but the haemolytic indices point away from these as the primary process. [1]

Key investigations (6 marks): [1]

• Transoesophageal echocardiogram (TOE) — the investigation of choice. TTE is relatively insensitive for paravalvular leaks and prosthetic regurgitation because of acoustic shadowing from the prosthetic material. TOE visualises the sewing ring and any regurgitant jet, and assesses for vegetations (endocarditis), thrombus, pannus and dehiscence.
• Blood cultures (three sets) and inflammatory markers — exclude endocarditis before attributing the picture to a paravalvular leak.
• Fluoroscopy — assesses leaflet motion of the mechanical valve; a leaflet that does not open fully suggests thrombosis or pannus obstruction.
• Cardiac CT — defines valvular and perivalvular anatomy, calcification, and any dehiscence; complementary to TOE.
• Bloods: reticulocytes, LDH, haptoglobin, film (schistocytes confirm intravascular haemolysis), iron studies, B12/folate, renal function.
• Urinalysis — haemoglobinuria/dark urine supports intravascular haemolysis. [1]

Management (6 marks): [1]

1. If a paravalvular leak is confirmed and is symptomatic or causing significant haemolysis: refer for percutaneous closure device (the preferred less-invasive option for suitable defects) or surgical re-operation (for large or dehiscent leaks). Transfusion support for severe anaemia; iron repletion if iron-deficient on top of haemolysis.
2. If endocarditis is confirmed: prolonged IV antibiotics per culture and modified Duke criteria; early surgical consultation (see infective-endocarditis topic).
3. If thrombosis is confirmed: management depends on obstruction severity and surgical risk — surgery for obstructive thrombus in left-sided valves if surgical risk acceptable; fibrinolysis if prohibitive surgical risk (higher embolic and bleeding risk); UFH plus warfarin for non-obstructive thrombus.
4. Anticoagulation: ensure INR remains in the mechanical mitral target (2.5–3.5); do not switch to a DOAC (contraindicated — RE-ALIGN, PMID 24040997).
5. Address the underlying cause definitively — haemolysis will persist as long as the structural lesion is present; supportive measures alone (iron, transfusion) are insufficient. [1]

Communication and follow-up (3 marks): [1]

• Explain the diagnosis and the rationale for TOE over TTE.
• Discuss procedural options (percutaneous closure vs surgery) and their risks.
• Baseline and follow-up echocardiography; lifelong surveillance; endocarditis prophylaxis education.
• Shared decision-making around reoperation risk in the context of the haemolytic anaemia severity. [1]