Valvular heart disease

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Valvular heart disease

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MITRAL STENOSIS

• ETIOLOGY AND PATHOLOGY
• predominant cause -Rheumatic fever
• Less frequently, congenital in etiology
• Very rarely , malignant carcinoid, systemic lupus
  erythematosus, rheumatoid arthriti
• Drug - Methysergide therapy

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MITRAL STENOSIS

• ETIOLOGY AND PATHOLOGY
• Approximately 25 per cent of all patients with
  rheumatic heart disease have pure MS
• Two-thirds of all patients with rheumatic MS are
  female.
• It probably takes a minimum of 2 years after the
  onset of acute rheumatic fever for severe MS to
  develop
• Symptoms commence most commonly in the third or
  fourth decade

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MITRAL STENOSIS

• ETIOLOGY AND PATHOLOGY
• Rheumatic fever results in four forms of fusion
  of the mitral valve apparatus leading to
  stenosis
• (1) commissural,
• (2) cuspal,
• (3) chordal,
• (4) combined.

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MITRAL STENOSIS

• PATHOPHYSIOLOGY
• normal adults the cross-sectional area of the
  mitral valve orifice is 4 to 6 cm.
• Mild MS , MVA 2.0 to 1.5 cm
• Moderate stenosis , MVA 1.0 to 1.5 cm
• Severe MS , MVA lt 1 cm

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MITRAL STENOSIS

• Intracardiac and Intravascular Pressure
• Left ventricular diastolic pressure is normal in
  patients with pure MS
• Coexisting MR, aortic valve lesions, systemic
  hypertension, ischemic heart disease, and
  cardiomyopathy may all be responsible for
  elevations of left ventricular diastolic
  pressure.

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MITRAL STENOSISIntracardiac and Intravascular
Pressure

• Schematic relationship of left ventricular,
  aortic, and pulmonary atrial wedge (PAW) pressures

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MITRAL STENOSIS

• Intracardiac and Intravascular Pressure
• Pulmonary hypertension in patients with MS
  results from
• (1) passive backward transmission of the elevated
  left atrial pressure
• (2) pulmonary arteriolar constriction, which
  presumably is triggered by left atrial and
  pulmonary venous hypertension (reactive pulmonary
  hypertension)
• (3) organic obliterative changes in the pulmonary
  vascular bed, which may be considered to be a
  complication of longstanding and severe MS

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MITRAL STENOSIS

• CLINICAL MANIFESTATIONS
• HEMOPTYSIS
• Sudden hemorrhage - the rupture of thin-walled,
  dilated bronchial veins
• Blood-stained sputum
• Pink, frothy sputum - rupture of alveolar
  capillaries.
• Pulmonary infarction, a late complication of MS
  associated with heart failure.

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MITRAL STENOSIS

• CLINICAL MANIFESTATIONS
• CHEST PAIN
• THROMBOEMBOLISM
• INFECTIVE ENDOCARDITIS - more common in patients
  with mild than with severe MS.
• HOARSENESS - Compression of the left recurrent
  laryngeal nerve by a greatly dilated left atrium,
  enlarged tracheobronchial lymph nodes, and
  dilated pulmonary artery

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MITRAL STENOSIS

• Physical Examination - AUSCULTATION
• opening snap (OS)
• a short A2-OS interval is a reliable indicator
  of severe MS
• During exercise the A2-OS interval narrows
• the A2-OS interval varies inversely with the left
  atrial pressure
• sudden standing with the resultant decrease in
  venous return causes a lowering of left atrial
  pressure and therefore widens the A2-OS interval
• presystolic murmur
• diastolic rumbling murmur

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MITRAL STENOSIS

• ELECTROCARDIOGRAPHY
• Left atrial enlargement (P-wave duration in lead
  II gt 0.12 sec, terminal negative P force in lead
  V1 gt 0.003 mV/sec, P-wave axis between 45 and
  -30 degrees) , 90
• Atrial fibrillation
• Right ventricular hypertrophy (a mean QRS axis
  greater than 80 degrees in the frontal plane and
  an RS ratio greater than 1.0 in V1 )

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MITRAL STENOSIS

• RADIOLOGICAL FINDINGS
• (combined with MR)
• left atrial enlargement
• Enlargement of the pulmonary artery, right
  ventricle, and right atrium
• Interstitial edema - manifested as Kerley B lines
  (dense, short, horizontal lines most commonly
  seen in the costophrenic angles)

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MITRAL STENOSIS

• MANAGEMENT
• Medical Treatment
• penicillin prophylaxis for beta-hemolytic
  streptococcal infections and infective
  endocarditis
• In symptomatic patients
• Oral diuretics and the restriction of sodium
  intake
• Digitalis glycosides
• not benefit patients with MS and sinus rhythm
• but are of great value in with atrial
  fibrillation and in the treatment of right-sided
  heart failure
• Anticoagulant therapy is helpful in preventing
  venous thrombosis and pulmonary embolism

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MITRAL STENOSIS

• Surgical Treatment
• INDICATIONS FOR OPERATION
• Operation (or balloon valvuloplasty) should
  therefore be carried out in symptomatic patients
  with moderate to severe MS (i.e., a mitral valve
  orifice size less than approximately 1.0 cm2/m2
  body surface area BSA - less than 1.5 to 1.7
  cm2 in normal-sized adults).

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MITRAL STENOSIS

• SURGICAL TECHNIQUES.
• closed mitral valvotomy
• open valvotomy, i.e., valvotomy carried out under
  direct vision with the aid of cardiopulmonary
  bypass
• mitral valve replacement

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MITRAL STENOSIS

• Balloon Mitral Valvuloplasty

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MITRAL STENOSIS
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MITRAL REGURGITATION

• ETIOLOGY AND PATHOLOGY
• ABNORMALITIES OF VALVE LEAFLETS
• ABNORMALITIES OF THE MITRAL ANNULUS
• ABNORMALITIES OF THE CHORDAE TENDINEAE
• INVOLVEMENT OF THE PAPILLARY MUSCLES

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CAUSES OF ACUTE REGURGITATION

• Mitral Annulus Disorders
• Infective endocarditis (abscess formation)
• Trauma (valvular heart surgery)
• Paravalvular leak due to suture
  interruption (surgical technical problems or
  infective endocarditis)

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CAUSES OF ACUTE REGURGITATION

• Mitral Leaflet Disorders
• Infective endocarditis (perforation or
  interfering with valve closure by vegetation)
• Trauma (tear during percutaneous mitral balloon
  valvotomy or penetrating chest injury)
• Tumors (atrial myxoma)
• Myxomatous degeneration
• Systemic lupus erythematosus (Libman-Sacks lesion)

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CAUSES OF ACUTE REGURGITATION

• Rupture of Chordae Tendineae
• Idiopathic, e.g., spontaneous
• Myxomatous degeneration (mitral valve prolapse,
  Marfan syndrome, Ehlers-Danlos syndrome)
• Infective endocarditis
• Acute rheumatic fever
• Trauma (percutaneous balloon valvotomy, blunt
  chest trauma)

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CAUSES OF ACUTE REGURGITATION

• Papillary Muscle Disorders
• Coronary artery disease (causing dysfunction and
  rarely rupture)
• Acute global left ventricular dysfunction
• Infiltrative diseases (amyloidosis, sarcoidosis)
• Trauma

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CAUSES OF ACUTE REGURGITATION

• Primary Mitral Valve Prosthetic Disorders
• Porcine cusp perforation (endocarditis)
• Porcine cusp degeneration
• Mechanical failure (strut fracture)
• Immobilized disc or ball of the mechanical
  prosthesis

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CAUSES OF CHRONIC REGURGITATION

• Inflammatory
• Rheumatic heart disease
• Systemic lupus erythematosus
• Scleroderma
• Infective
• Infective endocarditis affecting normal,
  abnormal, or pros thetic mitral valves

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CAUSES OF CHRONIC REGURGITATION

• Degenerative
• Myxomatous degeneration of mitral valve leaflets
  (Barlows click-murmur syndrome, prolapsing
  leaflet, mitral valve prolapse)
• Marfan syndrome
• Pseudoxanthoma elasticum
• Calcification of mitral valve annulus

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CAUSES OF CHRONIC REGURGITATION

• Structural
• Ruptured chordae tendineae (spontaneous or
  secondary to myocardial infarction, trauma,
  mitral valve prolapse, endocarditis)
• Rupture or dysfunction of papillary muscle
  (ischemia or myocardial infarction)
• Dilatation of mitral valve annulus and left
  ventricular cavity (congestive cardiomyopathies,
  aneurysmal dilatation of the left ventricle)
• Hypertrophic cardiomyopathy
• Paravalvular prosthetic leak

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CAUSES OF CHRONIC REGURGITATION

• Congenital
• Mitral valve clefts or fenestrations
• Parachute mitral valve abnormality in association
  with
• Endocardial cushion defects
• Endocardial fibroelastosis
• Transposition of the great arteries
• Anomalous origin of the left coronary artery

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MITRAL REGURGITATION

• CLINICAL MANIFESTATIONS
• Do not develop in patients with chronic MR until
  the left ventricle fails
• In severe MR
• hemoptysis
• systemic embolization
• infective endocarditis,
• rupture of chordae tendineae.

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MITRAL REGURGITATION

• Physical Examination
• S1, produced by valve closure, is usually
  diminished.
• The abnormal increase in the flow rate across the
  mitral orifice during the rapid filling phase is
  usually associated with an S3
• Systolic murmur - the most prominent physical
  finding in MR (radiation to the axilla and left
  infrascapular area )

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MITRAL REGURGITATION

• LABORATORY EXAMINATION
• ELECTROCARDIOGRAPHY
• left atrial enlargement
• atrial fibrillation
• left ventricular enlargement (1/3 patients)
• right ventricular hypertrophy (15 patients)

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MITRAL REGURGITATION

• MANAGEMENT - Medical Treatment
• The treatment of heart failure (Digitalis
  glycosides, diuretics )
• Afterload reduction is of particular benefit in
  the management of MR
• intravenous nitroprusside may be lifesaving in
  acute MR
• chronic afterload reduction with an angiotensin
  inhibitor or oral hydralazine

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MITRAL REGURGITATION

• MANAGEMENT - Surgical Treatment

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MITRAL REGURGITATION

• MANAGEMENT - Surgical Treatment
• INDICATIONS FOR OPERATION
• recommended operation for patients with chronic
  severe MR only if they were in functional Class
  III or IV
• severe MR who are in Class II and if end-systolic
  volume and diameter are elevated (gt50 ml/m2 BSA
  and gt45 mm, respectively).

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MITRAL VALVE PROLAPSE

• DEFINITION - many names
• systolic click-murmur syndrome
• Barlow syndrome
• billowing mitral cusp syndrome
• myxomatous mitral valve
• floppy valve syndrome
• redundant cusp syndrome

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MITRAL VALVE PROLAPSE

• ETIOLOGY
• commonly in heritable disorders of connective
  tissue that increase the size of the mitral
  leaflets and apparatus including
• Marfan syndrome
• Ehlers-Danlos syndrome
• osteogenesis imperfecta
• pseudoxanthoma elasticum

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MITRAL VALVE PROLAPSE

• PATHOLOGY
• myxomatous degeneration of the valve
• postinflammatory changes
• secondary to papillary muscle dysfunction

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MITRAL VALVE PROLAPSE

• CLINICAL MANIFESTATIONS
• observed in patients of all ages and in both
  sexes
• reported to occur in 6 per cent of healthy young
  women surveyed by echocardiography

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MITRAL VALVE PROLAPSE

• during the straining phase of the Valsalva
  maneuver,
• sudden standing,
• early during the inhalation of amyl nitrite,
• ? LV volume decreases and the click and murmur
  occur earlier in systole

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MITRAL VALVE PROLAPSE

• Physical Examination
• leg raising, squatting, isometric exercise such
  as handgrip,
• slowing of the heart rate with propranolol
• ?all increase LV volume and delay the click and
  murmur

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MITRAL VALVE PROLAPSE

• History
• fatigability,
• palpitations,
• neuropsychiatric symptoms,
• symptoms of autonomic dysfunction
• syncope, presyncope,
• chest discomfort - typical of angina but most
  often it is atypical

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MITRAL VALVE PROLAPSE

• MANAGEMENT
• Asymptomatic patients - follow-up cardiac echo
  examinations every 3 to 5 years
• Endocarditis prophylaxis is advisable in patients
  with a typical systolic murmur
• Symptomatic patients or those who have
  ventricular arrhythmias or Q-T prolongation
  should undergo ambulatory (24-hour)
  electrocardiographic monitoring or exercise
  electrocardiography or both to detect
  arrhythmias.
• Beta-adrenoceptor blockers are useful in the
  treatment of palpitations

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AORTIC STENOSIS ETIOLOGY AND PATHOLOGY

• CONGENITAL AORTIC STENOSIS
• unicuspid, severe obstruction in infancy - fatal
  valvular aortic stenosis
• bicuspid, stenotic with commissural fusion at
  birth
• tricuspid, the cusps of unequal size and some
  commissural fusion
• there may be a dome-shaped diaphragm

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AORTIC STENOSIS ETIOLOGY AND PATHOLOGY

• ACQUIRED AORTIC STENOSIS
• Rheumatic AS
• degenerative (senile) calcific AS
• atherosclerotic aortic valvular stenosis

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AORTIC STENOSIS ETIOLOGY AND PATHOLOGY
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AORTIC STENOSIS ETIOLOGY AND PATHOLOGY

• PATHOPHYSIOLOGY

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AORTIC STENOSIS

• CLINICAL MANIFESTATIONS
• commence most commonly in the sixth decade of
  life, are
• angina pectoris - the time of death is
  approximately 5 years
• Syncope - the time of death is approximately 3
  years
• heart failure - the time of death is
  approximately 2 years

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AORTIC STENOSIS

• Physical Examination
• S1 is normal or soft
• S4 is prominent - atrial contraction is vigorous
  
• The systolic murmur of AS is usually late-peaking
  - transmitted along the carotid vessels and to
  the apex (Gallavardin phenomenon )
• the more severe the stenosis, the longer the
  duration of the murmur

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AORTIC STENOSIS

• MANAGEMENT - Medical Treatment
• Digitalis glycosides are indicated if there is an
  increase in ventricular volume or reduced
  ejection fraction.
• Diuretics are beneficial when there is abnormal
  accumulation of fluid, they must be used with
  caution to avoid hypovolemia.

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AORTIC STENOSIS

• Surgical Treatment
• INDICATIONS FOR OPERATION
• The aortic valve should, in general, be replaced
  in patients who have hemodynamic evidence of
  severe obstruction (aortic valve orifice lt 0.8
  cm2 or lt 0.5 cm2/m2 BSA) and symptoms believed to
  result from AS
• Surgical risk is high in LVEF lt 35
• Balloon Aortic Valvuloplasty
• in children, adolescents, and young adults with
  congenital noncalcific AS

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AORTIC REGURGITATION

• ETIOLOGY AND PATHOLOGY
• caused by primary by
• the aortic valve leaflets
• the wall of the aortic root
• or both
• Rheumatic fever
• Syphilis
• Systemic hypertension
• Marfan syndrome
• Infective endocarditis
• Prolapse from VSD

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AORTIC REGURGITATION
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AORTIC REGURGITATION

• CLINICAL MANIFESTATIONS
• CHRONIC AORTIC REGURGITATION
• Exertional dyspnea,
• orthopnea,
• paroxysmal nocturnal dyspnea

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AORTIC REGURGITATION

• CLINICAL MANIFESTATIONS
• ACUTE AORTIC REGURGITATION
• cardiovascular collapse,
• weakness,
• severe dyspnea,
• hypotension secondary to the reduced stroke
  volume

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AORTIC REGURGITATION

• Physical Examination
• de Mussets sign - the head frequently bobs with
  each heartbeat
• Corrigans pulse - the pulses are of the
  water-hammer or collapsing type with abrupt
  distention and quick collapse
• Traube sign (pistol shot sounds) - booming
  systolic and diastolic sounds heard over the
  femoral artery
• Mullers sign - systolic pulsations of the uvula

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AORTIC REGURGITATION

• Physical Examination
• Duroziezs sign - a systolic murmur heard over
  the femoral artery when it is compressed
  proximally and a diastolic murmur when it is
  compressed distally
• Quinckes sign - Capillary pulsations detected by
  pressing a glass slide on the patients lip or by
  transmitting a light through the patient?
  fingertips
• Hills sign - popliteal cuff systolic pressure
  exceeding brachial cuff pressure by more than 60
  mm Hg.

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AORTIC REGURGITATION

• Medical Treatment
• antibiotic prophylaxis for endocarditis.
• Cardiac glycosides
• intravenous hydralazine
• sublingual nifedipine
• oral prazosin.

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AORTIC REGURGITATION

• INDICATIONS FOR OPERATION
• the left ventricular ejection fraction declines
  to 50 per cent,
• the left ventricular end-systolic diameter
  exceeds 45 to 50 mm,
• Or the left ventricular end-systolic volume
  exceeds 55 ml/m2?

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PULMONIC STENOSIS

• Valvular PS is the most common form of isolated
  right ventricular obstruction
• The most common symptoms of PS during infancy are
  acidemia and hypoxemia
• Percutaneous transluminal balloon valvuloplasty
  is the initial procedure of choice in patients
  with typical valvular PS and moderate to severe
  degrees of obstruction
• The electrocardiogram is usually normal in mild
  PS, whereas moderate and severe PS is associated
  with right axis deviation and RV hypertrophy.

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PROSTHETIC CARDIAC VALVES

• prosthetic valve endocarditis
• absolute indications for operation
• the presence of congestive heart failure,
• ongoing sepsis,
• fungal etiology,
• valvular obstruction,
• unstable prosthesis
• recent-onset heart block
• positive blood cultures despite 2 weeks of
  appropriate antibiotic therapy

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PROSTHETIC CARDIAC VALVES

• prosthetic valve endocarditis
• Relative indications for operation
• mild congestive failure,
• nonstreptococcal etiology,
• early prosthetic valve endocarditis,
• embolism,
• perivalvular leak,
• vegetations on echocardiography,
• relapse,
• culture-negative endocarditis without clinical
  response to empiric antibiotic therapy

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