Aortic stenosis — bedside and severity viva

Interpretation

The examiner presents a patient with a slow-rising carotid pulse and a crescendo–decrescendo ejection systolic murmur at the right second ICS radiating to the carotids, and asks: "What is the bedside diagnosis, how would you confirm and grade severity, and what is your management plan?"^[1]

• Bedside phenotype of severe AS: pulsus parvus et tardus (slow-rising, small-volume carotid pulse); ejection systolic murmur at the right 2nd ICS radiating to the carotids; ejection click (mobile/bicuspid valve, disappears when calcified); soft or absent A2 (immobile valve) with paradoxical splitting of S2 (delayed A2 from prolonged LV ejection); S4 (stiff hypertrophied LV). Sustained, heaving, non-displaced apex from concentric LVH.^[1]
• Clinical context: the symptom triad — angina, syncope, heart failure — defines severe symptomatic AS. Mean survival after symptom onset in the classical series: angina 5, syncope 3, heart failure 2 years.^[3]

Key points

The examiner will probe each of these; defend them at viva depth:

1. Dynamic manoeuvres — AS vs HOCM (a favourite). AS murmur softens on Valsalva/standing (↓ preload) and gets louder on squatting (↑ preload + afterload); HOCM is opposite. The HOCM pulse is jerky/bisferiens, not slow-rising, and the murmur does not radiate to the carotids.^[1]
2. Echo severity: Vmax at least 4.0 m/s or mean gradient at least 40 mmHg defines severe AS; the AVA is typically 1.0 cm2 or less (indexed 0.6 cm2/m2 or less) but is supportive rather than required — a small area with a low gradient is the low-flow problem, not automatically severe AS. Very severe = Vmax at least 5.0 m/s or mean gradient at least 60 mmHg. AVA is calculated by the continuity equation: AVA = (CSA_LVOT × VTI_LVOT) / VTI_aortic.^[1][2]
3. Low-flow low-gradient AS — classical (LVEF under 50%) vs paradoxical (LVEF at least 50%, stroke volume index 35 mL/m2 or less). Confirm true severity with dobutamine stress echo (gradient rises to at least 40 mmHg with flow while AVA stays 1.0 cm2 or less if truly severe; AVA opens above 1.0 cm2 if pseudo-severe) or the CT aortic valve calcium score (2021 ESC: severe highly likely above 3000 AU in men and 1600 AU in women). Absence of contractile reserve (stroke-volume rise under 20%) marks higher procedural risk.^[2]
4. Pathophysiology — pressure overload → concentric LVH (Laplace: wall stress = P×r/2h). Angina with normal coronaries = demand ischaemia plus a selectively and markedly reduced coronary flow reserve (compression of intramural vessels, low diastolic perfusion gradient). Syncope = fixed cardiac output on exertion. Decompensation progresses diastolic → systolic. Calcific AS is an active process with similarities to atherosclerosis — leaflet lipid infiltration and inflammation, then fibrosis and calcification.^[1]
5. Management — Class I AVR: symptomatic severe AS; asymptomatic with EF under 50%; severe AS undergoing other cardiac surgery. AVR is the only survival-modifying therapy. Statins failed (SEAS 2008, ASTRONOMER 2010).
6. SAVR vs TAVI — 2020 ACC/AHA: under 65 SAVR, over 80 transfemoral TAVI, 65–80 either after shared decision-making. 2021 ESC: SAVR if under 75 and low surgical risk; TAVI if 75 or over, high surgical risk or unsuitable for surgery. SAVR favoured in young, bicuspid (unfavourable TAVI anatomy), concomitant CABG/mitral/aortic surgery, hostile iliofemoral access, and for the Class 2a asymptomatic triggers. TAVI favoured in elderly/frail, high/prohibitive surgical risk, porcelain aorta, prior thoracotomy.^[1][2]
7. Complications and pitfalls — post-TAVI new LBBB and high-grade AV block: in the Evolut low-risk trial a self-expanding valve needed a new pacemaker in 17.4% at 30 days versus 6.1% after surgery, while balloon-expandable TAVR in PARTNER 3 showed no significant difference from surgery; also paravalvular leak, stroke and prosthetic deterioration. Softening of the murmur is NOT improvement — a failing LV can no longer generate the gradient. Heyde syndrome (GI bleed from acquired von Willebrand syndrome). Exercise testing is contraindicated (Class 3, Harm) in symptomatic severe AS.^[4][5][1]
8. Bicuspid valve — lifelong serial imaging of the aortic sinuses and ascending aorta once the diameter reaches 4.0 cm, at least annually once it exceeds 4.5 cm; surgical replacement above 5.5 cm (5.0 to 5.5 cm with a risk factor for dissection), and concomitant aortic replacement at SAVR once it is 4.5 cm or more; screen for coarctation (and vice versa).^[1]

References

1. Otto CM, et al. 2020 ACC/AHA Valvular Heart Disease Guideline. Circulation 2021.^[1]
2. Vahanian A, et al. 2021 ESC/EACTS Valvular Heart Disease Guidelines. European Heart Journal 2022.^[2]

References5ShowHide

1. [1]Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease. Circulation, 2021.PMID 33332150
2. [2]Vahanian A, Beyersdorf F, Praz F, et al. 2021 ESC/EACTS Guidelines for the management of valvular heart disease. European Heart Journal, 2022.PMID 34453165
3. [3]Ross J, Braunwald E Aortic stenosis. Circulation, 1968.PMID 4894151
4. [4]Popma JJ, Deeb GM, Yakubov SJ, et al. Transcatheter Aortic-Valve Replacement with a Self-Expanding Valve in Low-Risk Patients. N Engl J Med, 2019.PMID 30883053
5. [5]Mack MJ, Leon MB, Thourani VH, et al. Transcatheter Aortic-Valve Replacement with a Balloon-Expandable Valve in Low-Risk Patients. N Engl J Med, 2019.PMID 30883058