NATURAL HISTORY, HEMODYNAMICS AND SURGICAL MANAGEMENT OF AORTIC STENOSIS

1. NATURAL HISTORY, HEMODYNAMICS
AND SURGICAL MANAGEMENT OF
AORTIC STENOSIS

2. Aortic Stenosis
• Etiology based on location
– Supravalvular
– Subvalvular-
– Valvular
Congenital
Bicuspid
Rheumatic
Senile degenerative

3. • Reduction of the size of the aortic orifice does
not result in a pressure drop across the valve at
rest until at least 50% of the valve area is
narrowed (i.e., aortic valve area of approximately
1 cm2).
• However, a prominent systolic murmur may be
present even in mild degrees of aortic stenosis.
• Hemodynamically significant aortic stenosis
occurs when the aortic valve area is reduced by
60 to 75%, resulting in a calculated aortic valve
area of 0.7 to 0.8 cm2 .
• Symptoms are likely to appear at this stage, and
definite evidence of left ventricular hypertrophy
is usually present.

4. Degenerative Calcific Aortic Stenosis
• Has a prolonged latent period during which symptoms are
minimal or even lacking.
• Once moderate aortic stenosis is present and symptomatic,
the average rate of progression of the valvular stenosis is-
- Decrease in the valve area of 0.1 cm2/yr.
- Increase in the jet velocity of 0.3 m/second/yr
- Increase in the mean pressure gradient of 7 mm
Hg/yr.
• Risk factors for atherosclerosis(such as age, smoking,
hypertension, obesity and diabetes, lipid abnormalities,
chronic renal failure ) and atherosclerotic disease itself
(such as concomitant coronary artery disease) are
associated with more rapid rates of progression of the
severity of the aortic stenosis.

5. Bicuspid aortic valve stenosis
• Bicuspid aortic valve stenosis presents one or two
decades earlier than the tricuspid aortic valve. The rate
of progression of degenerative aortic stenosis can be
faster in patients with bicuspid aortic valve than in
those with congenital or rheumatic disease.
• Bicuspid aortic valve functions without any significant
pressure gradient during childhood. However, the
thickening and calcification of the valves may be
detectable pathologically and on echocardiography by
the second decade.
• Approximately 75% of bicuspid aortic valves progress
into aortic stenosis requiring operative correction

6. • The annual mortality rate is < 1% per year in
asymptomatic patients. Only 4% of sudden
cardiac deaths that occur in patients with aortic
stenosis occur in those patients who are
asymptomatic.
• Medical treatment of newly diagnosed moderate
to severe symptomatic aortic stenosis is
associated with a 25% mortality at one year and a
50% mortality at two years. Half of the deaths are
due to sudden cardiac death.

7. Data from postmortem studies
• The average durations of various symptoms
were:
– Angina pectoris: 3 years,
– Syncope: 3 years,
– Dyspnea: 2 years and
– Congestive heart failure: 1.5 to 2 years.

8. Causes of death
• Congestive heart failure: 50-60%.
• Infective endocarditis: 15-20%.
• Sudden death: 15-20%.-----
Tended to occur in patients with symptoms.
65-80% of patients had history of angina pectoris,heart
failure, or syncope.
12-20% of patients had evidence of old or
recent myocardial infarction.
Only 3-5% of deaths appear to occur
suddenly in patients without symptoms.

9. Changing Spectrum of AS
• Aortic stenosis in the 21st century is the result of
2 main pathological processes*
– Congenital bicuspid aortic valves and
– Atherosclerotic/calcific aortic valves.
• The present patient population is older.
• They have more associated coronary artery
disease.
• There has been improvements in the treatment
of heart failure and infective endocarditis.

10. 622 patients with asymptomatic AS with mean follow up of 5.4±4.0
years.
Peak systolic velocity ≥ 4 m/s.
Predictors of symptom development:-
AV area
LVH.
Predictors of all-cause mortality:-
Age
CRF
Inactivity
AV velocity

11. • Most patients with asymptomatic,
hemodynamically significant AS will develop
symptoms within 5 years.
• Sudden death without preceding symptoms
occurred in 11 (4.1%) i.e. ≈1%/y.
• Patients with peak velocity ≥4.5 m/s had a higher
likelihood of developing symptoms (relative risk,
1.34) or having surgery or cardiac death (relative
risk, 1.48).

13. • 116 consecutive asymptomatic patients with
median follow up of 41 months.
• Very severe isolated aortic stenosis defined by
a peak aortic jet velocity (AV-Vel)≥5.0 m/s.
• End points: Cardiac death or indication for
aortic valve replacement according to the
accepted guidelines.

15. • Patients with asymptomatic very severe aortic
stenosis have a poor prognosis with a high
event rate and a risk of rapid functional
deterioration.
• Early elective valve replacement surgery
should therefore be considered in these
patients.

16. Stenosis progression in aortic stenosis

18. Pathophysiology
Pressure gradient across the aortic valve increases exponentially (not
linearly) with decreasing aortic valve area

19. Pathophysiology
• Increase in afterload
• Progressive hypertrophy-Concentric
hypertrophy-- II sarcomeres
• Decrease in systemic and coronary flow

20. Framework for how mechanical stress (σ) is
transduced into pressure versus volume overload
hypertrophy.

22. Compensatory Mechanisms
• Adaptive and maladaptive
• Progressive worsening of left ventricular
outflow obstruction leads to hypertrophy
• Compensatory hypertrophy required to
maintain wall stress (afterload)
• Augmented preload with increased atrial kick
preserve LV systolic function

23. Subendocardial ischemia
• Perivascular fibrosis- ECM ellaboration
• Large diameter myocytes impairing O2 diffusion
• High LVEDP- dec coronary diastolic perfusion
• Inc O2 consumption from increase mass and wall stress
• Epicardial CAD

25. • ↓ EF:-
1) Normal Contractility
increased - Afterload “ mismatch”
increased preload- noncompliant vent
asynchronous uncoordinated contraction- wall stress
2) decreased contractility- multifactorial
↓ supply to endocardium
↓ coronary flow reserve
cytoskeletal abnormalities
diastolic dysfunction
pathological LVH

28. • In mild AS, intracardiac pressures and CO - normal
• As the valve becomes more stenotic- normal at rest, unable
to increase CO during exercise
• Progressive narrowing of the valve leads to decreased stroke
volume and cardiac output even at rest
• In moderate to severe AS, patients may develop elevated
filling pressures to compensate for the increase in LV end-
diastolic pressure
• In a minority of patients LV systolic failure occurs- further
elevation in intracardiac pressures

30. • the degree to which hypertrophy may go on is limited by the
coronary blood flow
• The aortic obstruction imposes some limits on the perfusion
pressure available for the coronary vessels, and also on the
output available for them.
• Moreover, the increased systolic resistance to flow in the
hypertrophied muscle cuts down on whatever coronary flow
normally does occur in systole.
• As the obstruction progresses to a critical level, the high
afterload “overwhelms” the left ventricle and systolic function
begins to decrease.
• With continued severe afterload excess, myocyte
degeneration and fibrosis occurs and produces irreversible
left ventricular systolic dysfunction

36. Angina
• Progressive LV hypertrophy from aortic
stenosis leads to increased myocardial oxygen
needs
– Hypertrophy may compress the coronary arteries
– Reduced diastolic filling may result in classic
angina, even in the absence of coronary artery
disease
• 35% presentation
• 50% die in 5 years

37. Syncope
• Cardiac output no longer increases with
exercise
• A drop in systemic vascular resistance that
normally occurs with exertion may lead to
hypotension and syncope
• Rest- arrythmias, av block
• 15% presentation
• 50% die in 3 years

38. Heart Failure
• Changes in LV function may no longer be
adequate to overcome the outflow
obstruction
– Hypertrophic remodeling leads to diastolic
dysfunction
– Afterload excess results in decreased ejection
fraction – systolic dysfunction
• 50% presentation
• 50% die in 2 years

40. There may be a plateau or an anacrotic pulse or a late peaking and small volume
pulse, pulsus parvus, and tardus
The pulse pressure may be reduced
In supravalvular AS, the right brachial and carotid pulsations are of greater
amplitude than the left-sided ones

42. • In supravalvular AS- the right brachial pulse and the
carotid may be stronger than the left brachial
• Coanda effect -properly directed jet , attach to a convex
surface instead of moving in a straight line
• Obstruction in the supravalvular AS is such that the high-
velocity jet is directed towards the right innominate artery

43. • The classic carotid pulse in aortic stenosis has
a slowed upstroke, reduced amplitude, and
sustained contour, with or without an
accompanying palpable thrill .
• The severity of the valvular obstruction is
roughly proportional to the degree of
abnormality of the carotid pulse.

44. Jugular Venous Pulse
• The venous pulse configuration and pressure are
unremarkable in aortic stenosis.
• Occasionally, the jugular A wave will be prominent in
the absence of an elevation in mean jugular pressure;
this effect probably results from decreased right
ventricular compliance in the setting of a hypertrophic
left ventricular chamber and septum (Bernheim
effect).
• If biventricular heart failure is present, the mean
jugular pressure will be elevated.

45. S2
• INTENSITY
Normal- Pliable, thin valves –BAV without calcification
Dec –thickened rigid valves , calcification
Severe -the stroke volume is ejected slowly and over a longer
period and also leads to poor distension of the aortic root--
softer A2
• SPLITTING
A2 moves into P2- 1) ↑ LV ejection 2) longer time for LV pr
to drop below aortic at end systole
• Single S2

46. • If LV ejection time is substantially delayed, reversed or
paradoxic splitting of S2.
• Detection of paradoxic splitting of S2 in aortic stenosis
in the absence of left bundle branch block or impaired
left ventricular function is an important observation,
which implies that the left ventricular-aortic gradient is
75 mmHg or greater, e.g., severe aortic stenosis.
• In approximately two thirds of older patients with
moderate to severe aortic stenosis, S2 will be single. S2
will be reversed or paradoxic in another 20 to 25% and
will be completely normal in a small number
ofpatients.

48. S4
• Correlates wit large LV-AO gradient and abnormally elevated LVEDP

49. Aortic Ejection Click
• It localizes the abnormality to the aortic valve (in the
absence of a dilated aorta or chronic hypertension).
• It suggests that the etiology of the valve abnormality is a
congenitally deformed aortic valve, usually a bicuspid
valve.
• its presence does not correlate with the severity of the
lesion.
• sudden cessation of opening motion of abnormal valve
leaflets(doming)
• Lost with calcification and thickening
• High frequency- 40-80 msec after S1 – best heard at apex-
constant

50. MURMUR
• Crescendo –decrescendo – shape of the pr diff bet LV-Ao
• Site of max intensity and radiation-
• Length of the murmur-severity
- time to peak intensity- 2nd half
• Frequency and pitch- rough ,grunting
Harsh- mixed frequency at base – effect of jet to Ao
high freq musical- vib fom leaflets with intact
commissures , at apex
-Gallavardin murmur
• Amplitude - generally louder –severe
- nonspecific

51. SEVERITY

52. Classification of Severity
Aortic Jet
Velocity
(m/s)
Mean
Gradient
(mm Hg)
Aortic valve
Area (cm2)
Mild 2.0 – 2.9 < 20 1.5 – 2
Moderate 3 – 3.9 20 – 39 1 – 1.5
Severe > 4 > 40 < 1

54. • Doppler data
– Peak instantaneous gradient over time
• Cath data
– Peak to peak data
• However, calculated mean P Grd are
comparable

57. Doppler derived gradients- using CW doppler @ vena
contracta
Catheter derived gradients- downstream vena contracta-
pressure recovery
GRADIENT DERIVED BY CATH IS LOWER THAN DOPPLER
DERIVED GRADIENT
Pressure recovery- exaggerated in
-Smaller aorta
-Stiffer aorta
-Hypertension

58. Hypertension may mask the severity of stenosis, an
Presence of stenosis may affect the optimal treatment of hypertension
Combination of AS and hypertension- “double-loads” the ventricle
Total afterload = the valve obstruction + elevated SVR
stenosis severity
Underestimated-
“recovered”
pressure, rather
than vencontracta
pressure, is rec

59. Stenotic valve area
Torricelli’s law
• F = A X V
A = F / V
A = F / V Cc
F- Flow
A- Valve area
V- Velocity of flow
Cc- coefficient of contraction

61. Mitral Valve = constant 0.7 (later changed 0.85)
Aortic valve: assumed to be 1

62. LOW OUTPUT LOW GRADIENT AS
• Mean gradient < 40 in the setting of AVA of 1.0 cm2 with an
aortic flow velocity <4 m/sec.
• Reduced or Preserved EF
• Dobutamine stress echo
• Stoppage pnt- 40µ / kg / min
- mean gradient > 40 mm hg
-CO inc by 50 %
-HR inc to < 140 / min
- intolerable symptoms / side effects

64. Aortic Stenosis: Surgical Management

65. Aortic Stenosis: Timing of Intervention
Recommendations COR LOE
AVR is recommended with severe high-gradient AS who
have symptoms by history or on exercise testing (stage
D1)
I B
AVR is recommended for asymptomatic patients with
severe AS (stage C2) and LVEF <50%
I B
AVR is indicated for patients with severe AS (stage C or
D) when undergoing other cardiac surgery
I B

66. Aortic Stenosis: Timing of Intervention (cont.)
Recommendations COR LOE
AVR is reasonable for asymptomatic patients with
very severe AS (stage C1, aortic velocity ≥5 m/s)
and low surgical risk
IIa B
AVR is reasonable in asymptomatic patients (stage
C1) with severe AS and decreased exercise
tolerance or an exercise fall in BP
IIa B
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
IIa B

67. Aortic Stenosis: Timing of Intervention (cont.)
Recommendations COR LOE
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
IIa C
AVR is reasonable for patients with moderate AS
(stage B) (aortic velocity 3.0–3.9 m/s) who are
undergoing other cardiac surgery
IIa C
AVR may be considered for asymptomatic patients
with severe AS (stage C1) and rapid disease
progression and low surgical risk
IIb C

68. Indications for Aortic Valve Replacement in Patients With Aortic Stenosis

69. Aortic Stenosis: Choice of Surgical or
Transcatheter Intervention
Recommendations COR LOE
Surgical AVR is recommended in patients who meet
an indication for AVR (listed in Section 3.4) with low
or intermediate surgical risk
I A
For patients in whom TAVR or high-risk surgical AVR is
being considered, members of a Heart Valve Team
should collaborate closely to provide optimal patient
care
I C
TAVR is recommended in patients who meet an
indication for AVR for AS who have a prohibitive
surgical risk and a predicted post-TAVR survival >12
months
I B

70. Aortic Stenosis: Choice of Surgical or
Transcatheter Intervention (cont.)
Recommendations COR LOE
TAVR is a reasonable alternative to surgical AVR for
AS in patients who meet an indication for AVR and
who have high surgical risk
IIa B
Percutaneous aortic balloon dilation may be
considered as a bridge to surgical or transcatheter
AVR in severely symptomatic patients with severe
AS
IIb C
TAVR is not recommended in patients in whom the
existing comorbidities would preclude the expected
benefit from correction of AS
III: No
Benefit
B

71. • In the adolescent or young adult with severe
congenital AS, balloon aortic valvotomy is
recommended for all symptomatic patients
and asymptomatic patients with a
transvalvular gradient higher than 60 mm Hg
or electrocardiographic ST-segment changes
at rest or with exercise

72. • In patients with severe aortic stenosis who
were not suitable candidates for surgery, TAVI,
as compared with standard therapy,
significantly reduced the rates of death from
any cause, the composite end point of death
from any cause or repeat hospitalization, and
cardiac symptoms, despite the higher
incidence of major strokes and major vascular
events.

73. • In intermediate-risk patients, TAVR was similar
to surgical aortic-valve replacement with
respect to the primary end point of death or
disabling stroke

74. • TAVR was a noninferior alternative to surgery
in patients with severe aortic stenosis at
intermediate surgical risk, had higher rates of
residual aortic regurgitation and need for
pacemaker implantation. TAVR resulted in
lower mean gradients and larger aortic-valve
areas than surgery

75. Indication:
Currently, there are no established indications or
guidelines for T
A
VRin the United States.Indications
are based on following trial andconsensus.
P
ARTNERTrial - Transcatheter aortic-valve
implantation for aortic stenosis in patients who
cannot undergo surgery. NEnglJMed. 2010 Oct 21.
363(17):1597-607.
ACCF/AATS/SCAI/STSexpert consensus
document on transcatheter aortic valve
replacement. JAmColl Cardiol. 2012 Mar27.
59(13):1200-54.

76. Indication No1:
Patients with calcific aortic valve stenosis withthe
following echocardiographiccriteria:
Mean gradient greater than 40 mm Hgor jet
velocity more than 4 m/s and an initial aortic valve
area (AVA)of lessthan 0.8 cm 2 or indexed effective
orifice area (EOA)of lessthan 0.5 cm 2/m 2;
Qualifying AVAbaseline measurement must be
within 45 days of the date of the procedure

77. Indication No2:
 One cardiac interventionalist and 2

experienced cardiothoracic surgeons agree that
medical factors either preclude operation or are
high risk for surgical aortic valve replacement,
based on aconclusion that the probability ofdeath
or serious irreversible morbidity exceedsthe
probability of meaningfulimprovement.
Thesurgeons' consult notes shall specify the
medical or anatomic factors leading to that
conclusion and include aprintout of thecalculation
of the Society of Thoracic Surgeons(STS)score to
additionally identify the risks in the patient; at least
1 of the cardiac surgeon assessorsmust have
physically evaluated the patient

78. Indication No3:
Patient is deemed to have symptomatic
aortic valve stenosis, asdifferentiated from
symptoms related to comorbid conditionsand
asdemonstrated by New YorkHeart
Association (NYHA)functional classII or
greater.

79. In the European Union, TranscatheterAortic
Valve Implantation is performed in patients
with severeaortic stenosis who are high-risk
surgical candidates with alogistic EuroScoreof
more than 20% and in patients who havea
contraindication to surgical aortic valve
replacement.

83. Aortic Regurgitation •AR is typically
paravalvular mild or
mild-moderate severity
•MostAR disappears
or reduces at 1 yr
follow-up.

84. (A) Left main coronary artery occlusionresultingfrom a bulkyleaflet displaced overthe
ostium.
(B) Successful percutaneous intervention restored leftcoronary
flow.

85. Theprincipal transcatheter aortic valveimplantation
devices currently inuse:
(A) EdwardsSapienXTbioprosthesis and
(B)Medtronic CoreValve®bioprosthesis

86. • Implanted since 2002
• Transfemoral, transapical,
alternate accessroutes
• Bovine pericardium leaflets
• Cobalt-chromium balloon
expandable stent
• Annular fixation
• Subcoronary implant

87. Medtronic CoreValve
Penrose program was the
first CoreValve program in
CO,NM, UT
,WY
Retrograde approach only
Equine Pericardium Leaflets
Nitinol Self-Expanding
Annular and Supra-coronary
fixation
18fr delivery system
Offers a31mm valve size

89. Conclusion….
• Catheter based treatment of aortic stenosisis
improving.
• Restenosis after valvuloplasty has beenovercome
after development ofTAVI.
• Indications for TAVIcan be expanded after the
availability of follow up of patients of the cohort.
• Teamapproach is essential for successfulprocedure.
• Trainingrequired for performance of TAVIand
dedicated imaging instruments.
• Patient selection is complex.