AORTIC VALVE DISEASE

4th Introductory
Cardiothoracic Course 2004
Ian W. Colquhoun

ANATOMY

Aortic Root - Anatomy

The AORTIC ROOT has four anatomic components:
The aortic annulus or aortoventricular junction
The leaflets
SINGLE
The aortic sinuses or sinuses of Valsalva FUNCTIONAL
UNIT
The sinotubular junction

Aortic Annulus (aortoventricular junction)

N

Fibrous tissue

Myocardium

Anterior leaflet of the mitral valve

Membranous septum

Normal:
Marfan/Bicuspid aortic valve:

55%
65%

Histology:
The aortic root is in fibrous continuity with the
anterior leaflet of the mitral valve and the
membranous septum; connective tissue (fibrous
strands) unites the aortic root to the
interventricular septum.

45%
35%

Sinotubular
Junctinon

Valve Leaflets
They are attached to the aortic root in a semilunar fashion

The triangular space underneath the leaflet

(trigone) is part of the left ventricle.
The highest point of the trigone where the
leaflets meet is called the commissure. The
commissures are localised immediately
below the Sinotubular Junction.
The 2 trigones underneath the commissures
of the noncoronary leaflet are fibrous
structures, whereas the other underneath
the commissure between the right and the
left leaflets is mostly a muscular structure.

Sinuses of Valsalva
The segment of the arterial wall
of the aortic root delineated by a
leaflet proximally and by the
sinotubular junction distally is
called the aortic sinus or sinus
of Valsalva.
They are 3 elliptical inlets that
have a very important role in the
dynamics of circulation :
Guaranteeing coronary artery
perfusion during systole;
Creating eddies to close the
aortic leaflets during diastole

Sinotubular Junction
It represents the terminal edge of the aortic root and it
is constituted by the imaginary line that connects
together the 3 commissures.
Young
adults
AA>STJ
Adults
AA =
STJ
Elderly
AA<STJ

BASE = Aortic Annulus (AA)

Anatomic and Echocardiographic Relationship

Between the Components of the Normal Aortic Root
120 degree - LAX

Annulus
Sinuses

Systole

ST junction
Tubular aorta
Diastole

AORTIC STENOSIS

Morphology

Calcific Aortic Stenosis

Congenitally bicuspid or unicuspid,
fused commissures, heavy
calcification, age 40-60
1% Population

Rheumatic Aortic Stenosis

Fibrous thickening, 3-cusp valve,
mild calcification, commisural fusion,
rheumatic fever history in

Degenerative Aortic Stenosis

Diffuse nodular calcification
3-cusp valve, no commissural fusion

Aortic Stenosis Aetiology /

Age

AGE <70

AGE >70

Levels of stenosis (1)

SUPRA VALVAR

WILLIAMS SYNDROME

Elfin-like facies
Hypervitaminosis D
Pulmonary stenoses valvar
& peripheral
Mesenteric artery stenosis
Thoracic aneurysm

Levels of stenosis (2)

SUB VALVAR

DISCRETE FIBROMUSCULAR RING

10% congenital AS
Presents <1year of age
50% have other cardiac defects

HOCM

ANOMALOUS ATTACHMENT of MITRAL VALVE

AV canal
Parachute deformity of mitral fused papillary
muscles

Aortic Stenosis:
Pathophysiology

Normal valve area = 2.5 3.5 cm2

Gorlan Formula

MILD AS
MODERATE
SEVERE
CRITICAL

>1.2cm2
1.0 1.2 cm2
0.8 1.2 cm2
<0.8cm2

Severe AS & normal cardiao output = transvalvar gradient >50mmHg

Pressure overload

Concentric left ventricular hypertrophy

increased wall stress, decreased ejection fraction
reduced coronary reserve, subendocardial ischaemia

Increased LVEDP
Higher preload required
Left atrial hypertrophy, prominent a wave
Loss of sinus rhythm serious clinical deterioration

Eventual failure and dilatation of LV

AS: Clinical Picture

Symptoms

Asymptomatic

Syncope

cerebral hypoperfusion vs. dysrhythmias

Angina

myocardial O2 supply/demand imbalance

Congestive Heart Failure

Sudden death

AS: Diagnosis
CVS:

Loud harsh crescendodecrescendo murmur

radiating to neck

Possible diastolic murmur (AI

murmur)

Split S2, possible S4 with

atrial hypertrophy

Prominent presystolic apical

impulse

Diminished carotid upstroke

ECG:

LVH

LA hypertrophy

conduction abnormalities

AS: Diagnosis
CXR

Left ventricular prominence with

possible cardiomegaly
Calcifications at level of aortic valve

Echocardiogram with Doppler

Heart Catheterization

Coronary artery anatomy

recommended for all pts
Visualization of aorta
Quantify gradient across valve
Calculate aortic valve area with
Gorlan formula
Quantify aortic regurgitation
Assess mitral valve, regional wall
motion disturbances, and left
ventricular function

ECHOCARDIOGRAPHY

Natural History - Stenosis

a) HAEMODYNAMICALLY SEVERE (symptomatic or asymptomatic)

Sudden death risk high

Immediate operation is indicated

b) HAEMODYNAMICALLY MILD MODERATE (asymptomatic)

50% event free for 4 years

Operation is not urgent, but patients should be followed

carefully as the disease advances rapidly

c) HAEMODYNAMICALLY MILD MODERATE (symptomatic)

One-third will die within 4 years

Prompt operation is indicated

Natural History Progression average of 0.1cm2 per year

Onset of Symptoms correlates with mortality risk

Stenosis Medical therapy

AORTIC
REGURGITATION

AR : Pathophysiology
Cusp Perforation
Cusp Prolapse
Restrictive Motion
Sinotubular Junction Dilatation
Annulus Dilatation
Annulo-aortic Ectasia

AR due to Abnormalities of the Leaflets

Infective endocarditis
Trauma
Iatrogenic cause

Cusp perforation

AR due to Abnormalities of the Leaflets

Excess of tissue
Disrupted commissure
Commissural malposition

Cusp prolapse

AR due to Abnormalities of the Leaflets

Fibrous thickening

Restrictive motion

AR - Abnormalities of the Aortic Wall

Sinotubular junction dilatation

Dilatation of the sinotubular junction displaces the commissures outward and prevents
the aortic leaflets from coapting, with resulting central aortic insufficiency

AR - Abnormalities of the Aortic Wall

Marfan syndrome
Connective tissue diseases
Ventricular dilatation
Chronic hypertension

Annular dilatation

AI due to Abnormalities of the Aortic Wall

Aortic root
aneurysm:
ST junction
dilatation
+
Sinuses of
Valsalva
aneurysm

Aortic Regurgitation (1)

CONGENITAL

Bicuspid valve
Supra-valvar
stenosis
Supra-cristal VSD
and right coronary
prolapse
Sinus of Valsalva
aneurysm

Aortic Regurgitation (2)

ACQUIRED

VALVE - Cusp prolapse or cicatricial

shortening of cusps with rolled edges

Rheumatic fever
Infective endocarditis
Rheumatoid disease
SLE
Hurlers syndrome

AORTIC ROOT - Dilation of sinus aorta,

failure of coaptation of cusps

Dissection
Syphilis
Cystic medial necrosis e.g Marfans
annulo-aortic ectasia
Arthritides with aortitis e.g. Ankylosing
spondylitis
Hypertension
Trauma

Aortic Valve Insufficiency

It may be due to alteration of the valve, the ascending aorta or both.

Etiology:

Idiopathic degenerative disease

Aortic dissection
Calcific aortic disease
Myxomatous degeneration
Rheumatic or postinflammatory
disease
Bicuspid aortic valve
Trauma
Infective endocarditis
Idiopathic dilatation of the aortic
root
VSD of the membranous septum

Systemic diseases (Whipple

disease; Crohns disease;)
Aortitis (Syphilis, viral
syndromes; giant cell
arteritis;Takayasu disease;
Chronic systemic hypertension
Connective tissue disorders
(Marfans syndrome; Reiters
disease; Ehlers-Danlos
syndrome; Osteogenesis
imperfecta; Rheumatoid
arthritis syndrome; Ankylosing
Spondylitis; SLE;)

Aortic Valve Insufficiency

Annulus
Annulo-aortic ectasia
Leaflets
Prolapse
Degeneration
Infectious disease

Acute
Chronic

Valve Sparing

Sinuses of Valsalva
Dilatation of one or more sinus
Ascending aorta dissection

Sinotubular Junction
Global dilatation (including ascending aorta)

ECHOCARDIOGRAPHY

AR - Diagnosis
Eponyms associate with AR

Austin-Flint murmur
vibrations of anterior mitral
leaflet
Duroziezs sign to and
fro femoral artery murmur
Quinckes pulse capillary
pulsation in finger tips
Traubes sign pistol shot
sound at femoral artery
De Mussets sign head
bobbing

Natural History Incompetence

a) Latent period to cardiac decompensation is long
Sudden death is not common

Once deterioration begins, the LV fails rapidly

b) Symptomatic patient with CHF, angina, syncope

Prompt operation is indicated
c) Asymptomatic patient
Follow carefully for LV enlargement or decreased LV
function by ECHO or MUGA
Operate at an appropriate time

Regurgitation Medical
therapy

Associated Coronary Artery

Disease
Treat significant
coronary artery disease
at the time of surgery
even if asymptomatic
CABG reduces risk of
AVR and improves longterm survival
Coronary angiography is
indicated in all patients
older than 45 years
who will be having AVR

ACC/AHA Guidelines for the

Management of Patients With
Valvular Heart Disease. Executive
Summary. A report of the American
College of Cardiology/American Heart
Association Task Force on Practice
Guidelines (Committee on
Management of Patients With
Valvular Heart Disease).
Bonow RO, Carabello B, de Leon AC, Edmunds LH Jr,
Fedderly BJ, Freed MD, Gaasch WH, McKay CR, Nishimura
RA, O'Gara PT, O'Rourke RA, Rahimtoola SH, Ritchie JL,
Cheitlin MD, Eagle KA, Gardner TJ, Garson A Jr, Gibbons RJ,
Russell RO, Ryan TJ, Smith SC Jr.
J Heart Valve Dis. 1998 Nov;7(6):672-707

MANAGEMENT - AS

ASYMPTOMATIC

SYMPTOMATIC

Mild moderate stenosis

AVR

Medical follow up
Regular ECHO
Avoid strenuous
exercise
Endocarditis prophylaxis
? Role for statins
Progress ~0.1cm2 per
year

Angina, syncope,
failure
Moderate AS + CAD
Reduced BP on
exercise
Severe AS & reduced
LV function

MANAGEMENT - AR
MEDICAL

Calcium channel
blocker
Regular ECHO
Avoid isometric exercise
Endocarditis
prophylaxis
Monitor for symptoms

SYMPTOMATIC

AVR

Symptom onset

Asymptomatic if:

Protracted course

LVESD
LVEDD
LVEF

> 50-55mm
> 70-75mm
< 55%

AORTIC VALVE
REPLACEMENT

Age and AVR

Advanced age most common
predictor of survival and cardiac
events
AVR very effective treatment even
in patients over age 70 or 80
Even the best patients over age 80
have reduced reserve

Trends in choice of
prosthesis
Age less than 55 years - Aortic allograft or

pulmonary autograft

Age between 55-75 years - Mechanical

prosthesis
Age greater than 75 years - Porcine
heterograft, stented or stentless
Allografts and autografts enlarge the orifice
by about 2 mm, porcine heterografts reduce
valve size by about 2 mm, and mechanical
valves reduce valve size by about 5-8 mm

Operative Principles

Restore unimpeded flow

through aortic annulus / left
ventricular outflow tract

Remove stenosis /
regurgitation

Match valve size to patient

Repair / replace abnormal

aorta reimplantation of
coronary arteries

Concomitant pathology
addressed:
CABG
Mitral valve

Pitfalls

Inadequate decalcification
Too vigorous decalcification
Heart block from suture
Coronary ostial occlusion from sewing
ring
Debris lodging in Left coronary ostium

Operative Results

Increased risk if

Emergency
NYHA Class III IV
>65 years old
Severe AS AVA<0.7 or AVG>70, LVEDP>20
Impaired LV systolic function
Need for other procedure (CABG)
Renal dysfunction
Small BSA
Redo operation

Post op complications:

Operative mortality: ~ 5%
Complete heart block
Ischemic heart disease (6 months from coronary ostial
stenosis)
CVA 3 5%

Long term survival

5 year survival

Normal LV function: 96%

Overall

80% @ 5 years
60% @ 10 years
Depressed LV function: 63%

Valve related morbidity responsible for >50% late

deaths

Bioprosthetic valve - Reoperation:

25% @ 10 years
65% @ 15 years

Surgical exposure

Valve excision /
debridement

Suturing technique

Minimally Invasive

Function of the Aortic Root

The function of the aortic valve is related to the
integrity of:
Leaflets and their coaptation area
Annulus
Sinuses of Valsalva
Commissures
supra valvular
Sinotubular junction
apparatus

Patient -Prosthesis
Mismatch
Understand the concepts of EFFECTIVE ORIFICE AREA rather than VALVE
SIZE
Not all similarly labelled valves are the same!!
a) 19 mm
Prohibitively high LV/Ao gradient
Enlarge the aortic root or perform stentless / Ross procedure instead
b) 21 mm
Adequate size if BSA 1.5-1.7 M2 and patient is sedentary
If BSA greater than 1.7 M2 = enlarge the aortic root
survival 80% vs 60%)
c) 23 mm or larger
Acceptable LV/Ao gradient in all patients

(10 year

Survival After AVR

a) Early (hospital) death - 3-6%
b) Time-related survival

5 years - 75%

10 years - 60%

15 years - 40%
c) Mode of death

Early due to CHF, hemorrhage, infection, CVA

Sudden - 20%

Device related - 20%

Risk Factors for Survival after

AVR
Advanced age
Functional status (NHYA class)
Depressed LV function (aortic
incompetence)
Coronary artery disease
Presence of endocarditis
Aneurysm of ascending aorta
Mismatch of prosthesis and body size

The Small Aortic Root (1)

Nicks Procedure
Manougian Procedure

Upsize valve x1 or
2

Simplest technique

The Small Aortic Root (2)

Konno Procedure

Upsize valve x2 or 3
sizes

Complex technique
Paediatric population

Aortic Root Infections

Prosthetic Valve Endocarditis