Valvular Heart Disease

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Valvular Heart Disease
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Reading

• Klabunde, Cardiovascular Physiology Concepts
• CD ROM material on Valve Disease

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Overview of Valves
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Major Factors That Affect Flow Across Any
Valvular Lesion

• The valve area
• The square root of the hydrostatic pressure
  gradient across the valve
• The time duration of transvalvular flow (applies
  to both systole and diastole)

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Valvular Heart Disease

• Increasing any of the major factors that affect
  flow across the valve increases transvalvular
  flow.
• Conversely, decreasing any of these major factors
  decreases transvalvular flow.

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Goals in Management of Various Valvular Lesions

• Regurgitant Lesions
• Reduce or minimize regurgitant flow across the
  mitral or aortic valve.
• Stenotic Lesions
• Maximize and enhance stenotic flow across the
  mitral or aortic valve

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Goals in Management of Various Valvular Lesions

• The valve area in regurgitant lesions can respond
  to changes in loading conditions (preload,
  afterload)
• The valve area with stenotic lesions is generally
  fixed

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Adult Valvular Heart Disease

• Aortic Stenosis
• Aortic Regurgitaiton
• Mitral Stenosis
• Mitral Regurgitation
• Hypertrophic Obstructive Cardiomyopathy

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Aortic Stenosis
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Aortic Stenosis

• Normal AVA 2.6 3.5 cm2
• Idiopathic Calcific Degeneration
• Congenital
• Bicuspid
• Endocarditis
• Other
• Pagets Disease
• Systemic Lupus Erythematosus

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Aortic Stenosis
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Aortic Stenosis Senile
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Natural History of AS

• May be a long asymptomatic period
• Symptomatic
• Usually have severe AS with AVA of 0.9 cm2 or
  less
• Presenting symptoms
• Angina
• Syncope
• CHF

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Natural History of AS

• Symptomatic patients without surgery show the
  following average life spans
• Angina 5 years
• Syncope 3 years
• CHF 2 years
• AS is considered an independent risk factor for
  perioperative morbidity

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Survival of Patients with Valvular Heart Disease
Treated Medically
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Pathophysiology of Aortic Stenosis
Aortic Stenosis
Obstruction to LV Ejection
Pressure Gradient Created Across the Valve
Chronic LV Pressure Overload
LV Hypertrophy
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Myocardial Function

• Develop left ventricular hypertrophy as an
  adaptation
• LVH reduces wall stress
• T (Pr)/h
• LVH causes increased diastolic stiffness

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Ischemia in AS

• Hypertrophied LV muscle mass
• Increased systolic pressure
• Prolongation of ejection
• Shortened diastolic time
• Relative decrease in myocardial capillary density
• High incidence of concomitant coronary artery
  disease

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Aortic Stenosis
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Measuring the Valve Gradient in AS

• Mean gradient
• Peak-to-peak gradient
• Peak instantaneous gradient

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Degree of Stenosis

• Critical AS
• Peak systolic pressure gradient gt 50 mmHg
• AVA lt 0.9 cm2
• Moderate AS
• 1.0 1.4 cm2
• Mild AS
• 1.5 2.0 cm2

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Aortic Stenosis
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AORTIC STENOSIS HEMODYNAMIC GOALS
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Aortic Regurgitation
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Aortic Regurgitation (Insufficiency)

• Rheumatic heart disease
• Endocarditis
• Aortic root dissection
• Trauma
• Connective tissue disorders
• Dexfenfluramine (appetite suppressant)

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Aortic Regurgitation
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Natural History

• Long asymptomatic period during which the LV
  undergoes progressive eccentric hypertrophy
• CHF
• Angina

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Aortic Regurgitation
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Pathophysiology of Aortic Regurgitation
Backward flow of blood from aorta into LV
(Diastolic)
Increased LV volume and pressure
Rapid fall of aortic pressure during diastole
Increased LA pressure
Increased SV (Frank-Starling Mechanism)
Increased pulmonary venous pressure
Peak systolic pressure increased because of
increased SV ejected into aorta
Pulmonary edema
Increased diastolic wall-tension produces
eccentric hypertrophy
Increased pulse pressure
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Pathophysiology

• LV overloading
• Increased diastolic wall-tension produces
  eccentric hypertrophy (increase both in chamber
  size and wall thickness)
• Reduced diastolic compliance (Acute AI)
• Very high diastolic compliance (Chronic AI)

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Eccentric Hypertrophy
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Pathophysiology

• Baseline myocardial oxygen demand higher than
  normal because of increased LV mass
• Reduced coronary perfusion pressure
• Lower diastolic pressure
• Increased LVEDP

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Pathophysiology

• Myocardial contractility is usually preserved
  until late in course of the disease
• Late in disease there is progression to
  irreversible contractile impairment

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Aortic Regurgitation
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AORTIC REGURGITATION HEMODYNAMIC GOALS
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Mitral Stenosis
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Normal MVA 4 6 cm2
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Mitral Stenosis

• Causes
• Rheumatic
• Women 4x gt Men
• Congenital
• Rheumatoid arthritis
• Systemic Lupus Erythematosus
• Carcinoid Syndrome
• Asymptomatic for approximately 20 years
• Presenting symptoms
• CHF (50)
• Atrial fibrillation

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Mitral Stenosis
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Pathophysiology of Mitral Stenosis
Obstruction to LA emptying
Decreased LV filling
Increased LA pressure
Increased LA size
Atrial fibrillation
Increased pulmonary venous pressure
Pulmonary edema
Increased pulmonary artery pressure
RV overload
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Mitral Stenosis
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Pathophysiology

• Chronic obstruction to left atrial emptying
  during diastole
• LV chronically volume-underloaded
• Chronic volume and pressure over-loading of the
  left atrium and structures behind it

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Pressure Gradient across the Mitral Valve

• Pressure Gradient
• CO Cardiac Output
• DFP Diastolic Filling Period

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Pathophysiology LV

• LV function is usually normal
• Decreased LVEF in about 1/3 of MS patients
• Rheumatic carditis
• Chronic volume underloading
• Concomitant CAD
• Septal hypertrophy in patients with pulmonary
  hypertension (PHT)

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Pathophysiology RV

• RV function is normal in absence of pulmonary
  hypertension (PHT)
• Severe pulmonary hypertension will result in RV
  failure and secondary abnormalities of LV function

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Mitral Stenosis
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MITRAL STENOSIS HEMODYNAMIC GOALS
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Mitral Regurgitation(Insufficiency)
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Mitral Regurgitation (Insufficiency)

• Valve leaflets
• Chordae tendineae
• Papillary muscles

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Mitral Regurgitation (Insufficiency)

• Rheumatic disease
• Endocarditis
• Mitral valve prolapse
• Mitral annular enlargement
• Ischemia
• Myocardial infarction
• Trauma
• Fenfluramine diet suppressants

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Prolapsed Mitral Valve Leaflet
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Mitral Regurgitation
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Pathophysiology of Mitral Regurgitation
Backward flow of blood from LV to LA (Systolic)
Left atrial enlargement
Increased LA volume and pressure
Increased pulmonary venous pressures
Increased LV filling (Increased LVEDV)
Pulmonary edema
Increased SV
Blood ejected into aorta
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Pathophysiology

• LV unloads itself into left atrium
• Chronic left atrial overload
• Chronic overload on left ventricle
• Volume of regurgitant flow determined by
• Ventriculo-atrial gradient
• Diastolic time
• Size of the regurgitant orifice
• Measurements of LV function tend to be slightly
  elevated
• Moderately depressed ejection fraction in a
  patient with MR may be indicative of a severely
  depressed inotropic state

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Natural History

• Chronic MR (variable course)
• Chronic MR may be protected from pulmonary
  congestion by dilated, highly compliant left
  atrium
• Acute MR usually with fulminant pulmonary edema

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Mitral Regurgitation
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MITRAL REGURGITATION HEMODYNAMIC GOALS
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Hypertrophic Cardiomyopathy
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Hypertrophic Cardiomyopathy

• Primary disease of cardiac muscle
• Histologic evidence of myocardial cellular
  disarray
• Characteristics
• LVH (often marked in the septum)
• Reduced diastolic compliance
• Subvalvular pressure gradient
• Ventricular arrhythmias
• May have Systolic Anterior Motion (SAM) of the
  mitral valve
• Blood is ejected into the LV outflow tract at
  high velocity which creates Venturi effect. This
  pulls the anterior leaflet of the mitral valve
  toward the septum during systole. This creates
  dynamic outflow tract obstruction and mitral
  regurgitation.

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Schematic Diagram of a Patient Undergoing
Surgical Septal Myectomy
Nishimura, R. A. et. al. N Engl J Med
20043501320-1327
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Hypertrophic Cardiomyopathy

• Management
• Avoid anything that causes reduction in left
  ventricular volume
• Decreased preload
• Increased contractility
• Decreased afterload
• Reduce determinants of myocardial oxygen
  consumption as thickened myocardium is
  predisposed to ischemia.

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HYPERTROPHIC CARDIOMYOPATHY HEMODYNAMIC GOALS
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The End