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Valvular Heart Disease: The Aortic Valve. Case. A 60 year old Asian female with a history of a heart murmur presents for a routine visit. She has no complaints. Vitals are normal. A 4/6 mid systolic murmur is noted at the left upper sternal border. An EKG shows no abnormalities. Case.

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slide2
Case
  • A 60 year old Asian female with a history of a heart murmur presents for a routine visit. She has no complaints.
  • Vitals are normal. A 4/6 mid systolic murmur is noted at the left upper sternal border.
  • An EKG shows no abnormalities.
slide3
Case
  • What is the next best step?
    • Do nothing, this murmur is benign
    • Do an exercise stress test to try to elicit symptoms of aortic stenosis.
    • Do nothing, the patient has had this murmur for a long time
    • Check an echocardiogram
    • Refer the patient to a cardiologist for further evaluation
slide5
Case
  • What is the next best step
    • Do nothing because aortic stenosis is not severe
    • Start a beta blocker and ACE-I for optimal blood pressure control
    • Refer the patient to a cardiac surgeon for repair
    • Refer the patient to a cardiologist for further evaluation
what makes a heart murmur
What Makes A Heart Murmur?
  • High blood flow through a normal or abnormal orifice
  • Forward flow through a narrowed or irregular orifice
  • Backward flow through an incompetent valve
these murmurs are benign
These Murmurs Are Benign
  • Mid systolic murmur at the left sternal border with grade 2 or less with a normal S1 and S2 and no other abnormal findings in an otherwise asymptomatic patient
  • Associated with normal or increased blood flow across normal valves
these murmurs need further evaluation
These Murmurs Need Further Evaluation
  • Diastolic Murmurs
  • Continuous Murmurs
  • Systolic
    • Loud
    • Early systolic
    • Late systolic
    • Holosystolic
when to order an echo
When To Order An Echo
  • Class I
    • Diastolic, continuous, holosystolic, late systolic, clicks, radiation to neck or back
    • Symptoms of underlying cardio-pulmonary disease
    • Grade 3 or louder mid systolic murmurs
  • Class III
    • Mid systolic mumur grade II or less thought to be innocent
aortic valve stenosis
Aortic Valve Stenosis
  • Obstruction of LV outflow
  • Common causes
    • Bicuspid
    • Degenerative calcific
    • Rheumatic
  • Rare causes
    • Congenital
    • Severe aortic atherosclerosis
    • Rheumatoid
    • Alkaptonuria

Flather. Lancet, 2000.

aortic valve characteristics
Aortic Valve Characteristics
  • Normal Aortic Valve
    • Valve area 3-4 cm2
  • Valve stenosis
    • 25% of normal valve area
  • Hemodynamic Progression
    • 0.12 cm2/year
    • 0.32 m/s increase in jet velocity/year
    • 7 mmHg increase in mean gradient/year
epidemiology
Epidemiology
  • Most common disease in western world
    • 50,000 valve replacements annualy
    • Age 65: 2% of patients
    • Age >80: >4%
    • 1 billion dollars annually in US
etiologies of aortic stenosis
Etiologies of Aortic Stenosis

Baumgartner. JASE, 2009.

etiologies of aortic valve disease
Etiologies of Aortic Valve Disease

Libby. Braunwald’s Heart Disease. 8th Ed.

bicuspid valve
Bicuspid Valve
  • 1-2% of births
  • Generalized arteriopathy: fragmentation of fibers of the elastic media
    • Coarctation, aortic dilation, dissection (5-9x risk)
  • Most common reason for valve replacement <70 years old
  • Roughly 66% of replaced valves < 70
  • More common in men: 70-80% of cases
  • Hemodynamic abnormalities predispose to earlier stenosis

Roberts. Circulation, 2005.

calcific as
Calcific AS
  • Most common cause of AS
  • Present in 2% of adults 65 or older
  • Becomes symptomatic age 60-80
  • Sclerosis present in 29% ≥ 65
  • Proliferative and inflammatory changes-> calcification and bone formation
  • Risk Factors: HL, tob, HTN, DM
rheumatic as
Rheumatic AS
  • Adhesions and fusion of commisures and cusps
  • Vascularization of leaflets-> retraction and stiffening of the free borders of the cusps
  • Calcific nodules
  • Small triangular orifice
  • Coexists with rheumatic mitral valve disease
development of as
Development of AS

Otto. NEJM. 2008.

pathophysiology of as
Pathophysiology of AS
  • Progressive obstruction and compensatory change
  • Pressure overload->increased wall stress->increased wall thickness
  • Increased myocardial collagen
  • Progressive systolic dysfunction
  • Progressive diastolic dysfunction
  • Decreased coronary blood flow
pathophysiology
Pathophysiology

Libby. Braunwald’s Heart Disease. 8th Ed.

law of laplace
Law of Laplace

Yousef. BMJ. 1999.

pathologic lv hypertrophy
Pathologic LV Hypertrophy

Sorajja. Contemporary Cardiology, 2009.

clinical course
Clinical Course
  • Outcome similar to normal in asymptomatic patients
  • Progression from sclerosis to severe AS: 2.5% in 8 years
  • Mortality is high in patients with symptomatic disease

Cosmi. Arch Int Med. 2002.

progression of asymptomatic as
Progression of Asymptomatic AS

Otto. Circulation. 1997.

mortality in symptomatic aortic stenosis is high
Mortality In Symptomatic Aortic Stenosis Is High

Levy. NEJM, 2002.

Ross J Jr, Braunwald E: Aortic stenosis. Circulation 38:V61, 1968

survival with or without valve replacement
Survival With Or Without Valve Replacement

Carabello. NEJM, 2002.

Schwarz. Circulation, 1982.

clinical presentation
Clinical Presentation
  • Age
    • Bicuspid: 50-70 years old
    • Calcific: > 70 years old
  • Symptoms
    • Progressive exercise intolerance
    • Angina (2/3 with significant CAD)
    • Syncope
    • Endocarditis, systemic embolization
physical examination
Physical Examination

Carotid upstroke

Parvus and tardus: slow rising, late peaking

Specific but insensitive

Systolic murmur

Late peaking heard at the base

Varies beat to beat

Louder with increased flow: squatting

Quieter with decreased flow: standing

Stops before A2

Can radiate to the apex (Gallivardin phenomenon)

Second heart sound

Absent A2 with severe disease

Signs of heart failure

Libby. Braunwald’s Cardiology. 8th Ed.

aortic stenosis carotid pulse waveforms
Aortic Stenosis Carotid Pulse Waveforms

Libby. Braunwald’s Heart Disease. 8th Ed.

dynamic auscultation
Dynamic Auscultation

Libby. Braunwald’s Heart Disease. 8th Ed.

ekg and cxr
EKG and CXR
  • EKG
    • LVH
    • Atrial enlargement
    • Conduction abnormalities
  • Chest XR
    • Rounding of LV border and apex
further assessment
Further Assessment
  • Unclear symptoms
    • Treadmill exercise testing
      • Development of symptoms
      • Failure to increase BP > 10 mmHg
      • NOT IN SYMPTOMATIC PATIENTS
  • Low left ventricular function
    • Dobutamine infusion
low cardiac output response to dobutamine infusion
Low Cardiac Output: Response to Dobutamine Infusion

Increase in CO.

No change in grad.

No change in CO, dec grad

and hypotension.

Increase in CO and grad.

No change in AVA.

Sorajja. Contemporary Cardiology, 2009.

echocardiogram in as
Echocardiogram in AS
  • Valve anatomy definition
  • LV hpertrophy and systolic function
  • Transaortic velocities and gradients
echo assessment of aortic stenosis
Echo Assessment of Aortic Stenosis

Baumgartner. JASE, 2009.

severity of aortic stenosis
Severity of Aortic Stenosis

Baumgartner. JASE, 2009.

non operative management of aortic stenosis
Non-Operative Management of Aortic Stenosis
  • Counseling to monitor for symptoms
  • Evaluate and treat CAD
  • Reassessment
    • For symptoms changes
    • Severe: Annually
    • Moderate: 1-2 years
    • Mild 3-5 years
  • Balloon valvulotomy
when to refer to cardiology
When To Refer To Cardiology
  • All symptomatic
  • AS with LV dysfunction
  • Asymptomatic progressive disease
  • Atypical presentations
operative management of as
Operative Management Of AS
  • Class I
    • Symptomatic
    • Severe AS undergoing cardiac surgery
    • Severe AS and EF < 50%
  • Class II
    • Moderate AS undergoing cardiac surgery
    • Asymptomatic with severe AS and abnormal ex response
    • Asymptomatic severe with risk of rapid progression
    • Mild AS undergoing cardiac sx, concern for rapid progression
    • Very severe asymptomatic with low op mortality
surgical mortality
Surgical Mortality
  • 3-4% for AVR alone
  • 5.5-6.8% with AVR plus CABG
  • 33% increased mortality in low volume centers
surgical risk calculator
Surgical Risk Calculator

euroscore.org/

www.sts.org/sections/stsnationaldatabase/riskcalculator/

transcatheter aortic valve replacement may be an option for high risk patients
Transcatheter Aortic Valve Replacement May Be An Option For High Risk Patients

http://www.edwards.com/eu/products/transcathetervalves/sapienthv.htm

aortic regurgitation
Leaflets (46%)

Degenerative (75% with some AR)

Endocarditis

Trauma

Congenital

Rhematic

Myxomatous

Systemic disorders: SLE, giant cell and Takayasu’s, ankylosing spondylitis, Whipple’s, Chron’s, weight loss drugs

Aorta (54%)

Age

Degenerative disease (Marfan)

Dissection

HTN

Syphilis

Ankylosing spondylitis

Giant cell arteritis

Behcet syndrome

Psoriatic arthritis

Osteogenesis imperfecta

Reieter syndrome

Relapsing poychondritis

Aortic Regurgitation

Rigolin. Contemporary Cardiology, 2009.

Roberts. Circulation, 2006.

pathophysiology1
Pathophysiology
  • LF ejection split between forward and back
  • Total stroke volume is increased
  • Left ventricle dilates to accommodate stroke volume
  • Increased LVEDP and hypertension -> increased preload and afterload -> eccentric hypertrophy
  • Mismatch-> systolic dysfunction -> fibrosis-> dysfunction becomes permanent
pathophysiology2
Pathophysiology

Libby. Braunwald’s Cardiology. 8th Ed.

clinical presentation1
Clinical Presentation
  • Long asymptomatic period
  • LV dysfunction -> EDV and EDP increase
  • Increase right sided pressures
  • Cardiac output falls
  • Exercise tolerance develops
physical exam
Physical Exam
  • Findings secondary to increased stroke volume and widened pulse pressure
  • Apical impulse: diffuse, laterally-inferiorly displaced, hyperdynamic
  • Carotid pulse: Corrigan’s, bifid
  • S1 normal, S2 variable
  • LSB blowing diastolic murmur, Austin Flint murmur

Libby. Braunwald’s Heart Disease. 8th Ed.

peripheral signs of ai
Peripheral Signs of AI

Rigolin. Contemporary Cardiology, 2009.

lvh and strain in aortic regurgitation
LVH and Strain In Aortic Regurgitation

Rigolin. Contemporary Cardiology, 2009.

cardiomegaly in aortic regurgitation
Cardiomegaly In Aortic Regurgitation

Rigolin. Contemporary Cardiology, 2009.

echo assessment of ai
Echo Assessment Of AI
  • LA size
  • Leaflet appearance
  • Jet width, density, deceleration, diastolic flow reversal
  • VC width, calculated regurgitant volume and EROA

Zoghbi. JASE, 2003.

echo assessment of ai1
Echo Assessment Of AI

Zoghbi. JASE, 2003.

medical therapy
Medical Therapy
  • Class I recommendation
    • Severe AR with symptoms or LV dysfunction and unable to undergo surgery
  • Class IIa
    • Bridge to surgery in patients with severe LV dysfunction
  • Class IIb
    • Long term in severe AR with LV dilation but normal function
  • Hydralazine, nifedipine have been studied
survival after ai repair by pre op ef
Survival After AI Repair By Pre-Op EF

Rigolin. Contemporary Cardiology, 2009.