JAY L. RUBENSTONE, D.O., F.A.C.C VALVULAR HEART DISEASE Fall 2012

JAY L. RUBENSTONE, D.O., F.A.C.C

VALVULAR HEART DISEASE

Fall 2012

NORMAL STRUCTUREMITRAL VALVE

• Cross sectional Area 4-6cm2• Anterior and Posterior Leaflets• Chordae Tendineae Papillary Muscles

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MITRAL STENOSISETIOLOGY & PATHOLOGY

• Rheumatic Fever- 99% • Other• Congenital • Carcinoid• Lupus• Amyloid• Infective Endocarditis• Mucopolysaccharide Disease

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PATHOPHYSIOLOGY

• Mild MS- orifice <2 cm2• Critical MS- <1 cm2• 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

• 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• Class III 38%-10yrs, 62% 5yrs• Class IV 15%-5yrs

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MANAGEMENT-MEDICAL

• 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• 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• 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• 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• 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 impairmentAs ejection fraction decreases operative risk increases.

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HISTORY

• 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• 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

• 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

• 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

• 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 VALVENORMAL 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

• 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• 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 REGURGITATIONETIOLOGY 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.• 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• 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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