Obstruction to LV outflow; classic SAD triad (Syncope, Angina, Dyspnea) signals need for AVR.
Also known as: AS, aortic stenosis, calcific aortic stenosis, bicuspid aortic valve, AVR, TAVR
Overview
Narrowing of the aortic valve orifice producing obstruction to LV outflow. Severity assessed by aortic valve area (AVA), peak transvalvular velocity, and mean gradient on echocardiography.
Epidemiology
Most common valvular heart disease requiring intervention in developed countries. Prevalence rises with age — present in ~5% of adults >75. Bicuspid aortic valve (1-2% of population) is the most common cause in patients under 65.
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Progressive valve calcification and fibrosis reduce orifice area. Increased afterload triggers compensatory LV hypertrophy (preserves stroke volume initially). Over years, LVH leads to diastolic dysfunction, increased oxygen demand (subendocardial ischemia → angina), and eventually systolic failure. The hypertrophied, stiff ventricle becomes preload-dependent — small drops in preload (nitrates, dehydration, hemorrhage) cause profound hypotension.
Clinical presentation
Symptoms
Classic SAD triad (onset of any symptom marks severe AS and dramatically worsens prognosis):
• Syncope — exertional; from inability to augment CO across fixed obstruction
• Angina — from subendocardial ischemia in LVH ± concomitant CAD
• Dyspnea / heart failure — late finding
Once symptomatic, untreated severe AS has 50% 2-year mortality
Signs / physical exam
Crescendo-decrescendo systolic ejection murmur at RUSB (2nd ICS right of sternum), radiating to carotids
Late peaking and softer S2 → more severe disease ('paradoxical splitting' if severe LV dysfunction)
Pulsus parvus et tardus — slow-rising, low-amplitude carotid pulse
Sustained, non-displaced PMI (LVH without dilation)
S4 from LVH
Carotid bruit may be a referred murmur from AS — verify with cardiac exam
Classic findings
Crescendo-decrescendo systolic ejection murmur at RUSB radiating to carotids, pulsus parvus et tardus, late-peaking murmur in severe disease.
Differential diagnosis
Aortic sclerosis — Aortic valve thickening WITHOUT obstruction; benign incidental finding; murmur present but valve area, gradient, and velocity normal; no symptoms
Hypertrophic obstructive cardiomyopathy (HOCM) — Dynamic LVOT obstruction; murmur LOUDER with decreased preload (Valsalva strain, standing) — opposite of AS; family history of sudden cardiac death; septal LVH on echo
Subvalvular AS (discrete membrane or muscular) — Younger patient, no aortic valve calcification on echo; obstruction visualized below the valve
Supravalvular AS — Williams syndrome (elfin facies, hypercalcemia, intellectual disability); narrowing above sinotubular junction
Mitral regurgitation — Holosystolic at apex, radiates to AXILLA (not carotids); intensity increases with handgrip (increased afterload)
Pulmonic stenosis — Right-sided systolic murmur at LUSB; INCREASES with inspiration (Carvallo sign); often congenital
Ventricular septal defect — Holosystolic at LSB with palpable thrill; murmur intensity inversely related to defect size
Diagnostic workup
Labs
Standard CV labs: lipid panel, A1c, BMP, BNP
Pre-operative workup if AVR planned
Imaging
ECG: LVH with strain (left precordial T-wave inversions), left atrial enlargement, occasionally LBBB or AV block from septal calcification
CXR: cardiomegaly late; aortic root calcification visible on lateral
• Mild: AVA >1.5 cm², mean gradient <20 mmHg, peak velocity <3 m/s
• Moderate: AVA 1.0-1.5, mean gradient 20-40, peak velocity 3-4
• Severe: AVA <1.0 cm², mean gradient ≥40, peak velocity ≥4 m/s
• Very severe (critical): AVA <0.6, mean gradient >60, peak velocity >5
Stress echo or dobutamine stress echo — clarify low-flow low-gradient AS (LVEF reduced)
Coronary angiography prior to AVR (rule out CAD requiring concomitant CABG)
CT for TAVR planning — annular measurements, vascular access
Diagnostic algorithm
flowchart TD
A[Severe AS<br/>AVA <1.0 cm²<br/>or mean gradient ≥40] --> B{Symptomatic?<br/>SAD: Syncope, Angina, Dyspnea}
B -->|Yes| C[AVR indicated<br/>Class I]
B -->|No| D{High-risk features?<br/>EF <50% / abnl exercise<br/>/ peak vel >5 m/s}
D -->|Yes| C
D -->|No| E[Monitor<br/>echo q6-12 mo]
C --> F{Choose AVR<br/>modality}
F --> G[SAVR<br/>younger, low risk,<br/>bicuspid + aortopathy]
F --> H[TAVR<br/>elderly, high risk,<br/>prior CABG]
G --> I{Valve type}
I --> J[Mechanical<br/>lifetime warfarin]
I --> K[Bioprosthetic<br/>limited AC, ~10-15 yr]
Aortic stenosis treatment algorithm — symptom onset is the inflection point. Modality (SAVR vs TAVR) depends on age, surgical risk, and anatomy.
Treatment
First-line
Asymptomatic AS — no proven benefit from medical therapy to slow progression
Treat concomitant HTN cautiously (avoid afterload reduction that worsens output across fixed obstruction); preferred agents: ACEi/ARB at low dose, titrated carefully
Lipid-lowering therapy does NOT slow progression of calcific AS (multiple negative trials)
Symptomatic severe AS → Aortic Valve Replacement (AVR)
Surgical AVR (SAVR)
Preferred in younger patients (<65-70), low surgical risk, bicuspid valve with aortic root pathology
Mechanical valve: lifetime warfarin (INR 2-3); preferred in younger patients without contraindication to AC
Bioprosthetic valve: shorter anticoagulation course; preferred in older patients or those who cannot tolerate warfarin; ~10-15 year durability
Transcatheter AVR (TAVR)
Now indicated across all surgical risk categories (high, intermediate, low risk in age >65)
Preferred for elderly (>80), high/prohibitive surgical risk, prior CABG
Balloon aortic valvuloplasty (BAV) — palliative or bridge to AVR in severely ill patients; restenosis within 6-12 months limits its standalone role
Asymptomatic patients with very severe AS (peak velocity >5 m/s), reduced LVEF <50%, or abnormal exercise test may benefit from early AVR — emerging area
Complications
Sudden cardiac death — risk rises sharply once symptoms develop
Heart failure (initially diastolic from LVH, then systolic)
Atrial fibrillation (LA dilation)
Conduction system disease — AV block (calcium extension into septum)
Acquired von Willebrand syndrome (shear stress destroys vWF multimers → mucosal bleeding, GI angiodysplasia — Heyde syndrome)
AVOID NITRATES IN SEVERE AS — preload reduction across a fixed obstruction causes profound hypotension and syncope. This is a high-yield board pitfall.
Heyde syndrome — triad of severe AS + GI angiodysplasia bleeding + acquired vWF deficiency. Bleeding resolves after AVR.
Bicuspid AV is associated with aortic root dilation (~30%) — image the ascending aorta routinely; if >5 cm, consider concomitant aortic surgery.
All patients with prosthetic valves need endocarditis prophylaxis for high-risk dental procedures (per AHA guidelines).
Severe AS with reduced flow ('low-flow, low-gradient AS') can underestimate severity — dobutamine stress echo distinguishes true severe from pseudo-severe AS.
References
ACC/AHA 2020 VHD — 2020 ACC/AHA Guideline for the Management of Patients with Valvular Heart Disease (Otto et al., Circulation 2021)
PARTNER 1 — Transcatheter versus Surgical Aortic-Valve Replacement in High-Risk Patients (Smith et al., NEJM 2011)
PARTNER 3 — TAVR with a Balloon-Expandable Valve in Low-Risk Patients (Mack et al., NEJM 2019)
Evolut Low Risk — TAVR with a Self-Expanding Valve in Low-Risk Patients (Popma et al., NEJM 2019)
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