Most common valvular disease. Classic triad: syncope, angina, heart failure. Once symptoms develop, prognosis is poor without valve replacement. Medical therapy does NOT change outcomes.
Once ANY symptom develops, mortality is steep. Asymptomatic patients have near-normal survival. The onset of symptoms is the critical inflection point, refer for valve replacement immediately.
Location: Best heard at right upper sternal border (RUSB, aortic area)
Radiation: To carotids bilaterally. Gallavardin phenomenon: may radiate to apex and mimic MR
Severity clues: Late-peaking murmur = more severe. Soft/absent A2 = severely calcified, immobile valve. Paradoxical splitting of S2
Pulsus parvus et tardus: Carotid pulse with diminished amplitude (parvus) and delayed upstroke (tardus), hallmark of significant AS
Maneuvers: Murmur ↓ with Valsalva and standing (except HCM, which ↑). This helps distinguish AS from HOCM
High-yield distinction: AS murmur decreases with Valsalva. HOCM murmur increases with Valsalva. Both are systolic crescendo-decrescendo murmurs, this maneuver is the key differentiator on boards and rounds.
Workup
Workup
TTE, gold standard for diagnosis and severity
ECG: LVH, LAE
BNP if HF symptoms
Cardiac cath: pre-op coronary assessment
RoundsRx Licensed Content - Unauthorized Use ProhibitedManagement
Management
Scenario
Management
Asymptomatic severe
Serial echo q6–12mo. Exercise testing if questionable
Symptomatic severe
VALVE REPLACEMENT (TAVR or SAVR)
High surgical risk
TAVR PARTNER Trials
Low risk / young
SAVR
No medical substitute for valve replacement. Diuretics may help symptoms but do not change natural history.
๐ Updated Practice: Old teaching: balloon aortic valvuloplasty (BAV) as treatment for severe AS. Current practice: BAV is a temporary bridge only, restenosis occurs within 6-12 months in nearly all patients. TAVR (transcatheter aortic valve replacement) has revolutionized AS management (PARTNER trials). TAVR is now approved for all surgical risk categories and is the standard for high/intermediate-risk patients.
TAVR vs SAVR Indications
Factor
Favors TAVR
Favors SAVR
Age
≥65–70 years
<65 years (durability concerns)
Surgical risk
High/intermediate STS score
Low STS score
Anatomy
Suitable vascular access, favorable anatomy
Bicuspid valve, small annulus, unsuitable access
Concomitant disease
Frailty, porcelain aorta, prior chest radiation
Concurrent CABG or other valve surgery needed
Valve durability
10–15 year data emerging PARTNER 3, 2019
20–25 year durability established
Complications
Lower bleeding, AKI, AF risk
Lower paravalvular leak, pacemaker rate
Recovery
Shorter hospitalization (1–3 days)
Longer recovery (5–7 days inpatient)
Shared decision-making: All patients with severe symptomatic AS should be discussed by a multidisciplinary Heart Valve Team. The choice between TAVR and SAVR depends on anatomy, life expectancy, comorbidities, and patient preference. Evolut Low Risk, 2019
Low-Flow, Low-Gradient AS
Diagnostic challenge: AVA <1.0 cm² but mean gradient <40 mmHg. Two scenarios:
Type
EF
Mechanism
Key Test
Classical (low EF)
<50%
Weak LV cannot generate gradient
Dobutamine stress echo, true severe AS: AVA stays <1.0, gradient rises. Pseudo-severe: AVA increases >1.0
Paradoxical (preserved EF)
≥50%
Small, hypertrophied LV with low stroke volume
Indexed AVA <0.6 cm²/m², stroke volume index <35 mL/m². CT calcium scoring aids diagnosis
Medications
Temporizing
Drug
Role
Caution
Furosemide
Symptom relief
Low doses. Aggressive diuresis → hypotension
ACEi/ARB
If concurrent HTN
Start very low. Dangerous hypotension in severe AS
On Rounds
Classic murmur of AS?
Crescendo-decrescendo systolic at RUSB, radiates to carotids. Late peaking = more severe. Pulsus parvus et tardus. Diminished A2.
Survival estimates once symptoms develop?
Without valve replacement: Angina ~5y, Syncope ~3y, HF ~2y. Steep mortality curve once any symptom appears.
How do you distinguish AS from HOCM on physical exam?
Both produce crescendo-decrescendo systolic murmurs. Key difference: Valsalva/standing, AS murmur decreases (less preload = less flow across valve), HOCM murmur increases (less preload = worse obstruction). Also, AS radiates to carotids with pulsus parvus et tardus; HOCM has a brisk, bifid carotid upstroke.
What is low-flow, low-gradient AS and how do you work it up?
AVA <1.0 cm² but mean gradient <40 mmHg. Classical type: Low EF (<50%), weak LV cannot generate gradient. Use dobutamine stress echo: true severe AS = AVA stays <1.0 with rising gradient; pseudo-severe = AVA opens >1.0. Paradoxical type: Normal EF but small hypertrophied LV with low stroke volume. Diagnosed by stroke volume index <35 mL/m² and CT aortic valve calcium scoring.
What are the major complications of TAVR?
Key TAVR complications: (1) Paravalvular leak, most common, due to incomplete seal between prosthesis and native annulus, (2) Conduction abnormalities, new LBBB or complete heart block requiring permanent pacemaker (~10–20%), (3) Vascular access complications, iliac/femoral injury, (4) Stroke, embolic risk from catheter manipulation, (5) Coronary obstruction, rare but catastrophic.
Why is exercise testing contraindicated in symptomatic severe AS?
Exercise causes peripheral vasodilation with a fixed cardiac output (cannot increase CO across severely stenotic valve). This mismatch → profound hypotension, syncope, ventricular arrhythmias, or sudden death. Exercise testing is ONLY appropriate in asymptomatic severe AS to unmask occult symptoms or an abnormal BP response.
What is the Gallavardin phenomenon?
The AS murmur sometimes has two components: the typical harsh, low-frequency murmur at RUSB radiating to carotids, AND a higher-pitched, musical component heard best at the apex. The apical component can mimic mitral regurgitation. This is a pitfall on physical exam, always check for radiation to carotids and pulsus parvus et tardus to avoid misdiagnosing AS as MR.
What is the most common cause of AS in patients under 65?
Bicuspid aortic valve, present in ~1–2% of the population (most common congenital cardiac anomaly). Develops premature calcification and stenosis, typically presenting 10–20 years earlier than degenerative AS. Associated with aortopathy (ascending aortic dilation, increased dissection risk), must image the ascending aorta.
Clinical Examples
๐ Case 1, Severe Symptomatic AS
Patient: 78M with progressive exertional dyspnea and two episodes of exertional near-syncope over 3 months. Known moderate AS on echo 2 years ago.
Exam: Late-peaking crescendo-decrescendo systolic murmur at RUSB radiating to carotids. Pulsus parvus et tardus. S4 gallop. Soft A2.
Echo: AVA 0.7 cm², mean gradient 52 mmHg, Vmax 4.8 m/s. LVEF 55%. Concentric LVH.
Management:
Severe symptomatic AS, Class I indication for valve replacement
STS score 6.2% (intermediate risk). Heart Valve Team discussion
CT angiography: suitable femoral access, no porcelain aorta
Proceeded with TAVR (transfemoral approach) PARTNER 2, 2016
Discharged day 2 on dual antiplatelet therapy (aspirin + clopidogrel x 3–6 months)
Teaching point: Classic presentation of severe symptomatic AS. Once symptoms develop, do not delay referral, survival drops steeply without intervention. TAVR is preferred for intermediate and high-risk patients.
๐ Case 2, Low-Flow, Low-Gradient AS
Patient: 72F with ischemic cardiomyopathy (EF 30%) and worsening HF symptoms despite optimal GDMT. Echo shows AVA 0.8 cm² but mean gradient only 22 mmHg.
Diagnostic dilemma: Is this true severe AS or pseudo-severe AS (valve appears stenotic because weak LV cannot open it fully)?
Workup:
Dobutamine stress echo: At peak dose, gradient increased to 48 mmHg, AVA remained 0.8 cm² = true severe AS
If AVA had increased >1.0 cm² = pseudo-severe (valve not intrinsically stenotic)
CT aortic valve calcium score: 1,850 AU (confirms severe calcification)
Management: Confirmed true severe AS with low EF. High surgical risk, proceeded with TAVR. Post-procedure, EF improved to 40% at 6-month follow-up (afterload reduction effect).
Teaching point: Low gradient does NOT exclude severe AS in patients with low EF. Dobutamine stress echo is the key test. CT calcium scoring provides complementary evidence.
๐ Case 3, Asymptomatic Severe AS
Patient: 68M, incidental finding of severe AS on echo done for AF workup. AVA 0.9 cm², mean gradient 45 mmHg, Vmax 4.2 m/s. LVEF 65%. Patient denies all symptoms.
Question: Should he undergo valve replacement now?
Workup:
Exercise stress test (appropriate in asymptomatic severe AS): Patient developed exertional dyspnea at 4 METs with SBP drop of 15 mmHg
Abnormal BP response = occult symptom = indication for intervention
BNP elevated at 380 pg/mL (suggests subclinical LV decompensation)
Management: Despite self-reported absence of symptoms, exercise test unmasked abnormal hemodynamic response. Referred for SAVR (age 68, low STS risk score 1.8%, long life expectancy favoring durable surgical valve).
Teaching point: Asymptomatic severe AS patients may be unknowingly limiting activity. Exercise testing can unmask symptoms and abnormal BP response. An abnormal BP response (failure to rise or drop >10 mmHg) is a Class IIa indication for AVR. Younger, low-risk patients generally favor SAVR for long-term durability.
Monitoring
Parameter
Frequency
Echo
q6–12mo severe; q1–2y moderate
Symptoms
Every visit. New symptoms = refer for valve replacement
Summary
Summary
Severe AS
AVA <1.0, gradient >40, Vmax >4.0.
Symptoms
SAD: Syncope, Angina, Dyspnea. Once present = valve replacement.
Treatment
Symptomatic = TAVR or SAVR. No medical therapy changes outcomes.