Valvular Heart Disease Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mr Nguyen is a 78-year-old Vietnamese-born retired farmer presenting with a 3-month history of exertional chest tightness and two episodes of near-syncope on walking uphill. He has a background of hypertension, type 2 diabetes, stage 3a chronic kidney disease (eGFR 48), and permanent atrial fibrillation on apixaban. [1]

His echo shows severe calcific aortic stenosis — valve area 0.7 cm², mean gradient 52 mmHg, peak velocity 4.8 m/s — with a preserved ejection fraction of 55%, moderate functional mitral and tricuspid regurgitation, and mild ascending aortic dilatation to 39 mm. [1]

His main problems are:

1. Severe symptomatic aortic stenosis (Stage D) — the primary problem requiring valve intervention
2. Moderate functional MR and TR — secondary to the AS afterload, expected to improve after AVR
3. Permanent AF, appropriately anticoagulated
4. CKD stage 3a and type 2 diabetes — influence procedural contrast and perioperative management
5. Mild ascending aortic dilatation — below surgical threshold, needs surveillance
6. Frailty and reduced functional reserve — influence the SAVR vs TAVI decision
7. Social: lives with his wife, limited English, relies on his daughter for translation and decisions." [1]

Examiner probing questions and model answers

Q1: "Is this patient's aortic stenosis severe, and how confident are you?" [1]

"Yes — confidently severe. He meets all the standard thresholds: valve area 0.7 cm² (severe is ≤1.0 cm²), mean gradient 52 mmHg (severe is ≥40 mmHg), and peak velocity 4.8 m/s (severe is ≥4.0 m/s). Because his ejection fraction is preserved at 55% and the gradient is high, this is classical high-gradient severe AS — I do not need a dobutamine stress echo, which is reserved for the low-flow low-gradient pattern where the gradient and valve area appear discordant in a patient with reduced ejection fraction." [1]

Q2: "He is symptomatic. What does that mean for his prognosis and management?" [1]

"Symptom onset is the inflection point in the natural history of aortic stenosis. Before symptoms, the annual mortality is low; once symptoms develop — angina, syncope, or heart failure — median survival falls to roughly 2 to 5 years without intervention, and the risk of sudden cardiac death rises. Symptomatic severe AS is therefore a class I indication for aortic valve replacement. The RECOVERY trial (PMID 31733181) reinforced the urgency of intervention in severe AS, showing benefit from early surgery even in selected asymptomatic patients with very severe AS. I would not delay his intervention for medical optimisation." [1]

Q3: "Why are you considering TAVI rather than open surgery in this man?" [1]

"The SAVR-versus-TAVI decision integrates surgical risk, age and life expectancy, anatomy, and comorbidity. He is 78 with CKD, diabetes, hypertension and likely frailty — an intermediate-to-high surgical risk profile. The durability advantage of a surgical valve matters less at this age and life expectancy. PARTNER 3 (PMID 30973341) showed TAVI with a balloon-expandable valve was non-inferior and at one year superior to SAVR in low-risk patients; the CoreValve US High Risk trial (PMID 24097881) showed the self-expanding prosthesis was superior to SAVR in high-risk patients. His position on that spectrum favours TAVI, provided his CT aortogram shows suitable annular dimensions and femoral access. I would refer him to the heart team for the final decision." [1]

Q4: "Does he need coronary angiography?" [1]

"Yes. Coronary artery disease commonly coexists with calcific AS, and identifying significant CAD changes management — if he proceeds to SAVR, significant coronary lesions are bypassed at the same operation; if he proceeds to TAVI, significant CAD may be stented beforehand or staged. In a 78-year-old with diabetes and exertional chest tightness, I would perform coronary angiography (or CT coronary angiography if the TAVI route is chosen and the pre-test probability is lower) as part of the work-up." [1]

Q5: "He is on apixaban for his atrial fibrillation. How do you manage his anticoagulation around TAVI?" [1]

"He stays on apixaban for his non-valvular AF throughout — apixaban is appropriate for native-valve AF and will remain appropriate after TAVI with a bioprosthetic valve. DOACs are contraindicated only in mechanical valves (the RE-ALIGN trial, PMID 24040997, showed dabigatran caused more thrombosis and bleeding than warfarin in mechanical valves). Periprocedurally, the valve team typically interrupts apixaban about 48 hours before TAVI and resumes once haemostasis is secure. After TAVI, antiplatelet therapy (often aspirin with clopidogrel for a few months then aspirin alone, or single antiplatelet) is added per local protocol, on top of his anticoagulation — with attention to bleeding risk." [1]

Q6: "What is his risk of needing a pacemaker after TAVI?" [1]

"Roughly 15 to 20 percent with a self-expanding valve and around 6 percent with a balloon-expandable valve — the self-expanding frames extend lower into the LV outflow tract and more often compress the conduction system near the atrioventricular node. A pre-existing right bundle branch block, which I would check on his ECG, substantially raises the risk of complete heart block. I would monitor his ECG closely post-procedure and have a low threshold for temporary then permanent pacing if high-degree block develops." [1]

Q7: "Should he be on a statin to slow his aortic stenosis?" [1]

"No — for the purpose of slowing the AS. The SEAS trial (PMID 18765275) and the ASTRONOMER trial both showed that lipid-lowering therapy does not slow the haemodynamic progression of aortic stenosis. He should be on atorvastatin 40 mg because he has diabetes and likely coronary disease risk, but I would be explicit with him that the statin is for his vascular risk, not for his valve." [1]

Q8: "How would you discuss the procedure with him and his family, given his limited English?" [1]

"I would use a trained medical interpreter — not a family member — to ensure accurate consent. I would explain the trade-offs clearly: TAVI means a shorter recovery (about a week versus four to six weeks for surgery), a small risk of needing a pacemaker, and uncertainty about valve durability beyond eight to ten years; SAVR means a longer recovery and higher upfront operative risk but a longer durability track record. I would ask about his values — what matters most to him at 78 (independence, avoiding major surgery, longevity) — and incorporate his daughter appropriately as his support person, while ensuring he gives consent himself. I would also discuss advance care planning given his comorbidity." [1]

Short Case Discussion — Cardiovascular Examination (Murmurs)

Scenario: "Examine this patient's cardiovascular system. You have 7 minutes for examination and 8 minutes for discussion."

Candidate presentation (model — aortic stenosis): [1]

"I examined Mrs Patel's cardiovascular system. She is comfortable at rest at 45 degrees. There is no clubbing, pallor or cyanosis. Hands reveal no splinter haemorrhages. The pulse is regular at 76 beats per minute, 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, suggesting 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, with a palpable praecordial thrill. There is no diastolic murmur. Lung fields are clear and there is no peripheral oedema. [1]

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

Examiner: "Why is the pulse pressure narrow, and what does paradoxical splitting of S2 mean?" [1]

"A narrow pulse pressure reflects the fixed outflow obstruction — the left ventricle cannot generate a high systolic pressure rapidly, so systolic pressure is lower, and the slow ejection delays valve closure. Paradoxical splitting means the aortic component (A2) is delayed so long that it closes after the pulmonary component (P2); on expiration, when P2 moves earlier, the split narrows or reverses. In severe AS, the delayed A2 is due to prolonged LV ejection through the stenotic valve. It is a sign of haemodynamically significant obstruction." [1]

Examiner: "How would you distinguish this murmur from hypertrophic cardiomyopathy?" [1]

"Both produce an ejection systolic murmur, but HOCM's murmur is typically at the lower left sternal edge, radiates poorly to the carotids, and — crucially — changes with manoeuvres. The HOCM murmur gets louder with Valsalva and on standing (reduced preload unmasks the obstruction), whereas the AS murmur gets softer with Valsalva. Handgrip makes the AS murmur softer (afterload reduces the gradient) but the HOCM murmur softer too; squatting-to-standing is the most reliable bedside discriminator. HOCM also has a bisferiens pulse and a preserved or loud A2, unlike the soft A2 of severe AS." [1]

Examiner: "What murmurs would you expect in aortic regurgitation, and how do they differ from aortic stenosis?" [1]

"Chronic aortic regurgitation gives an early diastolic, high-pitched, decrescendo murmur best heard at the left sternal edge, third intercostal space, with the patient sitting forward and breath held in expiration. The pulse is collapsing — a water-hammer pulse — with a wide pulse pressure. There may also be a flow-related ejection systolic murmur from the increased total stroke volume, and an Austin Flint mid-diastolic murmur at the apex from the regurgitant jet striking the anterior mitral leaflet. The key discriminator from AS is the diastolic component and the wide rather than narrow pulse pressure. Severe AS has a slow-rising pulse, narrow pulse pressure, and no diastolic murmur." [1]

Examiner: "Describe the murmur of mitral regurgitation and how you localise it at the bedside." [1]

"Mitral regurgitation produces a pansystolic murmur at the apex radiating to the axilla, louder on expiration, with a soft first heart sound and often a third heart sound. The apex is displaced and hyperdynamic from volume overload. To localise it, I listen at the apex with the diaphragm during expiration, then compare with the lower left sternal edge — a pansystolic murmur loudest at the apex radiating to the axilla is MR, whereas one loudest at the lower left sternal edge that increases on inspiration is tricuspid regurgitation. Handgrip increases an MR murmur (afterload up) while reducing an AS murmur, which is another useful discriminator. I would confirm mechanism and severity with echocardiography, particularly a transoesophageal echo if surgical repair is being considered." [1]