Transcript Mitral Stenosis

Valvular Heart Disease
ADRIEL E. GUERRERO, MD, FPCP, FPCC
Training Officer
Section of Cardiology, Dept of Medicine
The Medical City
Mitral Stenosis
Diagnostic Features of MS@
 2/3 are females; Pure MS are generally rheumatic
 History:
 Exertional Dyspnea, PND, Orthopnea and Hemoptysis
 PE:
 Opening snap, loud S1, diastolic rumble at the apex
 ECG and Chest Xray:
 Evidence of left atrial enlargement with normal left
ventricular size; RVH in later stages
 2DECHO
Chest Xray MS
Common Etiologies of MS
 Rheumatic Heart Disease
 Congenital Heart disease
 Congenital MS
 Lutembachers syndrome (MS and ASD)
 Mitral Annular Calcification (elderly)
Mitral Stenosis@
Pathophysiology
Obstruction to LV filling
Increase LA pressure
RV Failure
Natural History of MS
 Pulmonary Hypertension
 Fibrous thickening of alveolar and pulmo capillary walls
 Thrombi and Emboli
 Left atrial appendage
 Increased: AF, older patients, reduced CO
 Pulmonary Infections, IE,
Natural History of Mitral Stenosis
MS - blue
MR - purple
Differential Diagnosis of MS
 Atrial Septal Defect
 RVE and accentuated pulmo markings
 Widely split S2 (fixed)VS Opening snap; diastolic flow across
the TV
 No LAE
 Left Atrial Myxoma
 Obstructing LA emptying, tumor-plop
 Mitral Regurgitation
 Systolic murmur; LVH
 Aortic Regurgitation (Austin Flint)
 Apical middiastolic murmur of AR. Becomes louder on handgrip
and decreases with amyl nitrate
Treatment of MS
 Penicillin Prophylaxis of B-hemolytic Streptococcal
Infections to prevent Rheumatic Fever and IE
 Sodium restriction, oral diuretics
 Oral Anticoagulation (Warfarin)
 INR target 2-3.1 (embolization, permanent AF)
 Heart Rate Controlling drugs
 To lengthen diastolic LV filling
 Digitalis in Atrial Fibrillation; Beta-blockers in sinus rhythm
 Nondihydropyridine Calcium Antagonists
Mitral Valvotomy
 Indicated in symptomatic patients with isolated MS
(<1.0 cm2/m2)
 Ideal for mobile, thin leaflets with no or little calcium
without extensive subvalvular thickening and with no or
mild MR
 Open valvotomy – mortality rate is 2%
 50% of all patients require reoperation by 10 years.
 Pregnant – carried out if pulmonary congestion occurs
despite intensive medical treatment
Mitral Valve Replacement
 MS with significant MR
 Distorted valves from previous transcatheter or
operative manipulation
 Operative Mortality is 6%
 Long term complications of valve replacement
 Overall 10 year survival is 70%
 Poor Recovery
 Old patients
 Marked disability
 Depressed Cardiac index
Mitral Stenosis
Percutaneous Trans-septal Mitral
Commissurotomy
Star Edwards Caged Ball Valve
Medtronic Hall Valve (BjorkShiley)
St Jude Bileaflet Valve
Carpentier Edwards Porcine Valve
Carpentier Edwards Pericardial
Valve
Mitral Regurgitation
 Frequent in males
 History:
 Easy Fatigue then exertional Dyspnea
 PE:
 Characteristic holosystolic murmur at the apex with
radiation to the axilla
Common Etiologies of MR
 MV leaflet abnormality
 Rheumatic heart disease
 Myxomatous alteration (including MVP)
 Infective Endocarditis
 Mitral annulus dilatation of any cause
 Dilated Cardiomyopathy
 IHD with dilated LV
 Ruptured chordae tendinae
 Trauma
 Myocardial Infarction
 Papillary muscle disorder
 Ischemic Heart Disease
Mitral Regurgitation
NORMAL
Pathophysiology of Mitral
Regurgitation
Pathophysiology of Mitral
Regurgitation
Pathophysiology of Mitral
Regurgitation
Laboratory Examination
 La enlargement; RAE maybe present if pulmonary HPN is
severe
 Atrial Fibrillation
 LVH
 ECG
 2DECHO – most accurate non-invasive technique
 CXR – LAE and LVE
Medical Treatment for MR
 Restrict Physical activities
 Reduce sodium intake and enhance sodium excretion
(diuretics)
 Increase forward cardiac output
 Vasodilators (ACEI) and digitalis
 Anticoagulants and leg binders to decrease likelihood of
venous thrombi and pulmonary emboli
 Endocarditis prophylaxis
Surgical Treatment of MR
 Non-surgical candidates: asymptomatic, or exercise limited to
strenuous exertion, normal LV function
 Surgery for severe MR even if asymptomatic or when LV
dysfunction is progressive (declining <60%) and/or LV ESD on
echo is >45mm
 MV replacement for markedly shrunken, deformed, calcified
leaflets
 MV repair (reconstruction) with annuloplasty
 Lessens problem on long term anticoagulation and
thromboembolism
 For ruptured chordae, annular dilatation and IE
 Not suitable for Mr due to myxomatous degeneration and patients
with calcified annulus
Natural History of Unoperated MR
Late Survival Rates after Surgical
Correction in MR (pre-op EF)
Mitral Valve Prolapse
 Barlow’s syndrome, floppy-valve syndrome, systolic
click-murmur syndrome, billowing mitral leaflet
syndrome
 Excessive or redundant mitral leaflet tissue. Posterior
MV leaflet is more affected than the AMVL
 May lead to excessive stress on the papillary muscles
leading to dysfunction. Rupture of chordae tendineae
with progressive annular dilatation and calcification
 Ventricular arrythmias
Clinical Features
 Females (14-30 years old)
 Clinical course is often benign
 Increased familial incidence – autosomal dominant
 Most common cause of isolated severe MR requiring
surgical treatment in North America
 Arrythmias (PVCs, SVTs, VTs) – palpitations,
lightheadedness and syncope. Sudden death is rare
 Chest pain substernal, prolonged, unrelated to exertion
Mitral Valve Prolapse
Mismatch between
elongated MV and LV
cavity
Laboratory Exams
 ECG – non specific STTW changes, PVCs
 Echo – demonstrates systolic displacement of MVL and
quantifies Mitral Regurgitation and LV function
Treatment of MVP
 IE prophylaxis
 Beta-blockers sometimes relieve chest pain
 For severe symptomatic MR, MV repair or rarely
replacement is indicated
 Antiplatelets for patients with TIA, anticoagulation if
recurrent TIAs
Survival Rates of MVP patients at
baseline risk factors
Primary Risk Factors
Mod-severe MR; EF <50%
Secondary Risk Factors
Mild-mod MR; LA > 40
Flail leaflet; AF; age > 50
Aortic Stenosis
 80% with symptomatic AS are males
 Age-related degenerative calcific AS – most common
cause of AS in Adults
Common Etiologies of AS
 Valvular (90% of all cases)
 Rheumatic heart disease
 Degenerative calcification (elderly)
 Bicuspid AV stenosis/ Congenital heart disease
 Subvalvular (9%)
 Hypertrophic Obstructive Cardiomyopathy (HOCM)
 Discrete
 Supravalvular (<1%)
 Infancy
NORMAL AORTIC VALVE
Aortic Stenosis - Rheumatic
Aortic Stenosis - Degenerative
Aortic Stenosis - Bicuspid
Pathophysio of AS
Pathophysio of AS
Aortic Stenosis
 History:
 Cardinal symptoms
 Exertional Dyspnea
 Angina Pectoris
 Syncope
 PE
 Carotid upstroke slowly rising and reduced in amplitude in
severe cases; Systolic ejection murmur radiating to the
carotid arteries
Laboratory Exam
 LV hypertrophy is the key finding
 ECG
 2DECHO – estimate valve area, LV size and function
 Cardiac catheterization
 Presence or absence of concomittant CAD
Natural History of Severe AS
 Death most commonly occurs in the 7th and 8th decade
 Average time from onset of symptoms to death:
 Angina – 3 years
 Syncope – 3 years
 Heart Failure – 1.5 – 2 years
 Sudden death 10-20% in AS patients 60 years old and above
Medical Treatment for AS
 Severe AS (<0.5 cm2/m2)Avoid strenuous physical
activities even if asymptomatic
 Sodium restriction
 Cautious administration of diuretics and digitalis in CHF
 Nitroglycerin to relieve angina
 Statins (HMGCoA reductase inhibitors) slows down
progression of calcification (?)
 No effect on long term survival
Surgery in Aortic Stenosis
 Indications for Surgery
 Severe Aortic Stenosis ( < 0.6 cm2/m2)
 Symptomatic with LV dysfunction (LV Ejection Fraction
<50%)
 Expanding poststenotic aortic root (even if asymptomatic)
 Those who undergo CABG even if asymptomatic
 Operative risk of Aortic Valve Replacement in
asymptomatic severe AS is 4%. In frank CHF – 15 – 20%
 10 year survival rate of patients with AVR = 60%
 30% of bioprosthesis fail in 10 yrs
 Mechanical prosthesis – hemorrhage fm anticoagulation
Management Strategy for Severe
Aortic Stenosis
Percutaneous Balloon Aortic
Valvuloplasty
 Preferred in children and young adults with congenital,
noncalcific AS
 High “restenosis” rate in calcific AS
 “bridge to operation”
Percutaneous Transcatheter
Placement of AV prosthesis
Percutaneous Transcatheter
Placement of AV prosthesis
Aortic Regurgitation
Etiology
 Primary Valve Disease
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Rheumatic – 2/3 of patients
Infective Endocarditis
Trauma
Bicuspid valve
 Primary Aortic Root Disease
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Degenerative heart disease
Syphilis
Marfan’s syndrome
Ankylosing Spondylitis
Aortic Aneurysm with dissection
Systemic hypertension
Giant Cell arteritis
Pathophysio of AR
Aortic Regurgitation
 History:
 Easy fatigue then exertional dyspnea (diminished cardiac
reserve) – orthopnea, PND and excessive diaphoresis
 PE:
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Wide pulse pressure with bounding pulses
Diastolic decresendo murmur at the base of the heart
Midsystolic ejection murmur at base of the heart
Austin Flint murmur – soft, low pitched rumbling
middiastolic bruit at the apex
Peripheral Signs of Chronic AR
 Corrigan’s pulse: Pulses with abrupt distension and quick
collapse; water hammer pulse
 De Musset’s sign: head bobbing
 Traube’s sign: Pistol shot sound on the femoral artery
 Duroziez’s sign: Systolic murmur heard over the femoral
artery when compressed proximally
 Muller’s sign: systoic pulsation of the uvula
 Quincke’s sign: Capillary pulsation
 Hill’s sign: Popliteal cuff SBP > brachial cuff SBP by
60mmHg
Differential Diagnosis of a
Bounding Pulse
 Cardiac Causes
 Aortic Regurgitation
 Patent Ductus Arteriosus
 Non-Cardiac Causes
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
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Arteriovenous Fistula
Fever
Thyrotoxicosis
Pregnancy
Symptomatology in AR
 Symptoms depend on the onset of AR (acute/chronic)
 Compensatory mechanisms
 LV dilatation
 Laplace Law ( myocardial wall tension = intracavitary
pressure x LV radius)
 Deterioration of LV function precedes the development of
symptoms
 Chronic Severe AR may have a long latent period. Patients
remain asymptomatic for as long as 10-15 years.
Laboratory Exam
 LV Hypertrophy
 2DECHO + myocardial contractility and function
 Cardiac catheterization and angiography
 Magnitude of AR and status of LV function
Survival without Surgery in
Chronic AR
Medical Treatment of AR
 Salt restriction
 Diuretics
 Vasodilators (ACEI)
 Nitrates not as helpful in relieving angina
 Syphilitic aortitis – penicillin tx
Surgical Treatment of AR
 Definitive treatment
 Should be done before development of Heart Failure
 Operation should be carried out even in Asymptomatic
patients with progressive LV dysfunction and a left
Ventricular Ejection Fraction < 55% or a LV end-systolic
volume > 55 mL/m2 ( 55/55 rule)
 AVR – mechanical or bioprosthesis
 Operative mortality for isolated AVR is 4.3%
 Patients with marked LVE and dysfunction
 OR mortality 10%
 Late operative mortality 5% per year
Post-operative Survival in AR
Post-operative Survival in AR
Tricuspid Stenosis
Treatment of TS
 Medical Tx
 Intensive salt restriction, diuretic tx
 Surgical Tx
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Definitive tx
Diastolic pressure gradient >4 mmHg
Tricuspid orifice < 1.5 to 2.0 cm
Open heart repair/prosthesis (preferably large
bioprosthetic valve)
Tricuspid Regurgitation
Treatment Considerations in TR
 Isolated TR, in the absence of Pulmo HPN, is well
tolerated and does not require operation
 Functional TR (secondary to PHPN with MV disease)
resolves with effective correction of the MV disease)
 - annuloplasty
 TVR for severe valve deformity
Pulmonic Valve Disease
 Pulmonic Regurgitation – most common acquired
abnormality of the PV secondary to dilatation of the PV
ring as a consequence of PHPN
 Graham Steell murmur (high pitched decresendo,
diastolic blowing murmur along the left sternal borderlike AR)
 Of little hemodynamic significance.
Four Guidelines to Follow in Assessing Patients with
Multiple Valvular Abnormalities
 Guideline 1: Determine the Predominant Lesion
 A. The most severe lesion is usually the predominant lesion
 Ex.1
 Ans.
Patient has MS mild, AS severe, MR mild
AS is the dominant lesion
 B. The lesion that causes the most corresponding chamber
enlargement is usually the predominant lesion
 Ex.2 Patient has AR moderate, MS moderate,
Severely dilated LV, slightly dilated LA
 Ans. AR is the predominant lesion
 Guideline No. 2: Left-sided lesions are more important
that right-sided lesions. Therefore tailor your treatment
more for the left-sided lesion.
 Guideline No. 3: Significant stenotic lesions (MS or AS)
should be given more serious attention compared to
regurgitant lesions (MR or AR)
 Guideline No. 4: In severe valvular disease, surgical
correction of the mechanical defect should be given
prime consideration. Response to medical treatment is
poor.
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