AORTIC STENOSIS( AS)

DEFINITION

AS is a progressive obstruction of the LV outflow

tract, resulting in pressure hypertrophy of the LV
& clinically present with a triad of chest pain,
palpitations & dyspnea.
 Introduction
Normal aortic valve : 3-4 sq.cm

Significant AS : 1 sq.cm

Critical AS : 0.5 sq.cm

80% symptomatic adults AS- males

 ETIOLOGY
Congenital ( bicuspid aortic valve)

Rheumatic

Degenerative ( age related)

Calcifications

Idiopathic
 Pathology in AS

May be congenital or may be worsened by

degenerative inflammation of the aortic valve
Rheumatic inflammation of the valve gradual
fibrosis, calcification
Abnormal architecture of the leaflets
Idiopathic calcific AS- wear & tear phenomenon
 Other LV outflow tract obstruction

HOCM- marked LV hypertrophy mainly inter-

ventricular septum
Discrete congenital subvalvular AS presence of
membrane diaphragm or a fibrous ridge just
below aortic valve
Supravalvular AS- Narrowing of the ascending
aorta, a congenital anomaly/ fibrous diaphragm
 Pathophysiology in AS

LV outflow tract obstruction leading to systemic

pressure gradient between LV & aorta
Progress to LV dilatation, decrease stroke volume
& later to LVH
LV systolic pressure severity of AS ( upto 300
mm of Hg)
Later, LA, pulmonary artery, RV pressure
increases
 Symptoms of AS
Chest pain Angina
Palpitations
Exertional dypsnea ( CO)
Exertional syncope ( CO)
Symptoms of RVF
Symptoms of LVF
SCD ( arrythmias)
 Chest pain ( angina) in AS

Increase O2 demand ( LV hypertrophy)

Interference to coronary blood flow- pressure
compressing the coronary arteries > coronary
perfusion pressure
Metabolic evidence of myocardial ischemia
( Lactate production in AS)
Presence of IHD ( age group 5-7 decade)
Hemodynamics in combined lesion

Rheumatic AS is usually associated with Rh.

Mitral valve disease
AS intensifies the severity of MR
When AS & MS co-exist, MS masks the findings
of AS
 Physical Findings
Slow rising carotid pulse
Pulsus parvus et tardus ( radial)
Nipping of the systolic BP ( 200 rules out severe
AS)
JVP- normal ( prominent a in RVF/CCF)
Apex beat down, out & heaving in nature
Signs of pul. HTN in severe AS
Systolic thrill at the base of the heart
 Auscultatory signs in AS

ESM low pitched, rough, rasping in character,

loudest at aortic area conducting to the carotids
S1 may be normal
As severity increases, A2 disappear- now single S2
Paradoxical split due to prolonged ejection (P2A2)
S4 presence indicates decrease LV compliance
 Investigations

Chest x ray cardiomegaly LV type

- calcification of the valve
-post stenotic dilatation of the
ascending aorta
ECG - LVH with strain pattern (85%)
-AV intraventricular defects
 Specialized investigations

2D- ECHO reveal LVH, valvular calcification

Doppler ECHO- Diagnostic, determine the cause
location & asses severity
Catheterization & Coronary angiography- in
severe AS, as a pre request to the surgery.
Preferred in young AS, LV obstruction with
normal valve, IHD patients.
 Medical Management of AS

Treatment of AS
Treatment of arrhythmias
Prophylaxis of RF
Prophylaxis of IE
Statins for hyperlipidemia
Anti-anginal drugs for angina
 Severity of AS

Aortic valve < 0.5 sq.cm

Reverse splitting of S2 (P2-A2)
Long murmur or late peaking
Gradient across aortic valve >50mm of Hg
Absent A2 ( single S2)
Presence of S4
 Indications for surgery

Symptomatic AS
Severe / critical AS
Failed medical line of treatment
AS with AR
AS before severe LV dysfunction
 Surgeries in AS

Balloon aortic valvuloplasty

- useful in children/adults/ congenital AS
-as a bridge to surgery with severe LV
dysfunction
Aortic Valve Replacement ( AVR)
- by mechanical valves
- by prosthetic valves
 Complications of AS

CCF
IE
Arrhythmias
Strokes- Adams attacks
SCD
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