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
• 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
Case I: Echocardiogram
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?
• 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
• 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
• Diastolic Murmurs• Continuous Murmurs • Systolic
– Loud– Early systolic– Late systolic– Holosystolic
Strategy For The Evaluation Of Cardiac Murmurs
Bonow. JACC. 2006.
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
• Obstruction of LV outflow• Common causes
– Bicuspid– Degenerative calcific– Rheumatic
• Rare causes– Congenital– Severe aortic atherosclerosis– Rheumatoid– Alkaptonuria
Flather. Lancet, 2000.
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
• 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
Baumgartner. JASE, 2009.
Etiologies of Aortic Valve Disease
Libby. Braunwald’s Heart Disease. 8th Ed.
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.
Bicuspid Aortic Valve
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
• 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
Time Between Rheumatic Fever and Symptoms of Stenosis
Development of AS
Otto. NEJM. 2008.
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
Libby. Braunwald’s Heart Disease. 8th Ed.
Law of Laplace
Yousef. BMJ. 1999.
Pathologic LV Hypertrophy
Sorajja. Contemporary Cardiology, 2009.
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
Otto. Circulation. 1997.
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
Carabello. NEJM, 2002.Schwarz. Circulation, 1982.
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• 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
Libby. Braunwald’s Heart Disease. 8th Ed.
Dynamic Auscultation
Intervention
Hypertrophic Obstructive Cardiomyopathy Aortic Stenosis
Mitral Regurgitation
Mitral Valve Prolapse
Valsalva ↑ ↓ ↓ ↑ or ↓Standing ↑ ↑ or
unchanged↓ ↑
Handgrip or squatting
↓ ↓ or unchanged
↑ ↓
Supine position with legs elevated
↓ ↑ or unchanged
Unchanged ↓
Exercise ↑ ↑ or unchanged
↓ ↑
Amyl nitrite ↑↑ ↑ ↓ ↑Isoproterenol ↑↑ ↑ ↓ ↑
Libby. Braunwald’s Heart Disease. 8th Ed.
EKG and CXR
• EKG– LVH– Atrial enlargement– Conduction abnormalities
• Chest XR– Rounding of LV border and apex
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
Sorajja. Contemporary Cardiology, 2009.
Increase in CO and grad.No change in AVA.
Increase in CO.No change in grad.
No change in CO, dec grad and hypotension.
Echocardiogram in AS
• Valve anatomy definition• LV hpertrophy and systolic function• Transaortic velocities and gradients
Echo Assessment of Aortic Stenosis
Baumgartner. JASE, 2009.
Severity of Aortic Stenosis
Mild Moderate Severe
Jet Velocity (m/s) 2.6-2.9 3.0-4.0 >4.0
Mean gradient (mmHg)
<20 20-40 >40
AVA (cm2) >1.5 1.0-1.5 <1.0
Baumgartner. JASE, 2009.
Medical Therapy For Aortic Stenosis
Bonow. JACC, 2006.
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
• All symptomatic• AS with LV dysfunction• Asymptomatic progressive disease• Atypical presentations
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
• 3-4% for AVR alone• 5.5-6.8% with AVR plus CABG• 33% increased mortality in low volume centers
Surgical Risk Calculator
www.sts.org/sections/stsnationaldatabase/riskcalculator/
euroscore.org/
Transcatheter Aortic Valve Replacement May Be An Option For
High Risk Patients
http://www.edwards.com/eu/products/transcathetervalves/sapienthv.htm
Transcatheter Aortic Valve Replacement For High Risk Patients
Leon. NEJM, 2010.
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
Rigolin. Contemporary Cardiology, 2009. Roberts. Circulation, 2006.
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
Pathophysiology
Libby. Braunwald’s Cardiology. 8th Ed.
Clinical Presentation
• Long asymptomatic period• LV dysfunction -> EDV and EDP increase• Increase right sided pressures• Cardiac output falls• Exercise tolerance develops
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
Rigolin. Contemporary Cardiology, 2009.
LVH and Strain In Aortic Regurgitation
Rigolin. Contemporary Cardiology, 2009.
Cardiomegaly In Aortic Regurgitation
Rigolin. Contemporary Cardiology, 2009.
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 AI
Zoghbi. JASE, 2003.
Aortic Regurgitation Clinical Course
Bonow. JACC, 2006.
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
No Benefit To Vasodilators In Asymptomatic AR
Evangelista. NEJM, 2005.
Survival After AI Repair By Pre-Op EF
Rigolin. Contemporary Cardiology, 2009.
Bonow. JACC, 2006.
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