Transcript Valvular Heart Disease

VALVULAR HEART DISEASE
JAY L. RUBENSTONE, D.O., F.A.C.C
Fall 2012
NORMAL STRUCTURE
MITRAL VALVE
• Cross sectional Area 4-6cm2
• Anterior and Posterior Leaflets
• Chordae Tendineae  Papillary Muscles
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MITRAL STENOSIS
ETIOLOGY & PATHOLOGY
• Rheumatic Fever- 99%
• Other
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Congenital
Carcinoid
Lupus
Amyloid
Infective Endocarditis
Mucopolysaccharide Disease
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PATHOPHYSIOLOGY
• Mild MS- orifice <2 cm2
• Critical MS- <1 cm2
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A-V pressure gradient >20mmHg
Increased LA Pressure
Increase Pulmonary Venous + Capillary Pressures
Increase Pulmonary Artery Systolic Pressure
Decrease RV Function (when PAS>30-60mmHg)
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PATHOPHYSIOLOGY
• Pulmonary HTN
• Passive Backward Transmission Of Incr. LA pressure
Pulmonary Arteriolar Constriction Organic Obliterative
Changes in Pulmonary Vascular Bed RV Failure
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HISTORY
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Exertional Dyspnea
Cough/Wheezing
Orthopnea/PND/CHF
Hemoptysis-Rupture of Pulm Vein-Brochial Vein
Shunts
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HISTORY
• Chest Pain-Increase RV Pressures or Unknown
Etiology
• Systemic Emboli (LA clots)
• Increased LA size, Decreased C.O., Atrial Fib, IE
• Significantly decreased w/anticoagulation
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DIAGNOSIS
• Cardiac Catherization
• Gorlin Equation
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NATURAL HISTORY
• Asymptomatic for 15-20yrs following Rheumatic
Fever
• Additional 5-10 yrs for progression from mild to
severe stenosis
• Stenosis progression approx. .09 cm2/yr
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NATURAL HISTORY
• Presurgical Survival Rates
• NYHA Class II 80%-10yrs
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Class III 38%-10yrs, 62% 5yrs
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Class IV 15%-5yrs
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MANAGEMENT-MEDICAL
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Endocarditis Prophylaxis
Activity Limitation
Diruetics- Decrease Na Intake
Heart Rate Control for A-fib or Sinus Rhythm
Anticoagulation
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PERCUTANEOUS BALLOON
ANGIOPLASTY
• Moderate-Severe MS
• Mild MS- if Pulmonary Artery Pressures or Wedge
Pressure Elevate with Exercise
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VALVE REPLACEMENT
• Indications
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Combined MS/MR
<1.5 cm2-NYHA III or IV
<1 cm2
Class II if Pulm Artery Pressure >70mmHg
• Mortality
• 3-8%
• Valve Type-Prosthetic or Bioprosthetic, TAVR
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MITRAL REGURGITATION
• Etiology
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Rheumatic Heart Disease
Infective Endocarditis
Collagen Vascular Disease
Cardiomyopathy
Ischemic Heart Disease
• Mitral Valve Prolapse-most common cause for valve
surgery in US
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PATHOPHYSIOLOGY
• Decreased Impedance to Ventricular Emptying
• Determinants of Regurgitant Flow
• Instantaneous Size of MV Orifice
• Dependent on Preload, Afterload, LV Contractility, LV Size
• LA-LV Pressure Gradient dependent on Systemic Vascular
Resistance, LV Pressure, & LV Size
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PATHOPHYSIOLOGY
• LV Compensation
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Increased End Diastolic Volume
Increased Wall Tension
Increased Preload
Increased LV Emptying
Normal Ejection Fraction should be Super Normal >65% to
maintain forward cardiac output and B/P
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PATHOPHYSIOLOGY
• LV Decompensation
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Increase End Systolic Volume
Increased End Diastolic Volume
Leads to Annulus Dilatation (MR begets MR)
Decreased Ejection Fraction and Stroke Volume
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PATHOPHYSIOLOGY
• Ejection Fraction in Mitral Regurgitation
• >65% normal in compensated MR
• 50-65% mild impairment
• 40-50% moderate-severe impairment
• <35% advanced impairment
As ejection fraction decreases operative risk increases.
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HISTORY
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Shortness of Breath
Exertional Dyspnea
Congestive Heart Failure
RHF
Significant symptoms in chronic MR usually do not
develop until LV decompensation occurs.
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HISTORY
• Medical Treatment Survival
• 80% 5yr
• 60% 10yr
• 30-45% 5yr if MR severe
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MANAGEMENT OF CHRONIC MR
• Medical
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Digoxin
Diruetics*
Afterload Reduction
Anticoagulation in A-fib
Endocarditis Prophylaxis
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MANAGEMENT OF CHRONIC MR
• Surgical
• Indications
• Asymptomatic Class I
• EF < 60% or LV Systolic Diameter >45mm
• Severe MR Class II, III, or IV
• generally considered for surgery unless EF <30%
• Valve Repair vs. Replacement
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MITRAL VALVE PROLAPSE
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Systolic Click-Murmur Syndrome
Barlow’s Syndrome
Billowing Mitral Valve Syndrome
Floppy Valve Syndrome
Myxomatous Valve Syndrome
Parachute Valve
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MITRAL VALVE PROLAPSE
• Over diagnosed
• 2.4% of population
• Females>Males 2:1
• Severe MR- Elderly Male>Young Female
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MVP ETIOLOGY
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Primary Valvular most frequent
Connective Tissue Diseases
Hyperthyroidism
Myotonic Dystrophy
Periarteritis Nodosa
Von Willebrands
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MVP PATHOLOGY
• Myxomatous Proliferation and Degeneration of
Valve Leaflets
• Increased Quantity of Acid Mucopolysaccharide in
Middle Layer of Valve Tissue
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MVP HISTORY
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Most are asymptomatic throughout life
Chest pain, fatigue, anxiety
Orthostasis-questionable autonomic dysfunction
Arrhythmia-SVT, PACs, PVCs
Symptoms of MR if present
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PHYSICAL EXAMINATION
• Ascultation
• Murmur- mid to late crescendo progressing to holosystolic if
MR becomes severe
• Click and murmur move closer to S1 during strain phase of
valsalva, sudden standing, and Amyl Nitrate
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NATURAL HISTORY
• Progressive MR in 15% over 10-15 yrs
• Infective Endocarditis
• Cerebral Emboli-tearing of endothelial covering of
myxomatous valve with platelet activation
• Sudden Cardiac Death-V fib, increased Q-T interval
(not well established)
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MVP MANAGEMENT
Endocarditis prophylaxis if MR present
Holter monitor-beta blocker for ectopy?
Aspirin if focal neurological events present
MR-treat like any other MR, valves usually amenable
to repair
• *MVP is usually a benign disease*
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AORTIC VALVE
NORMAL STRUCTURE
• Valve sits at the base of Aortic Root
• Three Leaflets (cusps)-non coronary, right coronary,
left coronary
• Cusps give rise to ostea of right coronary artery and
left main coronary artery
• Normal cross-sectional area 3-4cm2
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AORTIC STENOSIS ETIOLOGY AND
PATHOLOGY
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Valvular
Supravalvular
Subvalvular
Hyperthrophic Cardiomyopathy
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CONGENITAL AORTIC STENOSIS
• Unicuspid
• Presents less than one year of age
• Bicuspid
• Adult Presentation
• Chronic turbulent flow
• Leads to fibrosis, rigidity, calcification
• Tricuspid
• Leaflets of unequal size
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ACQUIRED AORTIC STENOSIS
• Rheumatic
• Rare
• Usually mitral valve also involved
• Degenerative or Senile
• Most common cause of adult AS
• Most common cause of valve replacement
• Years of normal mechanical stress leads to
calcium deposits on leaflets
• Inflammatory or Infectious component??
• >age 65 2% frank AS, 30% Aortic Sclerosis
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HEMODYNAMICS
• Severe AS
• Mean systolic pressure gradient ≥ 40mmHg in the
presence of normal cardiac output
• Valve area ≤ 1.0cm2
• Moderate AS
• 1-1.5cm2
• Mild AS
• 1.5-2cm2
• Aortic Sclerosis
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HISTORY
• Long latent period of increasing obstruction
• Symptoms usually begin in 5th or 6th decade
• Angina in 2/3 of patients
• Hyperthrophied myocardium
• Increased ventricular systolic pressure
• All of which increase myocardial oxygen
consumption
• Oxygen supply-demand imbalance leads to
subendocardial ischemia
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HISTORY
• Syncopy
• Reduced cerebral perfusion
• Vasodilation in the presence of fixed cardiac
output leads to hypotension
• Baroreceptor-vasodepression due to high LV
systolic pressure
• Dyspnea (CHF)
• Particularly with exertion due to fixed cardiac
output
• Pulmonary Venous HTN can lead to CHF
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NATURAL HISTORY
• Asymptomatic latent period
• With moderate-severe AS valve area can decrease
on average 0.12cm2 per year
• *Angina, synocopy or CHF
• Average 1-3 year survival 50%
• Sudden cardiac death rare
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SURGERY (VALVE REPLACEMENT)
• Indications
• Symptomatic Patients -valve area ≤ 1.0cm2 Asymptomatic
Patients-progressive LV disfunction (EF <35%) or hypotensive
response to mild exercise
• Delaying surgery in asymptomatic patients with good exercise
tolerance is controversial
• Valve type Prosthetic, Bioprosthetic or TAVR
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KEEPSURGERY (VALVE REPLACEMENT)
• Results
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Effective prosthetic valve area not normal
Surgery replaces Critical AS with Non-critical AS
Symptoms can persist if valve-patient mismatch occurs
10 year survival –85%
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AORTIC REGURGITATION
ETIOLOGY AND PATHOLOGY
• Valvular
• Rheumatic-Fibrotic Retraction of Leaflets
• Ankylosing Spondylitis, Behcets, Psoratic Arthritis, Giant
Cell Arteritis
Degenerative AS-75% w/AR
Infective Endocarditis-Leaflet Distruction
Trauma-ascending aortic tear
Bicuspid aortic valve-prolapse or incomplete
closure
• Myxomatous Degeneration-like MVP
• Appetite suppressant drugs-serotonin related
valve deposits
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ETIOLOGY AND PATHOLOGY
• Aortic Root Disease-More common than primary
valvular. Root Dilatation leads to non-coaptation of
leaflets.
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Degenerative-Hypertensive Aortic Dilatation
Cystic Medial Necrosis-Classic Marfans Syndrome
Aortic Dissection
Syphilitic Aortitis
Rheumatic Disease-same as valvular
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HISTORY
• Acute AR
• LV cannot accommodate acute regurgitant volume
• can lead to cardiovascular collapse
• Chronic AR
• Gradual LV enlargement-eccentric hypertrophy
• Exertional dyspnea, orthopnea, PND, CHF
• Presents 4th or 5th Decade
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NATURAL HISTORY
• Acute AR
• Cardiovascular collapse
• Inotrophic agents and vasodilators
• Prompt surgical intervention
• Chronic AR
• 75% Five Year Survival
• 50% Ten Year Survival
• Progressive downhill course of CHF, Episodic
Pulmonary Edema, Sudden Cardiac Death
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MEDICAL TREATMENT
• Acute AR
• As above
• Chronic AR
• Asymptomatic Mild-Moderate
• Follow by Echo Yearly
• Endocarditis Prophalaxis for all AR
• May not require medical treatment
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MEDICAL TREATMENT
• Symptomatic Moderate-Severe AR
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Limit exertional activity
Aggressively treat B/P
Diuretics
Salt Restriction
Digoxin
Vasodilators (Nifedipine?)
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SURGICAL TREATMENT
• Indications
• Defer surgery for chronic severe AR if good exercise
tolerance, EF greater than 50%, end systolic diameter < 50
mm, and end diastolic diameter < 70 mm
• Be aware that progressive decline in LV function or size
increases surgical morbidity and mortality
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SURGICAL TREATMENT
• Mortality
• 3-8% perioperative
• 5-10% late mortality with significant preop LV dysfunction
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