Timing of aortic

valve surgery
Moch. Arif Nugroho, FIHA
Indonesian Society of Echocardiography
Disclossure

▪ No conflict of interest
Aortic Stenosis
Valvular Aortic Stenosis

Start: Leaflet changes (Risk)

Asymptomatic
PROGRESSIVE

End: Obstruction of left

ventricular outflow
Resulting in inadequate cardiac output, decreased
exercise capacity, heart failure, and death from
cardiovascular causes
 Epidemiology

Death rate
50-59 year > 75 years > 80 years > 50% in 2 year in
symptomatic AS

 Diagnosed with Aortic Stenosis

 Aortic stenosis 2% US population >65yrs old

 Aortic sclerosis 29% US population> 65 yrs old

 Aortic sclerosis 50% greater risk of mortality

and myocardial infarction.

 Aortic sclerosis progresses to aortic stenosis in 9%

over 5 years
What Causes Aortic Stenosis?

Age-Related Calcific Aortic Aortic stenosis in patients over the age of 65 is

Stenosis usually caused by calcific (calcium) deposits
associated with aging

Adults who have had rheumatic fever may

Rheumatic Fever also be at risk for aortic stenosis

In some cases adults may develop aortic

Congenital Abnormality stenosis resulting from a congenital
abnormality
Aortic Stenosis Is Life Threatening
and Progresses Rapidly
Echocardiographic Guidelines are the Gold
Standard in Assessing Severe Aortic
Stenosis

 According to the 2014 ACC/AHA guidelines, severe aortic stenosis is defined

as:
 Aortic valve area (AVA) less than 1.0 cm2
 Mean gradient greater than 40 mmHg or jet velocity greater than 4.0 m/s
 Stages of the disease
STAGE DESCRIPTION DEFINITION
A At risk Aortic valve sclerosis or bicuspid
valve
Vmax of <2 m/sec
B Progressive Mild-to-moderate calcification or
rheumatic changes with reduced
leaflet Motion. Vmax of 2 to 3.9
m/sec or mean transaortic pressure
gradient of 20 to 39 mm Hg
OURCOME MANAGEMENT
Associated with a 50% Assessment of
increase in the risk of cardiovascular risk factors
myocardial infarction and and primary prevention
cardiovascular death over
5 yr
Vmax of 2 to 3.9 m/sec or Hemodynamic progression
mean transaortic in most patients
pressure gradient Assessment of cardio-
of 20 to 39 mm Hg vascular risk factors
and primary prevention;
periodic clinical and echo-
cardiographic monitoring;
patient education about
disease progression and
STAGE DESCRIPTION DEFINITION OUTCOME MANAGEMENT
C1 Asymptomatic, Severe calcification or rheumatic Symptom onset in 50 to Frequent clinical monitoring
severe aortic changes with reduced leaflet 80% of patients within 3 (≤6 mo) and
stenosis with normal motion; Vmax of ≥4 m/sec or mean yr; low risk of sudden echocardiographic
left ventricular transaortic pressure gradient of death; variability in monitoring (≤12 mo) for
function ≥40 mm Hg with an ejection severity at symptom symptom onset and disease
fraction of ≥50% onset; symptom onset in progression; consider
>50% of patients with treadmill exercise testing or
very severe aortic testing serum levels of brain
stenosis (Vmax of >5 natriuretic peptide;
m/sec) within 2 yr AVR is reasonable with
asymptomatic very severe
aortic stenosis
C2 Asymptomatic, Severe calcification or rheumatic If other causes of left AVR is recommended to
severe aortic changes with reduced leaflet ventricular dysfunction preserve left ventricular
stenosis motion; Vmax of ≥4 m/sec or mean are absent, the ejection function
with ejection transaortic pressure gradient of fraction is likely to
fraction <50% ≥40 mm Hg with an ejection normalize after AVR
fraction <50%
STAGE DESCRIPTION DEFINITION
D1 Symptomatic, Severe calcification or rheumatic
severe, high gradient changes with reduced leaflet
aortic stenosis motion; Vmax of ≥4 m/sec or mean
transaortic pressure gradient of
≥40 mm Hg
D2 Symptomatic, Severe calcification or rheumatic
severe, low-gradient changes with reduced leaflet
aortic stenosis with motion; baseline AVA of ≤1 cm2
ejection fraction with Vmax of <4 m/sec with an
<50% ejection fraction of <50%; Vmax of
≥4 m/sec with AVA of ≤1 cm2 at
any flow rate on low-dose
dobutamine stress testing
D3 Symptomatic, Severe calcification or rheumatic
severe, low-flow, changes with reduced leaflet
low gradient aortic motion; baseline AVA of ≤1 cm2
stenosis with normal and Vmax of <4 m/sec with an
ejection fraction ejection fraction of ≥50%; Indexed
AVA of ≤0.6 cm2/m2 with stroke
volume index of <35 ml/m2 when
patient is normotensive
OUTCOME MANAGEMENT
Mortality is 50% at 1 yr, 70 Prompt AVR is the only
to 80% at 2 yr without effective therapy
AVR
Mortality at 2 yr is about AVR is reasonable if severe
80% with medical therapy, aortic stenosis is present;
as compared with 40% the ejection fraction is
with AVR; operative likely to improve after AVR,
mortality is higher and even in patients without
survival lower in patients contractile reserve
without contractile
reserve
Mortality at 2 yr is 50 to AVR is reasonable in
70% without AVR symptomatic patients
if evaluation indicates the
presence of severe aortic
stenosis and there is no
other cause for symptoms
Timing of Intervention

▪ Class I
▪ AVR is recommended with severe high-gradient AS who
have symptoms by history or on exercise testing (stage
D1)
▪ AVR is recommended for asymptomatic patients with
severe AS (stage C2) and LVEF <50%
▪ AVR is indicated for patients with severe AS (stage C or
D) when undergoing other cardiac surgery
Timing of Intervention
▪ Class IIa
▪ AVR is reasonable for asymptomatic patients with very
severe AS (stage C1, aortic velocity ≥5 m/s) and low surgical
risk
▪ AVR is reasonable in asymptomatic patients (stage C1) with
severe AS and decreased exercise tolerance or an exercise
fall in BP
▪ AVR is reasonable in symptomatic patients with low-flow/low-
gradient severe AS with reduced LVEF (stage D2) with a low-
dose dobutamine stress study that shows an aortic velocity
4 m/s (or mean pressure gradient 40 mm Hg) with a valve
area 1.0 cm2 at any dobutamine dose
Timing of Intervention

▪ Class IIa
▪ AVR is reasonable in symptomatic patients who
have low-flow/low-gradient severe AS (stage D3)
who are normotensive and have an LVEF ≥50% if
clinical, hemodynamic, and anatomic data support
valve obstruction as the most likely cause of
symptoms
▪ AVR is reasonable for patients with moderate AS
(stage B) (aortic velocity 3.0–3.9 m/s) who are
undergoing other cardiac surgery
Timing of Intervention

▪ Class IIb
▪ AVR may be considered for asymptomatic patients
with severe AS (stage C1) and rapid disease
progression and low surgical risk
Aortic Regurgitation
Etiology of AR (Chronic)

▪Two major causes:

A. Intrinsic structural valve problem
1. Congenital : Bicuspid valve
2. Acquired : - Inflammatory (Rheumatic,
Connective tissue diseases)
- Infectious (IE)
- Degenerative
Etiology of AR (Chronic)

B. Abnormality of the Ascending Aorta

1. Congenital : Marfans disease
2. Infectious : Syphilis (15-25yr after infection)
3. Inflammatory : Connective tissue diseases
4. Idiopathic : progressive dilation (cystic medial
necrosis)
Etiology (Acute)

▪ Trauma
▪ Aortic dissection
▪ Infective endocarditis
 Aortic regurgitation ↓ effective Stroke volume

Excess volume to the LV

↑LV end diastolic pressure

↓ Myocardial O2 supply
Stretching of Myocardium

LV failure
(Ischemia)
↑ wall stress

Eccentric LV hypertrophy ↑ Myocardial O2 demand

(Ischemia)
 T I M E

Developing Compensatory Heart Failure

Hypertrophy Hypertrophy
Physiologic Incerased Increased LV Contractile
Preload and volumes and dysfunction
Afterload Mass
Cellular Signal Increased Necrosis anad
transduction sarkomer and fibrosis
fibroblast
Molecular Increased Isoenzymatic Irreversible
Protein synthesis shift, collagen disfunction
synthesis
STAGE DESCRIPTION VALVE ANATOMY VALVE HEMODYNAMIC CONSEQUENCES
A At risk - Bicuspid aortic valve (or other AR severity: None None
congenital valve anomaly)
- Aortic valve sclerosis
- Diseases of the aortic sinuses or
ascending aorta
- History of rheumatic fever or
known rheumatic heart disease
- IE
B Progressive - Mild-to-moderate calcification Mild AR: - Normal LV systolic
of a trileaflet valve bicuspid o Jet width <25% of LVOT; function
aortic valve (or other congenital o Vena contracta <0.3cm; - Normal LV volume or
o RVol <30 mL/beat;
valve anomaly) mild LV Dilation
o RF <30%;
- Dilated aortic sinuses o ERO <0.10 cm2;
- Rheumatic valve changes o Angiography grade 1+
- Previous IE Moderate AR:
o Jet width 25%–64% of
LVOT;
o Vena contracta 0.3–0.6 cm;
o RVol 30–59 mL/beat;
o RF 30%–49%;
o ERO 0.10–0.29 cm2;
o Angiography grade 2+
STAGE DESCRIPTION VALVE ANATOMY
C Asymptomatic - Calcific aortic valve disease
severe AR - Bicuspid valve (or other
congenital abnormality)
- Dilated aortic sinuses or
ascending aorta
- Rheumatic valve changes
- IE with abnormal leaflet closure
or Perforation
D Symptomatic - Calcific aortic valve disease
severe AR - Bicuspid valve (or other
congenital abnormality)
- Dilated aortic sinuses or
ascending aorta
- Rheumatic valve changes
- IE with abnormal leaflet closure
or Perforation
VALVE HEMODYNAMIC
Severe AR:
o Jet width ≥65% of LVOT;
o Vena contracta >0.6 cm;
o Holodiastolic flow reversal
o RVol ≥60 mL/beat;
o RF ≥50%;
o ERO ≥0.3 cm2;
o Angiography grade 3+ to4+;
o evidence of LV dilation
Severe AR:
o Jet width ≥65% of LVOT;
o Vena contracta >0.6 cm;
o Holodiastolic flow reversal
o RVol ≥60 mL/beat;
o RF ≥50%;
o ERO ≥0.3 cm2;
o Angiography grade 3+ to4+;
o evidence of LV dilation
CONSEQUENCES
C1: Normal LVEF ( 50%)
and mild-to-moderate LV
dilation (LVESD 50 mm)
C2: Abnormal LV systolic
function with depressed
LVEF (<50%) or severe LV
dilatation (LVESD >50 mm
or indexed LVESD >25
mm/m2)
- Symptomatic severe AR
may occur with normal
systolic function (LVEF
>50%), mildto-moderate
LV dysfunction (LVEF
40% to 50%), or severe
LV dysfunction (LVEF
<40%);
- Moderate-to-severe LV
dilation is present.
Treatment

▪ Medical treatment
▪ Treatment of hypertension (systolic BP >140 mm Hg) is
recommended in patients with chronic AR (stages B and C),
preferably with dihydropyridine calcium channel blockers or
ACE inhibitors/ARBs. (Level of Evidence: B)

▪ Medical therapy with ACE inhibitors/ARBs and beta blockers

is reasonable in patients with severe AR who have symptoms
and/or LV dysfunction (stages C2 and D) when surgery is not
performed because of comorbidities. (Level of Evidence: B)
Timing of Surgery

▪ Class I
▪ AVR is indicated for symptomatic patients with severe AR
regardless of LV systolic function (stage D). (Level of
Evidence: B)
▪ AVR is indicated for asymptomatic patients with chronic
severe AR and LV systolic dysfunction (LVEF <50%) at rest
(stage C2) if no other cause for systolic dysfunction is
identified. (Level of Evidence: B)
Timing of Surgery

▪ Class I
▪ AVR is indicated for patients with severe AR (stage C or
D) while undergoing cardiac surgery for other
indications. (Level of Evidence: C)
▪ Class IIa
▪ AVR is reasonable for asymptomatic patients with severe
AR with normal LV systolic function (LVEF >50%) but with
severe LV dilation (LVESD >50 mm or indexed LVESD >25
mm/m ) (stage C2). (Level of Evidence: B)
2
Timing of Surgery

▪ Class IIa
▪ AVR is reasonable in patients with moderate AR (stage B)
while undergoing surgery on the ascending aorta, CABG, or
mitral valve surgery. (Level of Evidence: C)
▪ Class IIb
▪ AVR may be considered for asymptomatic patients with
severe AR and normal LV systolic function at rest (LVEF >50%,
stage C1) but with progressive severe LV dilatation (LV
enddiastolic dimension >65 mm) if surgical risk is low. (Level
of Evidence: C)
Conclussion

▪ aortic valve replacement improves survival and

quality of life in symptomatic patients with severe
aortic stenosis or regurgitation
▪ Even when left ventricular systolic dysfunction is
present preoperatively, patients with both aortic
stenosis and regurgitation show an improvement in
systolic function after valve replacement
▪ Aortic valve surgery in the asymptomatic patient with
aortic stenosis remains controversial except in patients
with severe stenosis undergoing other cardiac surgical
procedures.
▪ Patients with chronic aortic regurgitation, periodic
echocardiography is indicated to identify patients who
develop evidence of left ventricular dysfunction before
symptom onset. If surgery is performed soon after the
onset of ventricular dysfunction, left ventricular size and
ejection fraction are likely to return to normal
postoperatively.