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This is a clinician-written, evidence-based summary aligned to the USMLE Step 2 CK Content Outline. It is intended for medical students preparing for USMLE Step 2 CK. Management reflects current ACC/AHA, USPSTF, and APA guidelines. Always cross-reference with UpToDate, institutional protocols, and clinical judgment.
The Bottom Line
- Most common cause: degenerative calcification (age >65); bicuspid aortic valve in younger patients
- Classic symptom triad: exertional angina, syncope, and heart failure (in order of onset)
- Once symptomatic: median survival 5 years (angina), 3 years (syncope), 2 years (HF) without intervention
- Diagnosis: echo showing peak velocity >=4 m/s, mean gradient >=40 mmHg, or AVA <=1.0 cm2 = severe
- Treatment: aortic valve replacement (SAVR or TAVR) once symptomatic or LVEF <50%. No medical therapy alters progression
Overview
Aortic stenosis (AS) is the most common valvular heart disease requiring intervention in the developed world. It involves progressive calcification and fibrosis of the aortic valve leaflets, leading to obstruction of left ventricular outflow. The resultant pressure overload causes concentric LVH as a compensatory mechanism, which eventually fails leading to systolic dysfunction and heart failure. The two major etiologies are degenerative calcific disease (most common in adults >65) and congenital bicuspid aortic valve (most common in adults <65, present in 1-2% of the population). Rheumatic heart disease is a less common cause in developed countries but remains prevalent globally.
Epidemiology
Prevalence of AS increases with age: ~2% of adults over 65 and ~4% over 85 have severe AS. Approximately 300,000 patients undergo aortic valve replacement annually worldwide. Risk factors for degenerative AS overlap with atherosclerotic risk factors: age, hypertension, hyperlipidemia, diabetes, smoking, CKD. However, statins have NOT been shown to slow progression (SEAS, SALTIRE trials). Bicuspid aortic valve has a male predominance (~3:1) and is associated with aortopathy (ascending aortic aneurysm).
Clinical Features
Symptoms
Exertional angina (increased myocardial O2 demand from LVH, reduced coronary flow reserve)
Exertional syncope or presyncope (inability to augment CO with exertion, vasodepressor reflex)
Exertional dyspnea progressing to heart failure (decompensated LV)
May be asymptomatic for decades despite severe obstruction
Sudden cardiac death (rare as first presentation, ~1%/year in asymptomatic severe AS)
Signs
Crescendo-decrescendo (diamond-shaped) systolic ejection murmur at RUSB, radiating to carotids
Murmur peaks later in systole as severity increases; soft/absent S2 (calcified immobile valve)
Pulsus parvus et tardus (slow-rising, low-amplitude carotid pulse) — classic but may be absent in elderly with stiff arteries
Narrow pulse pressure
S4 gallop (non-compliant hypertrophied LV)
Sustained, non-displaced PMI (concentric LVH — displaced PMI suggests decompensation)
Gallavardin phenomenon: high-frequency component of murmur at apex mimicking MR
Investigations
First-line
Transthoracic echocardiogramGold standard for diagnosis and grading. Severe AS: peak velocity >=4 m/s, mean gradient >=40 mmHg, AVA <=1.0 cm2. Also assess LVEF, LVH, diastolic function, and aortic root dimensions (especially bicuspid valve)
ECGLVH with strain pattern (ST depression, T-wave inversion in lateral leads), LAE, possible conduction disease (LBBB)
Second-line
Low-dose dobutamine stress echoFor low-flow, low-gradient AS with reduced LVEF — differentiates true-severe AS (AVA stays <=1.0 with increased gradient) from pseudo-severe (AVA increases >1.0)
CT aortic valve calcium scoreAortic valve calcium >=2000 AU (men) or >=1200 AU (women) supports severe AS, especially in discordant echo findings
Cardiac catheterizationIndicated if non-invasive data discordant or pre-operative coronary assessment needed
Specialist
CT angiographyPre-TAVR planning: annular sizing, vascular access assessment, coronary height, calcium distribution
Exercise stress testingCan be performed in ASYMPTOMATIC severe AS to unmask symptoms or abnormal BP response — CONTRAINDICATED in symptomatic severe AS
1
Indications for valve replacement
- Symptomatic severe AS (angina, syncope, HF) = Class I indication for AVR
- Asymptomatic severe AS with LVEF <50% = Class I
- Asymptomatic severe AS with abnormal exercise test (symptoms, drop in BP) = Class I
- Asymptomatic very severe AS (peak velocity >=5 m/s) with low surgical risk = Class IIa
- Asymptomatic severe AS undergoing other cardiac surgery = Class I to do concurrent AVR
2
Choice of intervention
- SAVR (surgical): standard for low/intermediate surgical risk patients <65 (longer durability of mechanical/bioprosthetic valves)
- TAVR (transcatheter): standard for high/prohibitive risk; now approved for all risk categories. Preferred for patients >=80 or high surgical risk
- Shared decision-making for intermediate-risk patients 65-80: consider anatomy, durability, lifestyle, frailty
- Mechanical valve: requires lifelong warfarin (INR 2.5-3.5) — consider for younger patients who can tolerate anticoagulation
- Bioprosthetic valve: no long-term anticoagulation but limited durability (10-15 years); preferred if anticoagulation contraindicated or in elderly
3
Medical management (supportive only — does NOT alter disease progression)
- Manage concurrent HTN carefully: avoid excessive afterload reduction; ACEi/ARBs are safe and may even be beneficial
- Diuretics for volume overload if HF develops (use cautiously — preload-dependent)
- Maintain sinus rhythm (AF poorly tolerated in AS due to loss of atrial kick)
- Statins do NOT slow AS progression (SEAS trial)
- Avoid excessive exertion in symptomatic severe AS
- Endocarditis prophylaxis: NOT routinely recommended for native valve AS (only for prosthetic valves or prior endocarditis)
4
Balloon aortic valvuloplasty (BAV)
- Bridge to SAVR/TAVR in hemodynamically unstable patients or those needing urgent non-cardiac surgery
- NOT a definitive treatment — restenosis occurs within 6-12 months in nearly all patients
- May be used for palliation when AVR is not an option
Complications
- Heart failure: Eventual decompensation of LVH — leading cause of death in untreated severe AS
- Sudden cardiac death: ~1%/year in asymptomatic severe AS, higher once symptomatic
- Infective endocarditis: Especially with bicuspid valve or prosthetic valve
- Heyde syndrome: AS + GI bleeding from acquired von Willebrand disease (type 2A) + intestinal angiodysplasia — resolves after AVR
- Conduction disease: AV block (especially post-TAVR — may require permanent pacemaker in 10-20%)
- Aortopathy: Ascending aortic dilation (especially bicuspid valve) — monitor with imaging
USMLE Step 2 CK Exam Tips
- 1Crescendo-decrescendo systolic murmur at RUSB radiating to carotids = AS until proven otherwise
- 2Once the symptom triad appears (angina, syncope, HF), prognosis is dismal without AVR: 5-3-2 year survival
- 3Severe AS + LVEF <50% = valve replacement even if asymptomatic
- 4NEVER perform exercise stress testing in SYMPTOMATIC severe AS (risk of sudden death). It IS appropriate in asymptomatic severe AS to unmask symptoms
- 5Low-flow low-gradient AS with low EF: use dobutamine stress echo to distinguish true-severe from pseudo-severe
- 6Statins do NOT slow AS progression — this is a common incorrect answer choice
- 7Heyde syndrome: AS + GI bleeding + angiodysplasia + acquired vWD type 2A — resolves after AVR
- 8Post-TAVR complication to know: paravalvular leak and need for permanent pacemaker (conduction disease)
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