Aortic Stenosis

Aortic stenosis occurs when valvular disease impedes blood flow across the valve during ventricular systole. The aortic valve is normally 2.6-3.5cm², and haemodynamically significant obstruction occurs when AVA approaches 1cm². The degree of stenosis is classified based on echocardiographic findings, using either:

Aortic valve pressure gradient/peak flow
- Pressure gradients are calculated by measuring flow across the valve, using the simplified Benoulli equation: \(\Delta P = 4v^2\)
- Peak gradients are calculated from peak flow during ejection
- Mean gradients are calculated by the average flow (area under the doppler envelope) during ejection
Aortic valve area
Derived using AV VTI, LVOT VTI, and LVOT area.
Dimensionless Index
Ratio of the LVOT VTI to the AV VTI, and therefore an area-independent measurement.

Grading of Aortic Stenosis
Technique	Mild	Moderate	Severe
Peak velocity (m/s)	2.6-2.9	3-4	>4
Mean Pressure Gradient	<30	30-50	>50
Aortic Valve Area	>1.5	1.5-1.0	<1.0
Dimensionless Index	0.5-0.75	0.25-0.5	<0.25

Pressure gradients are dependent upon flow across the valve, and may under-predict severity in failure states because the failing LV cannot generate enough pressure to produce a high flow.

Low-flow, low-gradient AS is:

Suggested by an impaired EF (<50%) and discordance between the MPG and AVA, i.e.:
- AVA <1cm²
- MPG <40mmHg
Divided into two types:
- True severe AS with impaired EF
  - ↑ Gradient with dobutamine challenge
  - Benefits from AVR
- Pseudo AS
  - No change in gradient but ↑ in AVA with dobutamine challenge
  - Does not benefit from AVR
  - Benefits from medical management

Epidemiology and Risk Factors

Risk factors include:

Male
CAD risk factors
- DM
- Hypercholesterolaemia
- Smoking
- Hypertension
- Haemodialysis
  Occurs in 10%.

Pathophysiology

In aortic stenosis:

Fixed outflow tract obstructions with valvular AS or presence of a sub-aortic membrane. Dynamic outflow tract obstruction typically occurs with HOCM.

There is a constant degree of fixed outflow tract obstruction
LV responds to obstruction by undergoing hypertrophy
Allows pressure gradient across the valve to be maintained without:
- Reduction in SV
- Ventricular dilation
LVH leads to impaired compliance and diastolic dysfunction
- Hypertrophied ventricle more dependent on atrial kick
LVH ↑ oxygen requirements, whilst ↑ LV diastolic pressures reduce coronary blood flow and oxygen delivery
Susceptible to ischaemia, especially when CO is high, even in absence of coronary artery disease.
LA hypertrophy/dilation may occur to maintain filling

Aetiology

AS may be caused by:

Degenerative calcification
Mechanical stress leading to progressive fibrosis and calcification.
- Most common cause
- Typically in those over 70
- Initially occurs as sclerosis
  Thickening/calcification of leaflets without stenosis.
Congenital bicuspid valve
Most common congenital cardiac malformation.
- Typically symptomatic in 40-60 year olds
  Accounts for 50% of AVR performed for AS in those under 70.

Assessment

Aortic stenosis typically has:

A long symptom-free period
Low morbidity and mortality over this period.
Variable onset of symptoms, depending on aetiology and degree of degeneration
- Rheumatic: 40-50
- Congenitally bicuspid: 15-65
- Degenerative: 70-90

History

Angina
Due to mismatch between LV oxygen consumption and demand.
Syncope
Late and bad sign. Occurs due to inadequate cardiac output, and may be related to either:
- ↑ demand in the setting of a relatively fixed cardiac output
- Arrhythmia
Dyspnoea
Due to LV failure, and typically occurs in late disease (as it represents a failure of LV compensation.)

Examination

Slow rising, low volume pulse
Reduced SBP and pulse pressure
Ejection systolic murmur
- Peaks in late systole
- Radiates to carotids and to apex
- May disappear in LV failure as flow through the valve orifice ↓

Investigations

Bedside:

Diagnostic TTE
Diagnostic and essential for risk stratification. Features include:
- Thickening
- Impaired mobility
- Congenital abnormalities
- Calcification of valve leaflets
ECG
- Normal in ~20%
- LAD
- LVH
- AV block
  Secondary to AV nodal calcium infiltration (extending from the aortic annulus).

Laboratory:

Imaging:

Other:

Dobutamine stress echo
Used in the setting with ↓ EF and apparent severe AS, to distinguish true AS from AS.
- Addition of inotrope improves LV function
- If the AVA is low solely due to poor LV function, then the improved VTI (with inotrope) ↑ AVA and the MPG remains similar
- If the AVA is low due to true stenosis, then the AVA does not improve (the valve is stenosed), and the MPG ↑ substantially

Diagnostic Approach and DDx

Management

Asymptomatic patients should be monitored for progression of AS or deteriorating LV function that would indicate requirement for AVR.

Resuscitation:

Specific therapy:

Pharmacological
Procedural
- Surgical AVR
- TAVI
- BAV
  Reserved for patients too high risk for surgery and inappropriate for TAVI. Results in regurgitation and risk of early restenosis.
Physical

Supportive care:

Disposition:

Preventative:

Anaesthetic Considerations

Assume a hypertrophied and non-compliant ventricle.

In mixed valvular disease, management should prioritise the most haemodynamically significant lesion. That said, in general:

In mixed AS and MR, the AS should generally be given precedence
MR tends to be improved by anaesthesia, AS tends to be worsened and is more likely to cause intraoperative crises.
In mixed AS and MS
Progression is typically similar to that with pure MS and pulmonary hypertension. Considerations include:
- Two fixed output lesions in series
- Generally high burden of pulmonary disease
- AS severity may be underestimated due to the ↓ AV flow
In mixed AS and MR, the AS should generally be given precedence
MR tends to be improved by anaesthesia, AS tends to be worsened and is more likely to cause intraoperative crises.

C
- Lesion assessment
  Preoperative TTE ideal to evaluate degree of stenosis and LV function.
  - If unable to evaluate preoperatively, treat as if patient has at least moderate severity disease
  - Impairment can be estimated by knowing that valve area reduces by ~0.1cm²/year
- Invasive arterial monitoring
- Defend:
  - Preload
    Poor ventricular compliance requires filling, therefore aim:
    - Sinus rhythm
      Aggressively manage tachyarrhythmias.
    - Low-normal (50-70) heart rate
      Adequate time for ventricular filling.
    - Euvolaemia
  - Perfusion pressure
    - Vasopressor infusions with aggressive use of boluses to maintain afterload
    - Use neuraxial techniques with caution

Marginal and Ineffective Therapies

Complications

Extensive cardiac remodelling, including:

LVH
LV diastolic dysfunction
LA dilation
MR
Due to annular dilatation.
PHTN

Prognosis

Asymptomatic severe AS:

Annual ↓ in AVA is ~0.1cm²/year
Median time to symptom development is 1-4 years
Within 5 years:
- 2/3^rds will develop symptoms
- 75% will have died or had valve replacement

Symptomatic severe AS:

Very poor prognosis without AVR
Mortality rapidly ↑ once symptoms develop
- Mean survival 0.5-2.8 years after onset of cardiac failure
- Mean survival 0.8-3.8 years after onset of syncope
- Mean survival 2-4.7 years after onset of angina
Pulmonary hypertension is an additional risk factor and worsens prognosis after valve replacement

Perioperative death and MI risk:

Symptomatic AS; OR 2.7
Co-existing moderate or severe MR; OR 9.8
Pre-existing CAD; OR 2.7

References

Brown J, Morgan-Hughes NJ. Aortic stenosis and non-cardiac surgery. Contin Educ Anaesth Crit Care Pain. 2005;5(1):1-4. doi:10.1093/bjaceaccp/mki001
Généreux P, Stone GW, O’Gara PT, et al. Natural History, Diagnostic Approaches, and Therapeutic Strategies for Patients With Asymptomatic Severe Aortic Stenosis. J Am Coll Cardiol. 2016;67(19):2263-2288. doi:10.1016/j.jacc.2016.02.057