Definition, Incidence and Prevalence of Aortic Stenosis

Definition of aortic stenosis

• Aortic stenosis (AS) is also called as aortic valve stenosis
• AS happens when has become narrow or constricted (stenotic) and does not open fully thus restricting blood flow
• Aortic valve is located between the left ventricle and aorta
• The left ventricle pumps oxygen rich blood out of the heart to the aorta through aortic valve
• When aortic valce becomes stenotic, the ability of left ventricle to pump out from heart to aorta is impaired
• As a result, organs receive an insufficient supply of oxygen rich blood (heart failure), and blood may back up into the lungs causing SOB

Incidence and Prevalence

1. in US…
• Aortic sclerosis increases in incidence with age and is present in:
• 29% of individuals older than 65 years and in
• 37% of individuals older than 75 years

• Patients with severe AS may be asymptomatic for many years despite the presence of severe LV outflow tract obstruction
• Such patients have a survival similar to those without aortic stenosis
• With the appearance of symptoms, however, their survival is reduced:

Symptoms ....................Survival Rate
Angina .......................4.5 years
Syncope/dizziness............2.6 years
Congestive heart failure.....1 year

2. Mortality/Morbidity Rate

Symptomatic Patients (moderate AS)

Mortality rates are around 25% at 1 yr & 50% at 2 years
More than 50% of deaths are sudden

Asymptomatic Patients(critical AS)

Excellent prognosis regarding survival with death rate less than 1% in a year
Only 4% of sudden cardiac death in severe aortic stenosis

3. In Western populations,

Aortic sclerosis................Aortic stenosis
25% over 65.....................3 % over 75

Around 16% of patients progress to stenosis in 7 yrs

4. Incidence of MI,

DISORDER............................................INCIDENCE OF MI
Septuagenarians with normal aortic valve.........6% over 5 years
Aortic scelerosis....................................8.6%
Aortic stenosis......................................11.3%

5. As our population ages, the prevalence of aortic stenosis inevitably rises.
• By 2020, about 3.5 million of a total population of 54 million in England can be expected to have aortic sclerosis and
• 150 000 to have severe aortic stenosis

Causes of AS

Divided into two:-

Congenital

Bicuspid aortic valve (1 – 2%)
A misshapen tricuspid aortic valve
Unicuspid aortic valve (rare)

Acquired

Heart conditions and other disorders
Age-related changes (scarring and calcification)
Rheumatic fever – damages the valve
Endocarditis – damages the valve

Complications & Prognosis

AORTIC STENOSIS

Prognosis

Adults without symptoms
- excellent prognosis
- normal life expectancy but should receive
- advised to receive antibiotic prevention – aortic valve infection

Adults with symptoms
a) Mild – usually leads a normal life, but some may progress to severe disease
b) Moderate – most end up with coronary artery disease within 10 years
c) Severe – once symptoms occur, death within 2-4 years if untreated, mortality rates of 75%

- Disease curable with surgery
- Moderate & severe stenosis eventually treated with surgery (progressive disease)
- eg : valve replacement (10 year survival rate = 75%)

- Post-surgical risks
a) Arrhythmias - sudden death
b) Blood clots – stroke
c) New valve not working & need to be replaced.

Complications

—Arrhythmias
—Endocarditis
—Left ventricular hypertrophy
—Sudden death
—Congestive heart failure
—Exacerbation of coronary artery disease
—Pulmonary oedema

a) Left ventricular hypertrophy
- Aortic valve narrowed
- Left ventricle has to work harder to pump sufficient blood to aorta and rest of the body - HYPERTROPHY
- Eventually weakens, leading to
i) Heart failure
ii) Arrythmias
iii) Cardiac arrest
iv) Angina

b) Endocarditis
- Narrowed aortic valve more prone to infection
- Turbulence damages endothelium
- Bacteria & inflammatory cells adhere & grow, forming an infected vegetation
- Increased risk of bacteria entering bloodstream

c) Cardiac failure
- Lack of sufficient blood flow to meet body’s needs.
- Causes : MI, IHD, hypertension
- Leads to : Pulmonary oedema (L), peripheral oedema (R)


ANGINA

Prognosis

- Stable angina is a marker of underlying CHD
- People with angina are 2–5 times more likely to develop other manifestations of CHD than people who do not have angina.
- People with angina had higher mortality than people with no history of coronary artery disease at baseline


Features that indicate a poorer prognosis :
Ø more-severe symptoms
Ø Male
Ø abnormal resting ECG
Ø previous MI
Ø left ventricular dysfunction
Ø easily provoked or widespread coronary ischaemia on stress testing
Ø significant stenosis of all three major coronary arteries or the left main coronary artery.


Complications
- If untreated, chronic stable angina --> unstable angina (untreated)
a) Severe arrythmias
b) Sudden cardiac death

Pathophysiology

Video
http://coursewareobjects.elsevier.com/objects/hao/anim/13-010ap.htm
http://www.med.yale.edu/intmed/cardio/echo_atlas/entities/aortic_stenosis_senile.html
3rd heart sound due to possible explanations include impact of the ventricle against the inner chest wall or a sound originating within the ventricular apex due to sudden limitation of longitudinal expansion.
4th heart sound due to forceful atrial ejection.
Pathophysiology of causes:
Calcium buildup on the valve. Calcium deposits result in stiffening of the leaflets of the valve.
Rheumatic fever. Rheumatic fever may result in scar tissue forming on the aortic valve. Scar tissue alone can narrow the aortic valve and lead to aortic valve stenosis.
Congenital heart defect.
Aortic valve narrows due to the causes above.
The blood flow of ejection is disturbed, causing a loud ejection systolic murmur.
The ventricles then have to hyperthrophy to compensate for the decrease in output. However, in the long run, the ventricles dilate and this decreases the compliance of the ventricles. The atria has to pump harder to fill the ventricles, thus the 4th heart sound.
Edema in lungs is due to backflow of blood.
Explanation in detail in PCL 

wiggers diagram

shows the blood pressure in the aorta, ventricles and atria, and the
ventricular blood volume, and ECG and heart sounds and valve opening
and closing in relation to eachother on a Y-axis agant an X-axis
denoting time. The purpose of this diagram is to make it easier to
see the relationship between these values.

http://library.med.utah.edu/kw/pharm/hyper_heart1.html

Medical Management for Aortic Stenosis

Surgical repairs increases survival rate greater than fourfold compared to medical treatment.

However there is no proven medical treatments that delay the progression of AS

Also most AS patients have cardiac conditions that are controlled using medication which is hypertension, AF, CAD

Hypertension –

Uses Angiotensin converting enzyme inhibitors for severe AS

Use second generation dihydropyridine calcium channel blockers for asymptomatic AS patients

Diuretics

AF –

Use beta blockers and rate slowing calcium channel blockers

CAD –

No smoking

Regular exercise

Aspirin prophylaxis

Antimicrobial prophylaxis

Statins

Antiplatelet therapy

Anticoagulant therapy

Signs & Symptoms

Symptoms

There are usually no symptoms until aortic stenosis is moderately severe (when the aortic orifice is reduced to one-third of its normal size). At this stage, exercise-induced syncope, angina, and dyspnoea develop. When symptoms occur, prognosis is poor- on average, death occurs within 2-3 years if there has been no surgical intervention.


Signs


Pulse

The carotid pulse is of small volume and is slow-rising or plateau in nature.

Precordial Palpation

The apex beat is not usually displaced because hypertrophy (as opposed to dilatation) does not produce noticeable cardiomegaly. However, the pulsation is sustained and obvious. A double impulse is sometimes felt because the fourth heart s

Publish Post

ound or atrial contraction (kick) may be palpable. A systolic thrill may be felt in the aortic area.

Auscultation

The most obvious auscultatory finding in aortic stenosis is an ejection systolic murmur that is usually 'diamond-shaped' (crescendo-descendo)
the murmue is usually rough in quality and best head in the aortic area. it radiates into the carotid arteries and also the pericardium. the intensity of the murmur is not a good guide to the severity of the condition because it lessened by reduced carotid output. in severe cases, the murmur may be inaudible.
other findings include:
systolic ejection click unless the valve has become immobile and calcified
soft or inaudible artic second heart sound when the aortic valve becomes inaudible
reversed splitting of the second heart sound (splitting on expiration)
prominent fourth heart sound unless coexisitng mitral stenosis prevents this.