Aortic stenosis

Narrowing of the aortic valve opening that obstructs left ventricular outflow, most often due to age-related calcific degeneration of a normal tricuspid valve in older adults, a congenital bicuspid valve in younger patients, or rheumatic commissural fusion.

• Most common valvular heart disease in developed countries (affecting ~2–3% of those >65). Once classic symptoms (exertional angina, syncope, dyspnea) appear, untreated AS has a poor prognosis (~50% 5-year survival without intervention). Early recognition of severe AS (e.g., harsh murmur with carotid radiation, SAD triad) and timely valve replacement is critical and frequently tested on exams.

• Long asymptomatic period (even with severe stenosis), then the classic triad of exertional dyspnea (heart failure), angina, and syncope develops in late stages.
• Cardiac exam: Harsh crescendo–decrescendo systolic murmur (mid-systolic ejection) best heard at the right upper sternal border with radiation to the carotids. Severe AS leads to a slow-rising, low-amplitude carotid pulse (pulsus parvus et tardus) and a soft or paradoxically split S2; an S4 gallop is often present (LV hypertrophy).
• Possible complications include heart failure (due to LV pressure overload), microangiopathic hemolytic anemia (schistocytes from high-velocity jet), and angiodysplasia-related GI bleeding (Heyde syndrome from von Willebrand factor degradation).

1. If AS is suspected (e.g., appropriate murmur or symptoms) → obtain a transthoracic echocardiogram to confirm diagnosis and assess severity (valve calcification, reduced cusp mobility, pressure gradient).
2. Severe AS is defined by a valve area ≤1.0 cm² (normal ~3 cm²) or jet velocity ≥4 m/s or mean gradient ≥40 mm Hg. Avoid exercise stress testing if symptomatic (risk of syncope).
3. Always evaluate for concomitant coronary artery disease before intervention (e.g., coronary angiography with catheterization). If echo findings are incongruent with symptoms, consider invasive hemodynamic assessment via cardiac cath.
4. ECG often shows left ventricular hypertrophy (due to chronic pressure load) and may show conduction blocks (e.g., LBBB); chest X-ray may reveal a calcified aortic valve or post-stenotic aortic root dilation, but imaging is usually nonspecific.

1. No medical therapy halts progression—definitive treatment is aortic valve replacement (AVR) for severe AS. Symptomatic patients with severe AS should undergo prompt valve replacement (improves survival).
2. Choose surgical AVR vs. TAVR (transcatheter AVR) based on patient’s surgical risk, age, and anatomy. TAVR is often preferred in older or high-risk patients, while younger low-risk patients usually get surgery.
3. Indications for AVR in asymptomatic severe AS: LVEF <50%, very high aortic velocity (≥5 m/s) or mean gradient ≥60 mm Hg, abnormal exercise test, or if the patient is undergoing other cardiac surgery.
4. Bridge therapy: in patients who are not immediate AVR candidates, balloon aortic valvuloplasty can provide temporary relief (especially in younger patients or as a bridge to TAVR), but the benefit is short-lived.
5. Manage heart failure symptoms cautiously (gentle diuresis for pulmonary edema, avoid excessive afterload reduction). Treat coexisting hypertension, but use vasodilators with caution (AS patients are preload-dependent).

• Mnemonic for symptoms: think SAD (Syncope, Angina, Dyspnea) as the triad of severe aortic stenosis.
• Pulsus parvus et tardus (weak, delayed carotid upstroke) is a classic finding specific to severe AS.
• Murmur maneuvers: The AS murmur decreases with Valsalva (less preload) – opposite of hypertrophic cardiomyopathy, which increases (useful in exam scenarios).
• Bicuspid aortic valve (younger patients) is associated with coarctation of the aorta and Turner syndrome (45,X), and leads to earlier stenosis than the typical degenerative form.
• Severe AS can cause an acquired von Willebrand disease (high shear stress cleaves vWF), explaining the classic association of AS with angiodysplasia GI bleeding (Heyde syndrome).

• Exertional syncope or angina in a patient with AS → signals critical stenosis; high risk of sudden death without intervention.
• Severe AS with hypotension or acute pulmonary edema (cardiogenic shock) – patients are extremely preload-dependent, so avoid nitrates/vasodilators; stabilize with fluids and pressors and arrange urgent valve intervention.
• Atrial fibrillation onset in AS can precipitate flash pulmonary edema (loss of atrial kick) – often requires urgent cardioversion to restore hemodynamics.

1. Suspected AS (murmur or risk factors) → obtain transthoracic echo to confirm and assess severity.
2. If severe AS (e.g., valve area ≤1 cm², Vmax ≥4 m/s) and patient is symptomatic or LV systolic dysfunction present → refer for aortic valve replacement (SAVR vs. TAVR).
3. If severe but asymptomatic (normal EF) → conservative management (close follow-up and repeat echos); consider AVR if any high-risk features (Vmax ≥5 m/s, EF dropping <50%, positive exercise test, or planned other cardiac surgery).
4. If mild/moderate AS → periodic monitoring with echo (e.g., every 1–2 years for moderate), manage risk factors (e.g., hypertension), and educate patient to report symptoms immediately.
5. Acute decompensation (e.g., flash pulmonary edema or syncope) in known AS → stabilize hemodynamics (maintain preload, avoid hypotension) and arrange emergent valve intervention (e.g., balloon valvuloplasty as bridge to AVR).

• Elderly man with exertional syncope, chest pain, and a late-peaking murmur radiating to the neck → Aortic stenosis (degenerative calcific).
• Middle-aged patient with bicuspid aortic valve and early-onset systolic murmur; history of Turner syndrome or coarctation → Premature aortic stenosis due to bicuspid valve.