Transcript AORTIC STENOSIS

AORTIC STENOSIS
De-huis T.J.
UFS
Bloemfontein
Aortic Stenosis
 Introduction ~
 Etiology:
 Calcification ~ normal trileaflet aortic valve:
 most common cause in adults with normal trileaflet or
 Congenital bicuspid valve
 Pathophysiology similar to atherosclerosis, thus
predisposing factors include ~
 Age
 Male gender
 Hyperlipidaemia
 Evidence of active inflammation
Aortic Stenosis
 Etiology ~
 Calcification:
 Usually in 6th to the 8th decade of life
 Mainly caused by solid calcific deposits in the cusps than
commissural fusion
 Calcification of congenital bicuspid aortic valve~
 1-2% of babies are born with a bicuspid Ao valve
 Mostly males
 Contributes more to the total number of AS cases than the
trileaflet
 Develops earlier than in Tricuspid leaflet ~ about the 2nd
decade
Aortic Stenosis
 Etiology ~
 Congenital Aortic Stenosis :
 Usually detected and treated early in childhood
and adolescence
 Usually a unicuspid unicommissural valve
 Sudden dearth is common due to LV strain
 Ejection fraction is usually supra normal with
concentric ventricular hypertrophy
Aortic Stenosis
 Etiology ~
 Rheumatic Valve Disease :
 Becoming rare in developed countries
 Mitral valve almost always affected
 Commissural fusion present
Aortic Stenosis
 Pathophysiology ~
 Pathophysiology and relation to symptoms :
Aortic Stenosis
 Pathophysiology ~
 Pathophysiology and relation to symptoms
 Asymptomatic patient have a good outlook even
with severe stenosis, whereas
 An individual with symptoms has a mortality rate of
25% per year
 Pressure Overload Hypertrophy
 Narrowing of valve orifice to half the normal
diameter of 3 cm² causes little obstruction to LVoutflow tract with a small gradient across the valve
Blase R Carabello
Aortic Stenosis
Aortic Stenosis
 Pathophysiology ~
 Pressure Overload Hypertrophy:
 LV hypertrophy → a major compensatory
mechanism, off setting the pressure overload
 Pressure overload →  LV afterload → ↓ ejection
performance
 Afterload ~
 wall stress σ = pr/2th ( Laplace Equation)
 P ~ ventricular pressure
 R ~ventricular radius
 th ~ ventricular thickness
Blase R Carabello
Aortic Stenosis
 Pathophysiology ~
 Pressure Overload Hypertrophy:
 As the LV pressure  so does the thickness (
concentric hypertrophy) ~ thus keeping the
afterload normal
 Maintenance of normal afterload → normal EF and
stroke volume
 Note ~
 Hypertrophy is a double edged sword, on the one hand
maintaining normal EF and on the other impeding
coronary artery blood flow reserve,
 It reduces diastolic function and
 Is associated with increased mortality
Blase A Carabello
Aortic Stenosis
 Natural History ~
 Severity of stenosis  with time
 Average rate of decrease in Ao valve ~ 0.12 cm² per year
 Progression is more in pts with degenerative disease than in
congenital or rheumatic etiology
 Survival
 35% of unoperated with usual AS symptoms are alive at 10
yrs ~ Grant
 Wood stated that 46% of such pts were alive at 1 to 7 yrs
later
 ACC/AHA guidelines ~ after onset of symptoms , average
survival is < than 2 to 3 yrs
Aortic Stenosis
 Survival ~
Aortic Stenosis
 Natural History ~
 Survival :
 15% to 20% of all deaths in AS are sudden
 VF
 Acute pulmonary edema from sudden LV failure
 Gradual cardiac failure after 5 yrs of diagnosis
 A few patients may display signs of moderate
pulmonary arterial hypertension and,
 Others develop RV failure
Kirklin/Barratt-Boyes
Aortic Stenosis
 Natural History ~
 Survival:
 Asymptomatic patients ~
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¼ develop symptoms within a year
½ by 3 yrs and
¾ by 4rs
Sudden death occurs in < 1%
Otto and colleagues
Aortic Stenosis
 Clinical Features and Diagnostic Criteria:
 Asymptomatic
 Symptomatic
 Classic triad (in 1/3 of pts) ~
 Angina pectoris
 50% to 70% of pts
 Common in pts with AS and CAD
 In severe AS than pts with less severe disease
 Syncope
 30% to 50% of pts
 Peripheral vasodilatation from faulty baroreceptor
mechanisms
 Pulmonary Venous Hypertension
 30% to 40%
 Dyspnea, orthpnea, PND, or frank pulmonary edema
 Associated with  LVEDP and systolic wall stress, ↓ CO and
EF
Aortic Stenosis
 Clinical Features and Diagnostic Criteria:
 10% of patients survive typical symptoms long
enough to develop secondary RV failure ~
  right atrial and jugular pressure,
 Hepatomegaly,
 Cardiac cachexia
 Tricuspid regurgitation (rarely)
Aortic Stenosis
 Clinical Features and Diagnostic Criteria:
 Physical examination
 Auscultation ~
 A crescendo-decrescendo systolic ejection murmur radiating to
the neck
From the collection of David Liff, MD, Emory University Hospital
Aortic Stenosis
 Clinical Features and Diagnostic Criteria:
 Physical examination
 Auscultation ~
 In mild disease
 murmur peaks in early systole
 S2 is physiologically split and
 Carotid upstrokes are normal
Aortic Stenosis
 Clinical Features and Diagnostic Criteria:
 Physical examination
 Auscultation ~
 As the AS progress
 The murmur becomes louder
 Peaks progressively later in systole, and
 Is associated with a thrill
 With further worsening of stenosis
 Murmur intensity becomes less due to ↓ in SV
 The carotid upstrokes are diminished in volume and rate of
rise is delayed (parvus et tardus)
 The apex beat is increased
Blase A Carabello
Aortic Stenosis
 Clinical Features and Diagnostic Criteria:
 Special Investigations ~ LV hypertrophy
Aortic Stenosis
 Clinical Features and Diagnostic Criteria:
 Special Investigations ~
 ECG ~
 Non specific ST-wave and T wave abnormalities ~ V6
lead – strain pattern)
 Chest Radiography ~
 Non specific
 LV hypertrophy with boot shape
 +/- calcification of Ao valve
Aortic Stenosis
Aortic Stenosis
 Clinical Features and Diagnostic Criteria:
 Echocardiography ~
 Thickened and calcified Ao valve with dense cusp echoes
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throughout cardiac cycle
Decreased separation of leaflets in systole with reduced
opening orifice ( 13-14 mm mild, 8-12 mm moderate, and < 8
mm in severe)
+/- doming in systole
Dilated Ao root
 thickness of LV wall (concentric LV hypertrophy)
Hyperdynamic contraction of LV (in compensated state)
↓ mitral EF slope (↓ LV compliance)
LA enlarged
 Ao gradient (Doppler)
↓ Ao valve area (unreliable)
www.learningradiology.com
Aortic Stenosis
 Clinical Features and Diagnostic Criteria:
 Echocardiography ~
Fig 3 Continuous wave Doppler echocardiogram in patient with severe aortic stenosis (same
patient as in figure 2).
Ramaraj R , Sorrell V L BMJ 2008;336:550-555
©2008 by British Medical Journal Publishing Group
Aortic Stenosis
 Clinical Features and Diagnostic Criteria:
 Bernoulli equation ~
Aortic Stenosis
 Clinical Features and Diagnostic Criteria:
 Bernoulli equation ~
G=4V²
 G ~ gradient
 V ~ peak transvalvular flow velocity
Aortic Stenosis
Aortic Stenosis
 Measurement of Aortic Valve Area ~
 Continuity equation
 Gorlin equation
 Hakki equation
Aortic Stenosis
 Clinical Features and Diagnostic Criteria:
 Graded exercise testing ~
 Not as risky in asymptomatic patients with AS
 May help in deciding on operative intervention, or if continued
observation is advised, recommendations concerning
vocational, recreational, or sports participation
 And is positive when ~
 Symptoms occur
 Inadequate blood pressure or drop in more than 10 mmHg or
greater
 Bradycardia
 Arrhythmia
 Conduction disturbances
 ST-segment depression (0.2 mV or more)
Kirklin/Barrat-Boyes
Aortic Stenosis
Aortic Stenosis
 Clinical Features and Diagnostic Criteria:
 Cardiac Catheterization ~
 Done if pt > than 40 yrs to asses coronary arteries
 If non invasive studies are inconclusive
 Transvalvular gradient and correct cardiac out
assessment are important ~ Gorlin equation to
determine Ao valve area
Kirklin/Barrat-Boyes
Blase A. Carabello
Aortic Stenosis
 Clinical Features and Diagnostic Criteria:
 Cardiac Catheterization ~
Aortic Stenosis
Aortic Stenosis
 Clinical Features and Diagnostic Criteria:
 Biomarkers and Symptomatic Status ~
 Brain Natriuretic Peptide (BNP)
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A maker of hypertrophy and
Use of preload reserve to maintain compensation
Is high in AS with symptoms
? Usefulness in asymptomatic patients
Renal failure, pulmonary hypertension and obesity
interfere with the predictable value of BNP measurement
Blase A. Carabello
Aortic Stenosis
 Treatment :
 Medical Treatment ~
 ?role of statins in progression of disease
 Cowell and colleagues
 Showed no benefit
 Other retrospective studies
 Showed benefit ~ ? Disease severity (Moura and
colleagues)
Blase A. Carabello
Aortic Stenosis
 Treatment:
 Medical Treatment ~
 Vasodilators
 Generally contraindicated in AS
 Hypotension and
 Syncope
 Except in concomitant hypertension and decompensated
heart failure
 ACE-I can be used
 Sodium nitroprusside
 ?  contractility ~ causes decrease ventricular filling
pressure → increased myocardial blood flow →
enhanced contractility
Blase A. Carabello
Aortic Stenosis
 Treatment:
 Surgical Treatment ~
 Indications
 Symptomatic patients with severe stenosis
 Patients with moderate or severe stenosis having operation for
coronary artery disease, other heart valve disease, or aortic
disease
 Asymptomatic patients with severe aortic stenosis
 LV systolic dysfunction
 Abnormal response to exercise (hypotension)
 Ventricular tachycardia
 Marked LV hypertrophy (≥15 mm)
 Aortic valve area (<0.6 cm²)
Kirklin/Barrat-Boyes
Aortic Stenosis
 Treatment:
 Surgical Treatment ~
 Isolated Aortic Valve replacement:
 Initial Steps ~
 Usual preparations
 Median sternotomy
 CPB established at 34˚C, single two-staged venous
cannula
 Cardioplegia – antegrade +/- retrograde
 Body is cooled down to 28˚C
 Ascending Aorta is Cross clamped ~ promptly if ventricular
fibrillation is allowed
 +/- LV vent
Aortic Stenosis
 Treatment:
 Surgical Treatment ~
Aortic Stenosis
 Treatment:
 Surgical Treatment ~
Aortic Stenosis
 Treatment:
 Surgical Treatment ~
Aortic Stenosis
 Treatment:
 Surgical Treatment ~
 Prosthetic Aortic Valve
 Interrupted suture technique
 Continuous suture technique
 Allograft Aortic Valve
 Subcoronary technique
 Root enlargement technique
Surgical techniques of posterior aortic root enlargement reported so far (Nick's-white
arrow, Nunez's-black arrow, Manouquian's-black plus black dotted arrows)
Nezic D. et al.; J Thorac Cardiovasc Surg 2008;135:1401-a-1402-a
Aortic Stenosis
 Special Features Of Postoperative Care:
 Mechanical Prosthesis ~
 Life long sodium warfarin (on the evening of the
2nd postoperative day)
 INR ~ around 2.5 (2-3)
 If AF or  atrium or impaired LV function ~ INR 3.0 (2.53.5)
 ? Addition of aspirin ~ benefits v/s hemorrhage
 ?enoxaparin ~ 1mg.kgֿ¹ for five days until INR reaches
therapeutic level
Aortic Stenosis
 Special Features Of Postoperative Care:
 Bioprostheses (human, porcine, bovine)
 No need for anticoagulation
 Aspirin can be used for 1 month if risk of
thromboembolism is great (81 mg daily)
 AF ~
 if patients are still in AF 48 hrs after surgery, then
warfarin is administered until sinus rhythm is
restored
Aortic Stenosis
 Special Features Of Postoperative Care:
 Patients with LV hypertrophy ~
 These require high LV filling pressures, thus
 Mean LA pressure of > 10 mmHg (15 to 18 mmHg)
 Sinus tachycardia ~
 If heart rate is > 100 beats . minֿ¹ for several days
without returning to normal, then beta blockers can
be started
Aortic Stenosis
 Results:
 Early (Hospital) Death ~
 3.4% hospital mortality for primary isolated aortic
valve replacement ( The Society of Thoracic Surgeons National Database)
 Risk higher for females than males (3.9% versus
3.0%)
 With CABG then STS National Database figures
rise to 6.3%
Aortic Stenosis
 Results:
 Modes of Death ~
 Early deaths
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Acute cardiac failure
Neurologic complications
Hemorrhage and
Infection
 Late deaths (20%)
 Cardiac failure
 Myocardial infarction
 Thromboembolism
Aortic Stenosis
 Results:
 Incremental Risk Factors for Premature Death
 Older age
 ?Ethnicity ( African-Americans at increased risk)
 Functional Status (NYHA)
 LV morphology and Function
 Ao regurgitation
 Gender
 Angina
 AF
Kirklin/Barrat-Boyes
Thank You