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]

DCE Short Case — Cardiovascular Examination (Murmurs)

Instruction

"Examine this patient's cardiovascular system. You have 7 minutes for examination and 8 minutes for discussion." [1]

Key signs the patient demonstrates (aortic stenosis)

• Slow-rising, small-volume pulse (pulsus parvus et tardus) — the cardinal bedside sign of AS.
• Narrow pulse pressure (e.g., 120/80).
• Sustained, non-displaced apex — concentric LV hypertrophy (pressure overload), unlike the displaced, hyperdynamic apex of volume overload (AR, MR).
• Ejection systolic murmur at the upper right sternal edge radiating to the carotids, late-peaking (the closer the peak to S2, the more severe the AS).
• Soft or absent A2; paradoxical splitting of S2 in severe AS.
• Palpable thrill over the murmur (grade 4/6).
• Carotid shudder/thrill transmitted from the murmur. [1]

Systematic examination routine (step-by-step)

1. End of bed: breathlessness, malar flush (mitral stenosis), cachexia, skeletal features (Marfan → AR).
2. Hands: splinter haemorrhages, Osler/Janeway (infective endocarditis), clubbing (cyanotic CHD). Pulse character — slow-rising (AS), collapsing/water-hammer (AR), alternans (severe LVF).
3. Blood pressure: narrow pulse pressure (AS) vs wide (AR).
4. Face: high-arched palate, lens dislocation (Marfan).
5. Neck: JVP (V wave in TR; elevated in right heart failure); carotid pulse character — delayed peak and thrill in AS.
6. Praecordium: apex site and character; parasternal heave (RV overload).
7. Auscultation — systematically at apex, lower left sternal edge, upper left sternal edge, upper right sternal edge, and back. Use dynamic manoeuvres: inspiration (TR louder), expiration/holding breath (AR louder), handgrip (MR and AR louder; AS softer), Valsalva/standing (MVP click-murmur earlier; HOCM louder — the key HOCM discriminator).
8. Back and abdomen: basal crackles, sacral oedema, pulsatile liver (TR). [1]

Presentation template

"I examined Mrs Patel's cardiovascular system. She is comfortable at rest at 45 degrees. There is no clubbing, pallor or cyanosis. The pulse is regular at 76, small in volume and slow-rising. The blood pressure is 120 over 80, with a narrow pulse pressure. The carotid pulse is delayed and weak, with a palpable thrill. [1]

The apex beat is in the fifth intercostal space, mid-clavicular line, and sustained in character, consistent with left ventricular pressure overload. There is no parasternal heave. On auscultation the first heart sound is normal and the second heart sound is soft, with paradoxical splitting. There is an ejection systolic murmur at the upper right sternal edge radiating to the carotids, peaking late in systole, grade four out of six, with a praecordial thrill. There is no diastolic murmur. The lungs are clear and there is no peripheral oedema. [1]

These findings are consistent with severe aortic stenosis. I would confirm the severity with echocardiography and assess for symptoms to determine the timing of valve intervention." [1]

Discussion questions

Q: "What is the significance of the late-peaking murmur?" [1]

"The timing of the peak of an ejection systolic murmur reflects the timing of maximal flow across the valve. In mild AS the murmur peaks early; as the stenosis worsens, peak flow is delayed because ejection is prolonged, so the murmur peak moves closer to the second heart sound. A late-peaking murmur is therefore a bedside marker of severe AS, and the soft or absent A2 confirms advanced disease." [1]

Q: "How would you grade the severity objectively?" [1]

"Echocardiographically: peak jet velocity ≥4.0 m/s, mean gradient ≥40 mmHg, and aortic valve area ≤1.0 cm² (or ≤0.6 cm² indexed to body surface area) define severe AS. The dimensionless index (ratio of LVOT velocity to aortic velocity) is ≤0.25 in severe AS. If the patient has reduced LV function and a low gradient despite a small valve area, I would perform a dobutamine stress echo to distinguish true severe AS from pseudo-severe AS (where a poorly-functioning LV fails to open a moderately diseased valve)." [1]

Q: "When would you refer this patient for surgery?" [1]

"Symptomatic severe AS is a class I indication for aortic valve replacement — so as soon as she has symptoms (angina, syncope, or dyspnoea), I refer to the heart team. For the asymptomatic patient with severe AS, I refer if the ejection fraction falls below 60%, if the AS is very severe (peak velocity ≥5 m/s), if an exercise test is abnormal, or if she is having other cardiac surgery. The decision between SAVR and TAVI is made by the heart team based on age, surgical risk, anatomy and life expectancy." [1]