Aortic Stenosis
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.
Overview
Etiology & Presentation
- Causes: Degenerative/calcific (elderly), bicuspid aortic valve (younger)
- Triad (SAD): Syncope, Angina, Dyspnea (HF)
- Murmur: Crescendo-decrescendo systolic, radiates to carotids. Pulsus parvus et tardus
Severity
| Parameter | Mild | Moderate | Severe |
|---|---|---|---|
| AVA (cm²) | >1.5 | 1.0–1.5 | <1.0 |
| Mean Gradient | <25 | 25–40 | >40 |
| Vmax (m/s) | <3.0 | 3.0–4.0 | >4.0 |
Do NOT give vasodilators aggressively in severe AS. These patients are preload-dependent. Vasodilation → syncope → death.
Symptom Triad & Natural History
| Symptom | Mechanism | Mean Survival Without AVR |
|---|---|---|
| Angina | LVH → ↑ O2 demand + ↓ coronary perfusion pressure | ~5 years |
| Syncope | Fixed CO + peripheral vasodilation (exercise) → cerebral hypoperfusion | ~3 years |
| Heart Failure | Chronic pressure overload → systolic dysfunction → decompensation | ~2 years |
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.
Classic Murmur Description
- Type: Crescendo-decrescendo (diamond-shaped) systolic ejection murmur
- 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
Management
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.
🔄 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
📋 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.
📋 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.
📋 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
Recognize It
The most common valvular disease. Classic triad of angina, syncope and heart failure. Murmur is crescendo-decrescendo, radiating to the carotids, with a delayed and diminished carotid upstroke in severe disease.
Severity on Echo
Severe: valve area < 1.0 cm², mean gradient > 40 mmHg, or peak velocity > 4.0 m/s. Moderate is 1.0 to 1.5 cm², gradient 25 to 40, velocity 3.0 to 4.0.
Symptoms Are the Inflection Point
Asymptomatic severe AS has near-normal survival; the moment symptoms appear the curve falls off a cliff. Untreated mean survival is roughly 5 years with angina, 3 with syncope and 2 with heart failure. Any new symptom means refer for valve replacement now, not at the next clinic visit.
No Medical Substitute
Nothing medical changes the natural history. Diuretics may ease congestion but do not alter outcome. Valve replacement is the only treatment.
The Dangerous Drug Error
Do not aggressively vasodilate severe AS. These patients are preload-dependent with a fixed cardiac output, so they cannot compensate for a drop in systemic resistance: vasodilation leads to syncope and death. Use nitrates, ACE inhibitors and propofol with great caution.
TAVR or SAVR
Decided by a multidisciplinary Heart Valve Team. High surgical risk or older age favors TAVR (PARTNER trials); younger, lower-risk patients and those needing other cardiac surgery favor SAVR, which also matters for valve durability. Anatomy, life expectancy and patient preference all feed the decision.
Balloon Valvuloplasty Is Only a Bridge
Old teaching treated BAV as definitive; it is not. Restenosis occurs within 6 to 12 months in nearly all patients, so it is a temporizing measure to get someone to TAVR or surgery.
Two Traps
Low-flow, low-gradient AS: a small valve area with a low gradient because the ventricle cannot generate one. Do not call it moderate; get a dobutamine stress echo to unmask true severity. Murmur mimic: the AS murmur decreases with Valsalva while HOCM increases, which is the bedside discriminator.
📄 One Pager
Text version
CARDIOLOGY · One Pager
Aortic Stenosis and TAVR
Asymptomatic severe AS has near-normal survival; the day a symptom appears the survival curve falls off a cliff, and no medication changes that, only a new valve does.
Diagnosis and Severity
- TTE is the gold standard for both diagnosis and severity grading; everything below comes off the echo.
- Severe AS: AVA <1.0 cm², mean gradient >40 mmHg, Vmax >4.0 m/s.
- Moderate: AVA 1.0–1.5, mean gradient 25–40, Vmax 3.0–4.0. Mild: AVA >1.5, gradient <25, Vmax <3.0.
- Murmur: crescendo-decrescendo systolic at the right upper sternal border radiating to both carotids. Late-peaking means more severe; a soft or absent A2 means a heavily calcified immobile valve.
- Pulsus parvus et tardus (low amplitude, delayed upstroke) is the hallmark of significant AS on the carotid exam.
- Supporting workup: ECG for LVH and LAE, BNP if HF symptoms, cardiac cath for pre-op coronary assessment before valve surgery.
Causes and the Symptom Clock
- Degenerative / calcific is the leading cause in the elderly. Bicuspid aortic valve is the cause in younger patients (~1–2% of the population), presenting 10–20 years earlier and carrying aortopathy, so image the ascending aorta.
- Triad is SAD: Syncope, Angina, Dyspnea (heart failure).
- Angina, mean survival ~5 years without AVR. LVH raises O₂ demand while coronary perfusion pressure falls.
- Syncope, ~3 years. Fixed cardiac output plus exercise-induced peripheral vasodilation means cerebral hypoperfusion.
- Heart failure, ~2 years. Chronic pressure overload leads to systolic dysfunction and decompensation.
- The onset of symptoms is the inflection point. Asymptomatic patients have near-normal survival, so refer the moment a symptom appears.
Management, Step by Step
1
Confirm severity on TTE and ask the one question that drives everything: is the patient symptomatic? Medical therapy does not change the natural history, so the decision is timing of valve replacement.
2
Symptomatic severe AS: valve replacement, TAVR or SAVR. Do not delay, because survival drops steeply once symptoms begin.
3
Asymptomatic severe AS: serial echo q6–12 months, plus exercise testing if the symptom history is questionable, because patients often unknowingly limit activity. An abnormal BP response (failure to rise or a drop >10 mmHg) counts as an occult symptom.
4
Low-flow, low-gradient AS (AVA <1.0 with mean gradient <40): sort out true severe from pseudo-severe before committing to a valve. See the block below.
5
Heart Valve Team decides TAVR vs SAVR using STS risk, anatomy, life expectancy, comorbidity, and patient preference. Every severe symptomatic AS patient should get this multidisciplinary discussion.
TAVR vs SAVR
- Favors TAVR: age ≥65–70, high or intermediate STS score, suitable vascular access, frailty, porcelain aorta, prior chest radiation.
- Favors SAVR: age <65 (durability), low STS score, bicuspid valve, small annulus, unsuitable access, or concurrent CABG / other valve surgery needed.
- Durability: TAVR has 10–15 year data emerging; SAVR has 20–25 year durability established, which is why younger patients lean surgical.
- Trade-offs: TAVR has less bleeding, AKI, and AF; SAVR has less paravalvular leak and a lower pacemaker rate.
- Recovery: TAVR 1–3 days in hospital vs SAVR 5–7 days inpatient.
Low-Flow, Low-Gradient and Monitoring
- Classical (EF <50%): the weak LV cannot generate a gradient. Dobutamine stress echo settles it: true severe AS keeps AVA <1.0 while the gradient rises; pseudo-severe opens the AVA >1.0.
- Paradoxical (EF ≥50%): a small hypertrophied LV with low stroke volume. Look for indexed AVA <0.6 cm²/m² and stroke volume index <35 mL/m²; CT calcium scoring adds supporting evidence.
- Echo q6–12 months for severe AS, q1–2 years for moderate, to catch progression before the patient decompensates.
- Ask about symptoms every visit. A new symptom is itself the referral trigger for valve replacement.
Pitfalls
- Aggressive vasodilators in severe AS. These patients are preload-dependent, so vasodilation leads to syncope and death. Start ACEi/ARB very low if HTN coexists.
- Aggressive diuresis. Furosemide relieves congestion but low doses only; over-diuresis causes hypotension.
- Exercise testing in a symptomatic patient. Fixed cardiac output plus exercise vasodilation causes profound hypotension, syncope, arrhythmia, or sudden death. It is only for asymptomatic severe AS.
- Calling a low gradient "not severe" when the EF is low. Get the dobutamine stress echo before dismissing it.
- Mistaking AS for MR (Gallavardin phenomenon) when the murmur radiates to the apex. Check carotid radiation and pulsus parvus et tardus.
- Mistaking AS for HOCM. The AS murmur decreases with Valsalva and standing; HOCM increases. HOCM also has a brisk bifid carotid upstroke.
- Treating balloon aortic valvuloplasty as definitive. It is a temporary bridge only; restenosis occurs within 6–12 months in nearly all patients.
Refer for Valve Replacement When
- Any symptom in severe AS (syncope, angina, dyspnea). This is the Class I indication and it does not wait for the next echo.
- Asymptomatic severe AS with an abnormal exercise BP response (failure to rise or a drop >10 mmHg), which is a Class IIa indication for AVR because it unmasks occult limitation.
- Confirmed true severe low-flow low-gradient AS on dobutamine stress echo, even though the resting gradient looks unimpressive.
- Known TAVR complications to counsel and watch for: paravalvular leak (most common), conduction disease with new LBBB or complete heart block needing a permanent pacemaker (~10–20%), vascular access injury, stroke, and rare but catastrophic coronary obstruction.
Key Evidence
- PARTNER Trials: established TAVR as non-inferior or superior to SAVR in high and intermediate surgical risk, which is why TAVR is now the standard for those groups.
- PARTNER 2, 2016: TAVR non-inferior to SAVR in intermediate-risk patients.
- PARTNER 3, 2019: TAVR non-inferior to SAVR at 5 years in low-risk patients, the basis for the emerging 10–15 year durability picture.
- Evolut Low Risk, 2019: TAVR non-inferior to SAVR at 2 years in low-risk patients; TAVR is now approved across all surgical risk categories, which is exactly why the Heart Valve Team, not a single number, makes the call.
- No trial supports medical therapy as a substitute. Diuretics ease symptoms but do not alter the natural history.
Related Topics
ACS OverviewAortic DissectionArrhythmiasAtrial FibrillationCardiac TamponadeHeart Block & Bradyarrhythmias