Aortic stenosis

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"aortic stenosis"[MeSH Terms] AND management

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aortic stenosis pathophysiology diagnosis management guidelines 2024 2025

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Aortic Stenosis

Overview

Aortic stenosis (AS) is obstruction to LV outflow across the aortic valve. It is the most common valvular heart disease in the developed world, present in ~15% of adults aged ≥65 years, and severe (AVA <1 cm²) in ~2%. Prevalence rises to ~3% by age 75.

Etiology

Type	Features
Calcific/Degenerative	Most common in adults >65. Calcium deposits on normal tricuspid cusps, causing progressive obstruction
Congenital Bicuspid Valve	1-2% of population; affects 66% of patients. Severe AS develops 1-2 decades earlier than in tricuspid valves. Often associated with aortic root dilation - risk of dissection/rupture
Rheumatic	Rare in Western countries. Results from fusion of commissures. Usually coexists with MS

Braunwald's Heart Disease, p. 1036
Grainger & Allison's Diagnostic Radiology, p. 338

Pathophysiology

Thickening and calcification of valve leaflets leads to progressive obstruction to LV outflow. The LV compensates with concentric hypertrophy (pressure overload pattern), which:

Maintains systolic function initially
Increases LV end-diastolic pressure -> diastolic dysfunction
Makes the LV noncompliant and highly dependent on atrial kick for filling (hence AF is very poorly tolerated)
Eventually reduces LV compliance and stroke volume

The three classic symptoms arise through distinct mechanisms:

Symptom	Mechanism	Mortality if untreated
Angina	Increased O₂ demand (hypertrophied LV) + decreased coronary perfusion time	50% 5-year mortality
Syncope	Fixed CO unable to meet demands on exertion; also baroreceptor reflex miscommunication	50% 3-year mortality
Dyspnea/HF	Elevated LVEDP -> pulmonary congestion	50% 2-year mortality

Symptom to Diagnosis, p. 9340

Clinical Features

Murmur: Harsh, crescendo-decrescendo (diamond-shaped) systolic ejection murmur, best heard at the right 2nd intercostal space, radiating to the carotids. Typically grade III/VI or louder in severe AS. Note: ~31% of patients with moderate-severe AS may not have a detectable murmur.

Pulse: Slow-rising, low-volume pulse ("pulsus parvus et tardus") - though this sign is less reliable in elderly patients with arterial stiffening.

Heart sounds: S2 may be softened or absent when calcification is extensive.

Other late features:

Atrial fibrillation (poorly tolerated - LV relies on atrial kick)
Acquired von Willebrand deficiency (large vWF multimers disrupted by turbulent flow across stenotic valve) - presents as GI bleeding (Heyde syndrome)

Diagnosis

Echocardiography (first-line)

Doppler echo is the gold standard. Key parameters:

Parameter	Mild	Moderate	Severe
Peak velocity (m/s)	<3.0	3.0-4.0	≥4.0
Mean gradient (mmHg)	<20	20-40	≥40
AVA (cm²)	>1.5	1.0-1.5	<1.0
AVA indexed (cm²/m²)	-	-	<0.6

AVA is calculated by the continuity equation (principle of conservation of flow):

EOA = (SV of LVOT) / (VTI across aortic valve)

Low-flow, low-gradient AS (LFLG-AS) - an important and challenging subset:

Valve area <1 cm² but mean gradient <40 mmHg
Occurs when LV stroke volume index is <35 mL/m²
More common in women with small LV cavities and in AF
Must distinguish true severe (low flow due to poor LV function) from pseudo-severe (moderate AS that appears severe at low flow)
Use dobutamine stress echo OR cardiac CT calcium scoring: an Agatston score ≥1600 in men / ≥1200 in women confirms severe AS without needing stress echo (2025 ESC/EACTS update)

Braunwald's Heart Disease, p. 1036

Chest X-ray

CXR: Rounded LV apex from LVH (white arrows) and ascending aortic dilation/arrowheads) - Grainger & Allison's, p. 338

Rounding of LV apex (LVH)
Poststenotic dilation of the ascending aorta
Aortic valve calcification visible on lateral view

Echocardiogram (B-mode)

Echocardiogram showing hyperechoic calcified aortic leaflets with mitral annulus calcification also visible

B-mode echo (horizontal long axis): Hyperechoic calcified aortic leaflets - Textbook of Clinical Echocardiography

Cardiac CT

Excellent for calcium scoring (Agatston score)
Allows direct planimetry of the valve orifice
Essential for pre-TAVR anatomy assessment (annulus sizing, coronary ostia height, access)
Agatston score of 150 is 100% sensitive for discriminating velocities <2.5 m/s from >2.5 m/s

CMR

Direct planimetry of valve orifice possible
Less sensitive than CT for calcium detection
Useful adjunct when echo is suboptimal

Management

Medical Therapy

There is no proven medical therapy that slows progression or replaces valve intervention once symptoms develop. Statins were trialed but did not reduce disease progression. Symptomatic patients who refuse or cannot undergo intervention should receive:

Diuretics cautiously for HF symptoms (avoid over-diuresis given diastolic dysfunction)
ACE inhibitors/ARBs - can be used cautiously; avoid vasodilators that precipitate hypotension
Rate control for AF (these patients are preload-dependent)

Intervention Indications

Class I - Intervention is indicated:

Symptomatic severe AS (dyspnea, angina, syncope) - this is the primary indication regardless of age or LV function
Asymptomatic severe AS with LVEF <50%
Asymptomatic severe AS undergoing cardiac surgery for another reason

Class IIa (2025 ESC/EACTS update):

Early intervention is a reasonable option vs. watchful waiting in asymptomatic severe AS with normal LVEF
Asymptomatic patients with peak velocity ≥5.5 m/s or very rapid progression (velocity increase >0.3 m/s per year) - intervention recommended even without symptoms

TAVR vs. SAVR

Patient Profile	Preferred Approach
High/prohibitive surgical risk	TAVR (any age)
Age >80 or life expectancy <10 years	TAVR
Age 65-80, low-intermediate surgical risk	Shared decision-making; TAVR or SAVR both acceptable
Age <65-70, low surgical risk	SAVR preferred (concern for long-term valve durability with TAVR)
Symptomatic, any age, high surgical risk + expected survival >12 months with acceptable QoL	TAVR

Key TAVR evidence:

PARTNER trial (inoperable patients, mean age 83): 1-year mortality 30% TAVR vs. 50% medical therapy
PARTNER low-risk trial: composite of death, stroke, or hospitalization at 1 year 8.5% (TAVR) vs. 15.1% (SAVR)
Registry data: 30-day TAVR mortality has declined from 4% to 2% over time

TAVR risks vs. SAVR: Higher risk of stroke (though declining), vascular complications, permanent pacemaker need, and paravalvular leak. Lower risk of new-onset AF and shorter hospital stay.

Braunwald's Heart Disease, p. 1036

2025 ESC/EACTS Guideline Update (Key Changes)

CT calcium scoring elevated to same level as dobutamine stress echo for LFLG-AS workup
Stronger recommendation for early intervention in asymptomatic patients (2A)
Continued 2A recommendation for high-risk asymptomatic patients (peak velocity ≥5 m/s)
TAVR expanded for intermediate-risk patients (previously required high risk)
For patients <70 at low surgical risk, SAVR remains preferred

Prognosis

Once symptoms develop, prognosis without intervention is poor (see table above). After successful AVR or TAVR, 5-year survival approaches that of age-matched controls. Bioprosthetic valve deterioration is slower in older patients, making repeat intervention less likely within their remaining lifespan.

Recent literature note: A 2025 JACC review on TAVR beyond severe AS (PMID 40044299) discusses expanding TAVR indications to moderate AS in HF patients - an evolving area to watch.

Hand drawn diagrams for examination

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