Aortic Stenosis Clinical

1. Introduction

Aortic stenosis (AS) is one of the most common and clinically significant forms of valvular heart disease, particularly in aging populations. Characterized by narrowing of the aortic valve orifice, it results in obstructed blood flow from the left ventricle (LV) to the aorta, leading to progressive pressure overload, left ventricular hypertrophy (LVH), and eventually heart failure.

AS has a classic triad of symptoms—angina, syncope, and dyspnea (heart failure)—and once these symptoms appear, the prognosis becomes poor without timely valve replacement. Clinical evaluation, including auscultation and pulse examination, combined with modern imaging (especially echocardiography), remains the cornerstone of diagnosis.

2. Pathophysiology of Outflow Obstruction

2.1 Normal Aortic Valve Function

The aortic valve has three semilunar cusps that open widely during systole to allow ejection of blood into the systemic circulation.
Normal valve area: 3–4 cm².
A pressure gradient across the valve in healthy individuals is minimal.

2.2 Mechanism of Stenosis

AS develops when the valve orifice narrows due to structural abnormalities, leading to an increased transvalvular pressure gradient. Major causes:

Calcific (degenerative) aortic stenosis: Most common in elderly; progressive calcification and stiffening of valve cusps.
Congenital bicuspid aortic valve: Leads to earlier calcification and stenosis.
Rheumatic aortic stenosis: Fusion of cusps due to post-rheumatic scarring (less common in high-income countries, still prevalent in LMICs).

2.3 Hemodynamic Consequences

Pressure Overload: The LV must generate higher pressures to overcome the obstruction.
Concentric LV Hypertrophy: Adaptive mechanism to maintain stroke volume but increases myocardial oxygen demand.
Diastolic Dysfunction: Hypertrophied LV becomes stiff, impairing filling and raising left atrial pressure.
Coronary Perfusion Imbalance: Elevated LV pressures reduce coronary flow reserve, leading to ischemia despite normal coronary arteries.
Decompensation: Eventually, LV contractile function declines, leading to heart failure.

2.4 Severity Classification

Based on echocardiographic parameters:

Mild AS: Valve area >1.5 cm², mean gradient <20 mmHg.
Moderate AS: Valve area 1.0–1.5 cm², mean gradient 20–40 mmHg.
Severe AS: Valve area <1.0 cm², mean gradient >40 mmHg, peak velocity >4 m/s.
Critical AS: Valve area <0.6 cm².

3. Symptoms: The Classic Triad

The hallmark of AS is its long asymptomatic latent period. Once symptoms develop, prognosis worsens dramatically without intervention.

3.1 Angina (Chest Pain)

Occurs in ~50% of symptomatic patients.
Mechanism:
- Increased LV mass and wall stress → higher oxygen demand.
- Reduced coronary perfusion due to high LV end-diastolic pressure.
Can occur even in the absence of coronary artery disease.
Prognosis: Average survival after onset is 5 years without treatment.

3.2 Syncope

Classically exertional syncope.
Mechanisms:
- Fixed obstruction prevents increase in cardiac output during exercise.
- Reflex vasodilation during exertion causes hypotension.
- Arrhythmias due to LV hypertrophy or conduction abnormalities.
Prognosis: Average survival 3 years after onset if untreated.

3.3 Heart Failure (Dyspnea, Fatigue, Orthopnea)

Represents end-stage AS when LV function fails.
Mechanisms:
- Elevated LV diastolic pressure → pulmonary venous hypertension → pulmonary edema.
- Progressive LV dysfunction and reduced ejection fraction.
Prognosis: Average survival 2 years without intervention.

3.4 Other Symptoms

Palpitations (often due to atrial fibrillation).
Sudden cardiac death (especially in severe untreated AS).
Fatigue and reduced exercise tolerance.

4. Physical Examination Findings

Clinical evaluation remains a vital skill in diagnosing AS.

4.1 General Appearance

Often elderly with evidence of chronic heart disease.
In advanced cases, signs of heart failure: pulmonary congestion, peripheral edema.

4.2 Pulse Characteristics

Pulsus parvus et tardus:
- Weak (parvus) and delayed (tardus) upstroke of the carotid pulse.
- Classic finding in severe AS.
Slow-rising pulse with low amplitude due to fixed obstruction.

4.3 Blood Pressure

Narrow pulse pressure (e.g., 110/90 mmHg).
Low systolic pressures in advanced disease.

4.4 Jugular Venous Pulse

May show prominent A waves in late stages due to reduced RV compliance secondary to LV dysfunction.

4.5 Cardiac Auscultation

Key finding: Harsh, crescendo-decrescendo systolic murmur.

Location: Best heard at right upper sternal border (aortic area).
Radiation: To carotids (pathognomonic).
Timing: Mid-systolic, peak later as severity increases.
Intensity: Does not always correlate with severity (may soften in advanced low-flow AS).

Additional sounds:

Ejection click (in younger patients, especially with bicuspid valves).
Soft/absent A2: Aortic component of second heart sound diminished due to immobile valve.
S4 gallop: Due to stiff LV.

4.6 Other Physical Findings

Heaving apex beat: Sustained, forceful, non-displaced due to LV hypertrophy.
Precordial thrill: Palpable in severe AS.
Signs of heart failure: Rales, hepatomegaly, peripheral edema in late stages.

5. Echocardiographic and Imaging Diagnosis

Modern imaging has revolutionized AS diagnosis, with echocardiography as the gold standard.

5.1 Echocardiography

Transthoracic Echo (TTE) is first-line.
Provides:
- Valve morphology (calcification, bicuspid anatomy).
- Valve area (continuity equation).
- Transvalvular gradients and velocities (Doppler).
- LV hypertrophy and function.
Stress echo may be used in low-flow, low-gradient AS to differentiate true severe from pseudo-severe AS.

5.2 Doppler Assessment

Peak aortic jet velocity (Vmax): >4.0 m/s = severe AS.
Mean gradient: >40 mmHg = severe AS.
Aortic valve area (AVA): <1.0 cm² = severe AS.
Dimensionless index (ratio of LVOT to aortic velocity) is useful when flow is low.

5.3 Transesophageal Echocardiography (TEE)

Better spatial resolution, especially for surgical planning.
Useful when TTE windows are poor.

5.4 Cardiac Catheterization

Historically used for hemodynamic assessment.
Now reserved for:
- Inconclusive non-invasive studies.
- Patients undergoing valve replacement with suspected coronary artery disease.

5.5 CT and MRI

CT Calcium Scoring: Quantifies valve calcification; useful in low-flow states.
Cardiac MRI: Provides detailed LV function, myocardial fibrosis assessment.
CT Angiography: Critical for planning transcatheter aortic valve implantation (TAVI).

5.6 Biomarkers

BNP and NT-proBNP: Elevated with symptomatic AS, correlate with severity and prognosis.
Still adjunctive, not diagnostic.

6. Diagnostic Approach

A systematic approach to suspected AS:

History: Age, rheumatic fever, congenital heart disease, symptom onset.
Examination: Murmurs, carotid pulse, signs of HF.
Echocardiography: Confirm severity, assess LV function.
Additional Imaging: CT/MRI if needed.
Risk Stratification: Identify candidates for surgical or transcatheter valve replacement.

7. Prognosis Without Treatment

Long asymptomatic phase; once symptoms appear, survival rapidly declines:
- Angina → 5 years.
- Syncope → 3 years.
- Heart failure → 2 years.
Untreated severe symptomatic AS has high risk of sudden cardiac death.