AORTIC STENOSIS
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Presentation
A classical triad is described, ‘SAD’
S – syncope (exertional)
A – angina
D – dyspnoea
Seen in around 40-50% of patients.
Murmur ® Ejection systolic, radiating to carotids
Other features include:
§ Epistaxis
§ Bruising
§ Sustained apex
§ Slow rising pulse
§ Narrow pulse pressure
§ Auscultation ® soft S2 (marker of severity), 4th heart sound/S4 (caused by atria contracting against stiff, hypertrophied
ventricles), reversed splitting.
It can also lead to acquired von Willebrand deficiency and clotting abnormalities.
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Pathophysiology
Aortic stenosis refers to the narrowing of the aortic valve.
§ Most common cause in western world is calcification of aortic valve
§ Calcification (degenerative) (80%)
o Caused by inflammation and progressive calcification
o Limits movement of aortic valve
o Affects patients later in life (>65)
o Risk factors ® hypercholesterolaemia, hypertension, smoking, diabetes
§ Bicuspid valve (congenital) (1-2%)
o Most common congenital abnormality of heart
o Males more commonly affected
o Valves are predisposed to become stenotic
o Stenosis appears at younger age (<65)
o Abnormal heart valves ® turbulent flow with subsequent fibrosis and calcification
§ Rheumatic heart disease
o Autoimmune condition following Streptococcal (group A) infection
o Inflammation results from molecular mimicry
o Affected tissues: heart, joints, CNS
o Becoming more uncommon over time.
§ Aortic stenosis ® problem of left ventricular outflow
o As valve becomes narrower, a pressure gradient develops across valve
o Initially leads to systolic dysfunction ® cannot pump out normal proportion of end-diastolic volume
o Compensatory mechanism ® left ventricular (concentric) hypertrophy
o May eventually lead to diastolic dysfunction through impaired relaxation and reduced compliance
o Cardiac failure results (features of left sided heart failure)
o Patients have reduced ability to adjust to increased myocardial demands ® exertional syncope
o Angina may develop also.
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-----------------------------------------------------------------------------------------------------------------------------------------------------
Presentation
A classical triad is described, ‘SAD’
S – syncope (exertional)
A – angina
D – dyspnoea
Seen in around 40-50% of patients.
Murmur ® Ejection systolic, radiating to carotids
Other features include:
§ Epistaxis
§ Bruising
§ Sustained apex
§ Slow rising pulse
§ Narrow pulse pressure
§ Auscultation ® soft S2 (marker of severity), 4th heart sound/S4 (caused by atria contracting against stiff, hypertrophied
ventricles), reversed splitting.
It can also lead to acquired von Willebrand deficiency and clotting abnormalities.
-----------------------------------------------------------------------------------------------------------------------------------------------------
Pathophysiology
Aortic stenosis refers to the narrowing of the aortic valve.
§ Most common cause in western world is calcification of aortic valve
§ Calcification (degenerative) (80%)
o Caused by inflammation and progressive calcification
o Limits movement of aortic valve
o Affects patients later in life (>65)
o Risk factors ® hypercholesterolaemia, hypertension, smoking, diabetes
§ Bicuspid valve (congenital) (1-2%)
o Most common congenital abnormality of heart
o Males more commonly affected
o Valves are predisposed to become stenotic
o Stenosis appears at younger age (<65)
o Abnormal heart valves ® turbulent flow with subsequent fibrosis and calcification
§ Rheumatic heart disease
o Autoimmune condition following Streptococcal (group A) infection
o Inflammation results from molecular mimicry
o Affected tissues: heart, joints, CNS
o Becoming more uncommon over time.
§ Aortic stenosis ® problem of left ventricular outflow
o As valve becomes narrower, a pressure gradient develops across valve
o Initially leads to systolic dysfunction ® cannot pump out normal proportion of end-diastolic volume
o Compensatory mechanism ® left ventricular (concentric) hypertrophy
o May eventually lead to diastolic dysfunction through impaired relaxation and reduced compliance
o Cardiac failure results (features of left sided heart failure)
o Patients have reduced ability to adjust to increased myocardial demands ® exertional syncope
o Angina may develop also.
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