Cardiology > Aortic Stenosis

   Background

Aortic stenosis (AS) is the narrowing of the aortic valve orifice, obstructing blood flow from the left ventricle into the aorta during systole. This results in increased left ventricular pressure, concentric hypertrophy, and eventually left ventricular dysfunction. If untreated, AS can lead to syncope, angina, heart failure, and sudden cardiac death.

II) Classification or Types

By Etiology: 

• • Calcific (Degenerative) AS: Most common in the elderly due to progressive calcium deposition on a trileaflet valve. 

• • Bicuspid Aortic Valve (Congenital): Predisposes to early calcification and stenosis; often presents before age 65. 

• • Rheumatic AS: Rare in high-income countries; commissural fusion from rheumatic fever. 

• • Radiation-Induced AS: Post mediastinal radiation leading to fibrosis and calcification. 

By Severity (Based on Echocardiographic Criteria): 

III) Epidemiology 

• • Sex: More common in males (especially bicuspid valve) 

• • Age: Degenerative AS typically manifests >65 years old 

• • Geography: Degenerative AS common in high-income countries; rheumatic causes still present in low- and middle-income regions 

• • Comorbidities: Often coexists with hypertension, coronary artery disease, and diabetes

     

  Etiology

I) What Causes It

• • Calcific degeneration of a normal or bicuspid valve 

• • Congenital bicuspid aortic valve 

• • Rheumatic heart disease 

• • Prior chest radiation 

• • Rare: systemic conditions (e.g., Paget disease, end-stage renal disease with hyperparathyroidism) 

1. II) Risk Factors

• • Age >65 years 

• • Congenital bicuspid aortic valve 

• • Rheumatic fever history 

• • Male sex 

• • Hyperlipidemia 

• • Smoking 

• • Hypertension 

• • Chronic kidney disease 

  Clinical Presentation

I) History (Symptoms)
Often asymptomatic until severe. Classic triad when symptomatic:

• • Angina: Due to increased myocardial oxygen demand and decreased perfusion 

• • Syncope: Especially on exertion from fixed cardiac output 

• • Dyspnea/Heart failure symptoms: From elevated LVEDP and pulmonary congestion 

Other symptoms: 

• • Fatigue 

• • Dizziness 

• • Decreased exercise tolerance 

• • Sudden cardiac death (in rare, advanced cases) 

1. II) Physical Exam (Signs)

Vital Signs: 

• • Narrow pulse pressure 

• • Delayed and diminished carotid upstroke (pulsus parvus et tardus) 

Cardiac Exam: 

• • Harsh crescendo-decrescendo systolic murmur at right upper sternal border, radiating to the carotids 

• • S4 gallop (due to stiff LV) 

• • Soft or absent A2 (delayed aortic valve closure) 

• • Paradoxical splitting of S2 

Pulmonary: 

• • Rales in advanced heart failure 

Peripheral: 

• • Cool extremities, signs of low output 

• • Peripheral edema (late) 

  Differential Diagnosis (DDx)

• • Hypertrophic obstructive cardiomyopathy (HOCM) 

• • Subaortic stenosis 

• • Mitral regurgitation 

• • Aortic sclerosis (no obstruction) 

• • Pulmonary embolism (if presenting with syncope) 

• • Anemia (if exertional symptoms are out of proportion)

     

  Diagnostic Tests

Initial Tests: 

• • Transthoracic Echocardiogram (TTE): 

• • • Determines severity (valve area, gradients, velocity) 

• • • Assesses LV function, wall thickness, and aortic root 

• • Electrocardiogram (ECG): 

• • • LV hypertrophy (LVH) 

• • • Left atrial enlargement 

• • • Possible conduction abnormalities (e.g., LBBB) 

• • Chest X-ray: 

• • • Post-stenotic dilation of the ascending aorta 

• • • Pulmonary congestion in decompensated heart failure 

• • BNP/NT-proBNP: 

• • • Elevated in symptomatic or decompensated patients 

• • Cardiac CT (Calcium Scoring): 

• • • Used if echo inconclusive, especially for valve morphology 

• • Cardiac Catheterization: 

• • • Confirms severity if noninvasive data is conflicting 

• • • Assesses coronary anatomy preoperatively 

  Treatment

I) Medical Management:
There is no medical therapy proven to halt disease progression; management focuses on symptom control and timely

• • Diuretics: For pulmonary congestion (use cautiously to avoid hypotension) 

• • Beta-blockers or ACE inhibitors: If comorbid conditions (e.g., hypertension, CAD) but cautiously in severe AS 

• • Statins: For concomitant atherosclerotic disease (not shown to slow AS progression) 

1. II) Interventional/Surgical:

• • Surgical Aortic Valve Replacement (SAVR): 

• • • Indicated in symptomatic severe AS or asymptomatic with EF <50%, or undergoing other cardiac surgery 

• • Transcatheter Aortic Valve Replacement (TAVR): 

• • • For severe symptomatic AS in high-risk or inoperable surgical candidates 

• • • Increasingly used in intermediate- and low-risk patients 

• • Balloon Aortic Valvuloplasty: 

• • Temporary measure in select non-surgical patients (e.g., bridge to TAVR) 

  Patient Education, Screening, Vaccines

• • Educate on symptoms that warrant urgent evaluation: syncope, worsening dyspnea, chest pain 

• • Emphasize need for regular follow-up and imaging 

• • Avoid strenuous activity in symptomatic patients 

• • Limit salt intake if volume overload present 

• • Maintain good dental hygiene to reduce endocarditis risk 

Vaccinations: 

• • Annual influenza vaccine 

• • Pneumococcal vaccination 

• • COVID-19 vaccination 

   Consults/Referrals

• • Cardiology: All moderate to severe AS, or symptomatic patients 

• • Cardiothoracic Surgery: For SAVR evaluation 

• • Interventional Cardiology: For TAVR eligibility 

• • Anesthesiology: If surgery planned (pre-op evaluation) 

• • Primary Care: For comorbidity optimization

     

   Follow-Up

• • Echocardiography: 

• • • Mild AS: every 3–5 years 

• • • Moderate AS: every 1–2 years 

• • • Severe AS: every 6–12 months (or sooner if symptomatic) 

• • • Monitor for symptom development (dyspnea, angina, syncope) 

• • • Assess LV function and new conduction abnormalities 

• • • Reevaluate for valve intervention as disease progresses 

• • • Optimize cardiovascular risk factors (e.g., BP, lipids, diabetes)