Aortic stenosis (AS) is the most common valvular heart disease, affecting 1%–2% of adults >65 years and ~12% of those >75 years, caused by calcification and fibrosis of the aortic valve leading to fixed left ventricular outflow obstruction. [1] Without valve replacement, symptomatic severe AS carries up to 50% mortality at 1 year. [1]
1. History
- Classic symptom triad: exertional dyspnea (most common initial symptom), exertional angina, and exertional syncope/presyncope [1-2]
- Characterize exercise tolerance — reduced exercise capacity may be the earliest and most subtle symptom; many elderly patients self-limit activity, masking symptoms [1]
- Timing and progression: gradual onset over months to years; acute decompensation may be precipitated by new atrial fibrillation, infection, anemia, or volume shifts [3]
- Associated symptoms: orthopnea, PND, lower extremity edema (late findings indicating HF) [2]
- Important negatives: absence of symptoms in known severe AS does not exclude high-risk disease — ask specifically about subtle exercise limitation [1]
- Inquire about prior echocardiograms, known murmur, history of bicuspid aortic valve, rheumatic fever [1]
2. Alarm Features
- Syncope or presyncope with exertion — suggests inability to augment cardiac output [2]
- New or worsening heart failure (dyspnea at rest, pulmonary edema) [4]
- Angina at rest or with minimal exertion
- Hemodynamic instability or cardiogenic shock [5]
- Rapid atrial fibrillation with acute decompensation (loss of atrial kick is poorly tolerated) [6]
- Acute GI bleeding (Heyde syndrome — acquired von Willebrand disease with angiodysplasia)
3. Medications
- No medical therapy slows AS progression — statins, bisphosphonates, and denosumab have all been ineffective in RCTs [1]
- Antihypertensives: ACE inhibitors/ARBs are safe and well-tolerated; β-blockers are a reasonable alternative. Start low, titrate cautiously [1][3]
- Use with caution:
- Nitroglycerin and other preload-reducing vasodilators — can cause precipitous hypotension due to fixed obstruction and preload dependence [5]
- Diuretics — excessive preload reduction can cause hemodynamic collapse in the small, hypertrophied LV [6]
- Calcium channel blockers — some evidence of being unsafe in AS [7]
- In acute decompensation:
- Hypotensive patients: norepinephrine (mixed shock/reduced EF) or phenylephrine (preserved EF) at lowest effective dose [4-5]
- Dobutamine can increase inotropy but may worsen ischemia and provoke arrhythmias [5]
- Nitroprusside may be used in non-hypotensive patients with acute pulmonary edema under invasive hemodynamic monitoring [5-6]
- Statins are indicated for standard atherosclerotic risk reduction, not for AS progression prevention [3]
4. Diet
- No specific dietary triggers for AS
- Standard heart-healthy diet; sodium restriction if concurrent HF
- Maintain adequate hydration — dehydration reduces preload and can precipitate hemodynamic compromise in severe AS
- Supplemental calcium may increase mortality in mild-moderate AS per some data; routine supplementation should be reconsidered [8]
5. Review of Systems
- Cardiovascular: chest pain, palpitations, lightheadedness, exercise intolerance, orthopnea, PND, leg swelling
- Pulmonary: dyspnea on exertion (most common initial symptom), cough (pulmonary congestion)
- Neurologic: syncope, presyncope, dizziness
- GI: GI bleeding (Heyde syndrome)
- Constitutional: fatigue, decreased functional capacity
6. Collateral History and Family History
- Family history of bicuspid aortic valve — autosomal dominant with variable penetrance; ~1/3 of families have >1 affected member [9]
- Familial clustering of calcific trileaflet AS has also been reported [9]
- NOTCH1 mutations associated with congenital aortic valve abnormalities and calcification [9]
- Elevated lipoprotein(a) has a genetic component and is associated with incident AS [9]
- Collateral: confirm functional status, symptom timeline, medication adherence, prior echocardiographic data
7. Risk Factors
- Bicuspid aortic valve (1%–2% of population; accounts for >80% of AVR in patients <60 years) [1]
- Aortic sclerosis (~25% of adults >65 years; ~2% annual progression to AS) [1]
- Older age (≥65 years), male sex [1]
- Hypertension (each 20 mm Hg increase in SBP → 41% higher AS risk) [1]
- Diabetes, smoking, elevated LDL cholesterol [9]
- Elevated serum lipoprotein(a) [1]
- Coronary artery disease [1]
- Chronic kidney disease / end-stage renal disease [8]
- Rheumatic heart disease (rare in developed countries, prevalent in low/middle-income countries) [9]
8. Differential Diagnosis
- Hypertrophic obstructive cardiomyopathy (HOCM) — dynamic LVOT obstruction; murmur increases with Valsalva (opposite of AS)
- Subaortic membrane — fixed subvalvular obstruction; distinguished by echo
- Supravalvular aortic stenosis (Williams syndrome)
- Mitral regurgitation — holosystolic murmur radiating to axilla vs. crescendo-decrescendo to carotids
- Aortic sclerosis — thickened valve without significant obstruction (Vmax <2 m/s) [3]
- Coronary artery disease — angina mimic; present in up to 50% of AS patients [2]
- Pulmonary stenosis — right-sided murmur, increases with inspiration
- Other causes of syncope/dyspnea: PE, arrhythmia, deconditioning, COPD [1]
9. Past Medical History
- Prior echocardiograms and known valve disease severity/trajectory
- Known bicuspid aortic valve or congenital heart disease
- History of rheumatic fever
- Prior cardiac surgery or interventions
- Coronary artery disease (common comorbidity)
- Hypertension, diabetes, CKD (accelerate progression) [1]
- Atrial fibrillation (poorly tolerated — loss of atrial kick)
10. Physical Exam
- Murmur: harsh, late-peaking crescendo-decrescendo systolic murmur, best heard at right upper sternal border, radiating to carotids. Among moderate-severe AS patients, 64% had grade ≥3/6 murmur, but 19% had only grade 1–2 [1-2]
- Carotid pulse: pulsus parvus et tardus (delayed, diminished upstroke) — specific for severe AS but often absent in elderly patients with stiff vasculature [2]
- S2: single or absent A2 component (loss of aortic valve closure sound) — a normally split S2 reliably excludes severe AS [6]
- PMI: sustained, non-displaced (concentric hypertrophy)
- S4 gallop: common due to diastolic dysfunction
- Signs of HF: elevated JVP, pulmonary crackles, peripheral edema (late findings)
- Vital signs: narrow pulse pressure; watch for hypotension
11. Lab Studies
- BNP/NT-proBNP: elevated levels correlate with severity and prognosis; BNP >3× upper limit of normal is a Class IIa indication for AVR in asymptomatic severe AS [1]
- Troponin: elevated high-sensitivity troponin indicates myocardial injury/fibrosis and worse prognosis [10]
- CBC: rule out anemia (can precipitate decompensation); thrombocytopenia (Heyde syndrome)
- BMP: renal function (CKD accelerates progression; pre-procedural assessment), electrolytes
- Coagulation studies: baseline, especially if considering intervention [4]
- Type and screen: if acute decompensation or procedural planning [4]
12. Imaging
- Transthoracic echocardiography (TTE) — gold standard for diagnosis and severity assessment [1][3]
- Measures: peak aortic velocity, mean gradient, aortic valve area (AVA), LVEF, LV hypertrophy, diastolic function, pulmonary pressures
- Severe AS: Vmax ≥4 m/s, mean gradient ≥40 mm Hg, AVA ≤1.0 cm² [1]
- Very severe AS: Vmax ≥5 m/s or mean gradient ≥60 mm Hg [3]
- Point-of-care ultrasound (POCUS): reasonable in the ED when formal echo is not immediately available [4]
- CT calcium scoring: useful in low-flow, low-gradient AS to confirm severity (sex-specific thresholds: ≥2000 Agatston units in men, ≥1300 in women) [3]
- Chest X-ray: boot-shaped heart (concentric LVH), possible aortic valve calcification on lateral view, pulmonary congestion [11]
- CT angiography: pre-procedural planning for TAVI (annulus sizing, coronary ostial distance, vascular access) [1]
The following figure from the 2024 JAMA review illustrates the management algorithm for AS across severity stages:
13. Special Tests
- Dobutamine stress echocardiography: for low-flow, low-gradient AS with reduced LVEF (Stage D2) — distinguishes true severe AS (fixed valve area with Vmax ≥4 m/s at any flow rate) from pseudosevere AS [3]
- Exercise stress testing: reasonable in asymptomatic severe AS to unmask symptoms or abnormal BP response (fall ≥10 mm Hg per ACC/AHA, ≥20 mm Hg per ESC). Contraindicated in symptomatic severe AS [12]
- Cardiac MRI: late gadolinium enhancement identifies midwall myocardial fibrosis — a strong predictor of adverse outcomes and may guide timing of intervention [10][13]
- Cardiac catheterization: when noninvasive data are discordant or coronary angiography is needed pre-operatively [6]
14. ECG
- LV hypertrophy (voltage criteria ± secondary ST-T wave changes/"strain pattern") — present in the majority but not all patients with severe AS [11][14]
- Left atrial abnormality (P-wave abnormality) — present in >80% of severe AS along with LVH or conduction delay [14]
- Conduction abnormalities: LBBB prevalence increases with AS severity (8.1% in severe AS); RBBB also seen; calcification extends into the conduction system [14-15]
- LV strain pattern (ST depression with asymmetric T-wave inversion in lateral leads) — specific marker of midwall myocardial fibrosis and independently predicts AVR or cardiovascular death (HR 2.67) [13]
- Atrial fibrillation: more common in older patients and those with hypertension [14]
- ECG is non-diagnostic for AS but supports the diagnosis and provides prognostic information [11]
15. Assessment
Severity Staging (2020 ACC/AHA): [3]
Typical presentation is an elderly patient with progressive exertional dyspnea. Atypical presentations include isolated fatigue, GI bleeding (Heyde syndrome), or acute decompensation triggered by new AF, sepsis, or anemia. Complications include heart failure, sudden cardiac death (<1%/year in asymptomatic severe AS), infective endocarditis (8.75× general population risk), and acquired von Willebrand disease. [1]
16. Treatment Plan
Initial Stabilization (ED/ICU)
- Maintain preload — patients are preload-dependent; avoid aggressive diuresis or vasodilation [5]
- Maintain sinus rhythm and normal heart rate (60–80 bpm); both bradycardia and tachycardia are poorly tolerated [4]
- Hypotension: norepinephrine (if reduced EF/mixed shock) or phenylephrine (if preserved EF) at lowest effective dose [5]
- Acute pulmonary edema without hypotension: cautious diuresis; nitroprusside under invasive monitoring [5-6]
- Consider PAC placement if hemodynamic uncertainty [5]
Definitive Treatment
- Aortic valve replacement (SAVR or TAVI) is the only definitive therapy for symptomatic severe AS [1]
- TAVI is recommended for patients ≥80 years or life expectancy <10 years (ACC/AHA); ≥75 years (ESC) [12]
- SAVR is recommended for patients <65 years with life expectancy >20 years (ACC/AHA); <75 years (ESC) [12]
- Shared decision-making with a Heart Team for intermediate-age patients [16]
- Balloon aortic valvuloplasty (BAV): temporizing bridge to definitive AVR in hemodynamically unstable patients; not a definitive treatment [17]
- ECMO/mechanical circulatory support: considered as rescue in refractory cardiogenic shock [5]
Chronic/Outpatient Management
- Treat hypertension (ACE inhibitors/ARBs preferred, β-blockers reasonable) — start low, titrate cautiously [1][3]
- Statins for standard atherosclerotic risk reduction (not for AS progression) [3]
- Optimal dental hygiene (increased endocarditis risk); antibiotic prophylaxis is not indicated for native AS without prior valve replacement [1]
- No medical therapy slows AS progression [1]
17. Disposition
- Admit (ICU): cardiogenic shock, acute pulmonary edema, hemodynamic instability, new symptomatic severe AS with syncope or HF [4-5]
- Admit (telemetry): new-onset symptoms attributable to known severe AS, new atrial fibrillation with AS, need for urgent echocardiography and cardiology consultation
- Observation: borderline symptoms with stable hemodynamics pending echocardiographic evaluation
- Discharge: known mild-moderate AS with stable symptoms, no acute decompensation, established outpatient follow-up
- Cardiology consultation: all patients with newly diagnosed or newly symptomatic severe AS; Heart Team referral for valve intervention planning [1]
18. Follow-Up / Return Precautions
Echocardiographic Surveillance Intervals: [1][3]
- Mild AS (Vmax 2.0–2.9 m/s): every 3–5 years
- Moderate AS (Vmax 3.0–3.9 m/s): every 1–2 years
- Severe AS (Vmax ≥4.0 m/s): every 6–12 months
Return precautions — instruct patients to seek immediate care for:
- New or worsening shortness of breath, especially with exertion
- Chest pain or pressure
- Lightheadedness, dizziness, or fainting
- Rapid or irregular heartbeat
- Sudden weight gain or leg swelling
Patient counseling
- Educate about the progressive nature of AS and the importance of reporting even subtle changes in exercise tolerance [1]
- Once severe AS is present, event-free survival is only 30%–50% at 2 years [3]
- The AHA's Target: Aortic Stenosis initiative recommends valve replacement within 90 days of meeting Class I guideline indications [1]
- Avoid strenuous exertion in severe AS; activity restrictions should be individualized
References
1. Calcific Aortic Stenosis: A Review. — Otto CM, Newby DE, Hillis GS. The Journal of the American Medical Association. 2024.
2. Asymptomatic Aortic Stenosis in the Elderly: A Clinical Review. — Manning WJ. The Journal of the American Medical Association. 2013.
3. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. — Otto CM, Nishimura RA, Bonow RO, et al. Journal of the American College of Cardiology. 2021.
4. Evaluation and Management of Aortic Stenosis for the Emergency Clinician: An Evidence-Based Review of the Literature. — Gottlieb M, Long B, Koyfman A. The Journal of Emergency Medicine. 2018.
5. Acute Decompensated Valvular Disease in the Intensive Care Unit. — Miller PE, Senman BC, Gage A, et al. JACC. Advances. 2024.
6. 2008 Focused Update Incorporated Into the ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease). Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. — Bonow RO, Carabello BA, Chatterjee K, et al. Journal of the American College of Cardiology. 2008.
7. Arterial Hypertension in Aortic Valve Stenosis: A Critical Update. — Basile C, Fucile I, Lembo M, et al. Journal of Clinical Medicine. 2021.
8. Unraveling the Mechanisms of Valvular Heart Disease to Identify Medical Therapy Targets: A Scientific Statement From the American Heart Association. — Small AM, Yutzey KE, Binstadt BA, et al. Circulation. 2024.
9. Aortic-Valve Stenosis — From Patients at Risk to Severe Valve Obstruction. — Otto CM, Prendergast B. The New England Journal of Medicine. 2014.
10. Early Intervention in Patients With Asymptomatic Severe Aortic Stenosis and Myocardial Fibrosis: The EVOLVED Randomized Clinical Trial. — Loganath K, Craig NJ, Everett RJ, et al. The Journal of the American Medical Association. 2025.
11. Aortic Stenosis. — Carabello BA, Paulus WJ. Lancet. 2009.
12. ACC/AHA and ESC/EACTS Guidelines For the Management of Valvular Heart Diseases: JACC Guideline Comparison. — Coisne A, Lancellotti P, Habib G, et al. Journal of the American College of Cardiology. 2023.
13. Left Ventricular Hypertrophy With Strain and Aortic Stenosis. — Shah AS, Chin CW, Vassiliou V, et al. Circulation. 2014.
14. Aortic Valve and Ascending Aorta Guidelines for Management and Quality Measures. — Svensson LG, Adams DH, Bonow RO, et al. The Annals of Thoracic Surgery. 2013.
15. Prevalence and Prognostic Relevance of Ventricular Conduction Disturbances in Patients With Aortic Stenosis. — Prihadi EA, Leung M, Vollema EM, et al. The American Journal of Cardiology. 2017.
16. Valvular Heart Disease: From Mechanisms to Management. — Praz F, Beyersdorf F, Haugaa K, Prendergast B. Lancet. 2024.
17. Aortic Valve Disease, Transcatheter Aortic Valve Replacement, and The Heart Failure Patient: A State-of-the-Art Review. — Okumus N, Abraham S, Puri R, Tang WHW. JACC. Heart Failure. 2023.