Valvular Heart Disease
M Saugi Abduh
Valvular Heart Disease
Heart contains
Two atrioventricular valves
Mitral
Tricuspid
Two semilunar valves
Aortic
Pulmonic
Valvular Disease
Normal Structure
Mitral Valve
Cross sectional Area 4-6cm
Anterior and Posterior Leaflets
Chordae Tendineae Papillary Muscles
Mitral Stenosis
Etiology & Pathology
Rheumatic Fever- 99%
Other
Congenital
Carcinoid
Lupus
Amyloid
Infective Endocarditis
Mucopolysaccharide Disease
Stenotic Pathology
Etiology & Pathology
Commissural
Cuspal
Chordal
Mixed
30%
15%
10%
Remaining
Valve becomes funnel shaped or fish mouthed
Thickened immobile leaflets or chordal
structures
Fig. 37-9
Fish mouth
Pathophysiology
Mild MS- orifice <2 cm
Critical MS- <1 cm
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)
History
Exertional Dyspnea
Cough/Wheezing
Orthopnea/PND/CHF
Hemoptysis-Rupture of Pulmonary VeinBronchial Vein Shunts
History
Chest Pain-Increase RV Pressures or
Unknown Etiology
Systemic Emboli (LA clots)
10
Increased LA size, Decreased C.O., Atrial Fib
Physical Exam
Auscultation
11
Diastolic Rumble
Assoc Murmur of MR
Loud S1-thickened leaflets
Increased P2-pulmonary hypertension
Decreased B/P if C.O. decreased
Prominent a wave if sinus rhythm present
Physical Exam
12
Mitral Facies-pink, purple facial patches
due to decrease CO and systemic
vasoconstriction
Hepatomegally
Edema
Ascites
Hydrothorax With Right Heart Failure
Diagnosis
ECG
Left Atrial Abnormality
13
P wave becomes bifid and greater than 0.12 sec in
duration in V1 and Lead II
RVH- right axis deviation
R wave > S wave in V1
Diagnosis
Chest X-ray
Echo- Cornerstone of Diagnosis
14
Dilated LA, RA, RV
Elevated Left Main stem Bronchus
Interstitial Edema
Thickened Calcified Leaflets
Doming of Leaflets on Opening
Natural History
15
Asymptomatic for 15-20yrs following
Rheumatic Fever
Additional 5-10 yrs for progression from mild to
severe stenosis
Stenosis progression approximately .09 cm/yr
Natural History
Presurgical Survival Rates
16
NYHA Class II 80%-10yrs
Class III 38%-10yrs, 62% 5yrs
Class IV 15%-5yrs
Percutaneous Balloon Angioplasty
18
Moderate-Severe MS
Mild MS- if Pulmonary Artery Pressures or
Wedge Pressure Elevate with Exercise
Valve Replacement
Indications
Mortality
19
Combined MS/MR
<1.5 cm-NYHA III or IV
<1 cm
Class II if Pulmonary Artery Pressure >70mmHg
3-8%
Valve Type-Prosthetic or Bioprosthetic
Mitral Regurgitation
Etiology
Rheumatic Heart Disease
Infective Endocarditis
Collagen Vascular Disease
Cardiomyopathy
Ischemic Heart Disease
Mitral Valve Prolapse-most common cause for valve
surgery in US
20
Pathophysiology
Decreased Impedance to Ventricular Emptying
Determinants of Regurgitant Flow
21
Instantaneous Size of MV Orifice
Dependent on Preload, After load, LV Contractility,
LV Size
LA-LV Pressure Gradient dependent on Systemic
Vascular Resistance, LV Pressure, & LV Size
Pathophysiology
LV Compensation
22
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
Pathophysiology
LV Decompensation
23
Increase End Systolic Volume
Increased End Diastolic Volume
Leads to Annulus Dilatation (MR begets MR)
Decreased Ejection Fraction and Stroke Volume
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.
24
History
25
Shortness of Breath
Exertional Dyspnea
Congestive Heart Failure
Right Heart Failure
Significant symptoms in chronic MR usually do
not develop until LV decompensation occurs.
History
Medical Treatment Survival
26
80% 5yr
60% 10yr
30-45% 5yr if MR severe
Diagnosis
Physical Exam
ECG
LA abnormality
LVH
RVH
Chest X-ray
27
Holosystolic Murmur
Increase Carotid Impulse
Increase LA, LV, RV, Interstitial Edema
Diagnosis
Echo
28
Transesophageal superior to transthoracic
Evaluation of Chamber Sizes, Regurgitant Jet,
Leaflets
Management of Acute MR
Medical
After load Reduction (Nitropresside & Intra
aortic balloon pump)
29
Decrease impedance to LV ejection
Decrease regurgitant volume into left atrium
Inotropic Support (Dobutamine)-if LV function
reduced
Management of Acute MR
Surgical Intervention
30
Progressive LV Failure or Hemodynamic
Deterioration
CHF
Hypertension
Valve Disruption
Management of Chronic MR
Medical
31
Digoxin
Diuretics*
After load Reduction
Anticoagulation in A-fib
Endocarditis Prophylaxis
Management of Chronic MR
Surgical
Indications
Asymptomatic Class I
Severe MR Class II, III, or IV
32
EF < 60% or LV Systolic Diameter >45mm
generally considered for surgery unless EF <30%
Valve Repair vs. Replacement
Aortic Valve
Normal Structure
33
Valve sits at the base of Aortic Root
Three Leaflets (cusps)-non coronary, right
coronary, left coronary
Normal cross-sectional area 3-4cm
Aortic Stenosis Etiology and
Pathology
34
Valvular
Supravalvular
Subvalvular
Hyperthrophic Cardiomyopathy
Congenital Aortic Stenosis
Unicuspid
Bicuspid
Adult Presentation
Chronic turbulent flow
Leads to fibrosis, rigidity, calcification
Tricuspid
35
Presents less than one year of age
Leaflets of unequal size
Acquired Aortic Stenosis
Rheumatic
Degenerative or Senile
36
Rare
Usually mitral valve also involved
Most common cause of adult AS
Most common cause of valve replacement
Inflammatory or Infectious component??
>age 65 30% Aortic Sclerosis
37
Hemodynamics
Critical (Surgical) AS
Moderate AS
38
1-1.5cm
Mild AS
Peak systolic pressure gradient > 50mmHg in the
presence of normal cardiac output
Valve area <0.7-0.8cm
1.5-2cm
Aortic Sclerosis
History
Long latent period of increasing
obstruction
Symptoms usually begin in 5th or 6th decade
Angina in 2/3 of patients
39
Hypertrophied myocardium
Increased ventricular systolic pressure
All of which increase myocardial oxygen
consumption
Oxygen supply-demand imbalance leads to
subendocardial ischemia
Diagnosis
Physical Examination
Systolic Murmur
Pulses Parvus
42
Diamond-Shaped, harsh, left sternal boarder to right
intercostal spaces, neck and apex
Late peak, obliteration of S2, Dx of Critical AS
Delayed and Prolonged Carotid Impulse
Diagnosis
ECG
Chest X-ray
Concentric LVH
Calcification of Aortic Valve
Echo
43
Classic LVH
calculation of LV-Aortic pressure gradient and
valve area
Diagnosis
44
Cardiac Catherization
Medical Management
45
Endocarditis Prophylaxis
Limit Physical Activity
Watch Beta Blockers and Diuretics
*Treatment of Critical AS in viable
candidates is surgery
Surgery (Valve Replacement)
Indications
Symptomatic Patients -valve area 0.7-0.8cm or
less
Asymptomatic Patients-progressive LV
dysfunction (EF <35%) or hypotensive response
to mild exercise
46
Delaying surgery in asymptomatic patients with good
exercise tolerance is controversial
Aortic Regurgitation
Etiology and Pathology
Valvular
Rheumatic-Fibrotic Retraction of Leaflets
47
Ankylosing Spondylitis, Behcets, Psoriatic Arthritis,
Giant Cell Arteritis
Degenerative AS-75% w/AR
Infective Endocarditis-Leaflet Destruction
Trauma-ascending aortic tear
Bicuspid aortic valve-prolapse or incomplete
closure
Myxomatous Degeneration-like MVP
Appetite suppressant drugs-serotonin related
valve deposits
Etiology and Pathology
Aortic Root Disease-More common than primary
valvular. Root Dilatation leads to non-coaptation of leaflets.
48
Degenerative-Hypertensive Aortic Dilatation
Cystic Medial Necrosis-Classic Marfans
Syndrome
Aortic Dissection
Syphilitic Aortitis
Rheumatic Disease-same as valvular
History
Acute AR
Chronic AR
49
LV cannot accommodate acute regurgitant
volume
can lead to cardiovascular collapse
Gradual LV enlargement-eccentric hypertrophy
Exertional dyspnea, orthopnea, PND, CHF
Presents 4th or 5th Decade
50
Physical Examination
Diastolic Murmur
51
Left sternal boarder
Decrescendo, high pitched
Best heard Sitting Up, End Expiration
Longer murmur equals worse AR
Physical Examination
de Mussetts Sign (head bobbing)
Corrigans Pulse water hammer
Bisferiens-pulse
Pistol shot sounds over femoral pulse
Duroziezs Sign
52
2 peaks
Traubes Sign
Abrupt Distention with Quick Collapse
Murmur over femoral pulse with compression
Physical Examination
Quinckes Sign
Mullers Sign
Systolic pulsations of uvula
Hills Sign
53
Capillary pulsations
Popliteal pulse exceed brachial pulse by >
60mmHg
Physical Examination
Korotkoff Sounds
54
Can persist to 0mmHg
Wide Pulse pressure
Diagnosis
ECG
Chest X-ray
55
Cardiomegaly predominantly inferior and leftward
Echo
LVH
Can aid in detecting etiology, quantifying degree of
regurgitation, and assessing LV size and function
Cardiac Catheterization
Medical Treatment
Symptomatic Moderate-Severe AR
56
Limit exertional activity
Aggressively treat B/P
Diuretics
Salt Restriction
Digoxin
Vasodilators (Nifedipine?)
Surgical Treatment
Indications
57
Defer surgery for chronic severe AR if good
exercise tolerance, EF greater than 50%, end
systolic diameter < 50 mmHg, and end diastolic
diameter < 70 mmHg
Be aware that progressive decline in LV function or
size increases surgical morbidity and mortality
Surgical Treatment
Mortality
58
3-8% perioperative
5-10% late mortality with significant preop LV
dysfunction
Tricuspid and Pulmonic Valve Disorders
Uncommon
Both conditions cause an increase in blood
volume in R atrium and R ventricle
Result in Right sided heart failure
Diagnostic Tests
Echo- assess valve motion and chamber size
CXR
EKG
Cardiac cath- get pressures
Medications
Like Heart Failure
ACE inhibitors
Digoxin
Diuretics
Vasodilators
Beta blockers
Anticoagulants
*Prophylactic antibiotics
Medical/ Surgical Treatment
Percutaneous balloon valvuloplasty
Surgical therapy for valve repair or replacement:
Valve repair is typically the surgical procedure
of choice
Open commissurotomy- open stenotic
valves
Annuloplasty- can be used for both
Valve replacement may be required for certain
patients Heart valve surgery
Mechanical-need anticoagulant
Biologic-only last about 15 years
Ross Procedure
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