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Valvular Heart Disease

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Presentation on theme: "Valvular Heart Disease"— Presentation transcript:

1 Valvular Heart Disease
Jay L. Rubenstone, D.O., F.A.C.C

2 Normal Structure Mitral Valve
Cross sectional Area 4-6cm² Anterior and Posterior Leaflets Chordae Tendineae  Papillary Muscles

3 Mitral Stenosis Etiology & Pathology
Rheumatic Fever- 99% Other Congenital Carcinoid Lupus Amyloid Infective Endocarditis Mucopolysaccharide Disease

4 Stenotic Pathology Etiology & Pathology
Commissural 30% Cuspal 15% Chordal 10% Mixed Remaining Valve becomes funnel shaped or “fish mouthed” Thickened immobile leaflets or chordal structures

5 Stenotic Pathology Debate: Smoldering rheumatic process or
Constant blood flow trauma leading to valve fibrosis and thickening

6 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)

7 Pathophysiology Pulmonary HTN
Passive Backward Transmission Of Incr. LA pressure Pulmonary Arteriolar Constriction Organic Obliterative Changes in Pulmonary Vascular Bed RV Failure

8 History Exertional Dyspnea Cough/Wheezing Orthopnea/PND/CHF
Hemoptysis-Rupture of Pulmonary Vein-Bronchial Vein Shunts

9 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

10 Physical Exam Auscultation Decreased B/P if C.O. decreased
O.S. 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

11 Physical Exam Mitral Facies-pink, purple facial patches due to decrease CO and systemic vasoconstriction Hepatomegally Edema Ascites Hydrothorax With Right Heart Failure

12 Diagnosis ECG Left Atrial Abnormality RVH- right axis deviation
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

13 Diagnosis Chest X-ray Echo- Cornerstone of Diagnosis
Dilated LA, RA, RV Elevated Left Main stem Bronchus Interstitial Edema Echo- Cornerstone of Diagnosis Thickened Calcified Leaflets Doming of Leaflets on Opening Bernoulli equation

14 Diagnosis Cardiac Catherization Gorlin Equation


16 Natural History Asymptomatic for 15-20yrs following Rheumatic Fever
Additional 5-10 yrs for progression from mild to severe stenosis Stenosis progression approximately .09 cm²/yr

17 Natural History Presurgical Survival Rates NYHA Class II 80%-10yrs
Class III 38%-10yrs, 62% 5yrs Class IV 15%-5yrs

18 Management-Medical Endocarditis Prophylaxis Activity Limitation
Diuretics- Decrease Na Intake Heart Rate Control for A-fib or Sinus Rhythm Anticoagulation

19 Percutaneous Balloon Angioplasty
Moderate-Severe MS Mild MS- if Pulmonary Artery Pressures or Wedge Pressure Elevate with Exercise

20 Valve Replacement Indications Mortality
Combined MS/MR <1.5 cm²-NYHA III or IV <1 cm² Class II if Pulmonary Artery Pressure >70mmHg Mortality 3-8% Valve Type-Prosthetic or Bioprosthetic

21 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

22 Pathophysiology Decreased Impedance to Ventricular Emptying
Determinants of Regurgitant Flow 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

23 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

24 Pathophysiology LV Decompensation Increase End Systolic Volume
Increased End Diastolic Volume Leads to Annulus Dilatation (MR begets MR) Decreased Ejection Fraction and Stroke Volume

25 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.

26 History Shortness of Breath Exertional Dyspnea
Congestive Heart Failure Right Heart Failure Significant symptoms in chronic MR usually do not develop until LV decompensation occurs.

27 History Medical Treatment Survival 80% 5yr 60% 10yr
30-45% 5yr if MR severe

28 Diagnosis Physical Exam ECG Chest X-ray Holosystolic Murmur
Increase Carotid Impulse ECG LA abnormality LVH RVH Chest X-ray Increase LA, LV, RV, Interstitial Edema

29 Diagnosis Echo Transesophageal superior to transthoracic
Evaluation of Chamber Sizes, Regurgitant Jet, Leaflets

30 Management of Acute MR Medical
After load Reduction (Nitropresside & Intra aortic balloon pump) Decrease impedance to LV ejection Decrease regurgitant volume into left atrium Inotropic Support (Dobutamine)-if LV function reduced

31 Management of Acute MR Surgical Intervention
Progressive LV Failure or Hemodynamic Deterioration CHF Hypertension Valve Disruption

32 Management of Chronic MR
Medical Digoxin Diuretics* After load Reduction Anticoagulation in A-fib Endocarditis Prophylaxis

33 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

34 Mitral Valve Prolapse Systolic Click-Murmur Syndrome Barlow’s Syndrome
Billowing Mitral Valve Syndrome Floppy Valve Syndrome Myxomatous Valve Syndrome Parachute Valve

35 Mitral Valve Prolapse Over diagnosed 2.4% of population
Females>Males 2:1 Severe MR- Elderly Male>Young Female

36 MVP Etiology Primary Valvular most frequent Connective Tissue Diseases
Hyperthyroidism Myotonic Dystrophy Periarteritis Nodosa Von Willebrands

37 MVP Pathology Myxomatous Proliferation and Degeneration of Valve Leaflets Increased Quantity of Acid Mucopolysaccharide in Middle Layer of Valve Tissue

38 MVP History Most are asymptomatic throughout life
Chest pain, fatigue, anxiety Orthostasis-questionable autonomic dysfunction Arrhythmia-SVT, PACs, PVCs Symptoms of MR if present

39 Physical Examination Body type Auscultation
Asthenic, low weight body habitus, straight back syndrome Auscultation Systolic click- multiple, non-ejection (after carotid upstroke) due to tensing of elongated chordae and prolapsing valve

40 Physical Examination Auscultation
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

41 Diagnosis ECG and Chest X-ray Echo Normally unremarkable
Billowing of one or both leaflets into the left atrium during systole at least 2mm Parasternal long axis view for diagnosis Associated MR Leaflet thickness

42 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)

43 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*

44 Aortic Valve Normal 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

45 Aortic Stenosis Etiology and Pathology
Valvular Supravalvular Subvalvular Hyperthrophic Cardiomyopathy

46 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

47 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

48 Is this atherosclerotic disease?
Degenerative A.S. accelerated in diabetes and hyperlipidemia. Associated with tobacco use and HTN. Potentially treated with HMGcoA agents?


50 Hemodynamics Critical (Surgical) AS Moderate AS Mild AS
Peak systolic pressure gradient > 50mmHg in the presence of normal cardiac output Valve area < cm² Moderate AS 1-1.5cm² Mild AS 1.5-2cm² Aortic Sclerosis

51 History Long latent period of increasing obstruction
Symptoms usually begin in 5th or 6th decade Angina in 2/3 of patients Hypertrophied myocardium Increased ventricular systolic pressure All of which increase myocardial oxygen consumption Oxygen supply-demand imbalance leads to subendocardial ischemia

52 History Syncope Dyspnea (CHF) Reduced cerebral perfusion
Vasodilatation 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

53 Diagnosis Physical Examination Systolic Murmur Pulses Parvus
Diamond-Shaped, harsh, left sternal boarder to right intercostal spaces, neck and apex Late peak, obliteration of S2, consistent with bedside Dx of Critical AS Pulses Parvus Delayed and Prolonged Carotid Impulse

54 Diagnosis ECG Chest X-ray Echo Classic LVH Concentric LVH
Calcification of Aortic Valve Echo Bernoulli (continuity) equation-calculation of LV-Aortic pressure gradient and valve area

55 Diagnosis Cardiac Catherization Gorlin Equation

56 Natural History Asymptomatic latent period
With moderate-severe AS valve area can decrease on average 0.12cm² per year *Angina, syncope or CHF Average 1-3 year survival 50% Sudden cardiac death rare

57 Medical Management Endocarditis Prophylaxis Limit Physical Activity
Watch Beta Blockers and Diuretics *Treatment of Critical AS in viable candidates is surgery

58 Surgery (Valve Replacement)
Indications Symptomatic Patients -valve area cm² or less Asymptomatic Patients-progressive LV dysfunction (EF <35%) or hypotensive response to mild exercise Delaying surgery in asymptomatic patients with good exercise tolerance is controversial

59 Surgery (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%

60 Aortic Regurgitation Etiology and Pathology
Valvular Rheumatic-Fibrotic Retraction of Leaflets 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

61 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

62 History Acute AR Chronic 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


64 Physical Examination Diastolic Murmur Left sternal boarder
Decrescendo, high pitched Best heard Sitting Up, End Expiration Longer murmur equals worse AR

65 Physical Examination de Mussett’s Sign (head bobbing)
Corrigan’s Pulse “water hammer” Abrupt Distention with Quick Collapse Bisferiens-pulse 2 peaks Traube’s Sign Pistol shot sounds over femoral pulse Duroziez’s Sign Murmur over femoral pulse with compression

66 Physical Examination Quinckes Sign Muller’s Sign Hill’s Sign
Capillary pulsations Muller’s Sign Systolic pulsations of uvula Hill’s Sign Popliteal pulse exceed brachial pulse by > 60mmHg

67 Physical Examination Korotkoff Sounds Can persist to 0mmHg
Wide Pulse pressure

68 Diagnosis ECG Chest X-ray Echo Cardiac Catheterization LVH
Cardiomegaly predominantly inferior and leftward Echo Can aid in detecting etiology, quantifying degree of regurgitation, and assessing LV size and function Cardiac Catheterization

69 Natural History Acute AR Chronic 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

70 Medical Treatment Acute AR Chronic AR As above
Asymptomatic Mild-Moderate Follow by Echo Yearly Endocarditis Prophylaxis for all AR May not require medical treatment

71 Medical Treatment Symptomatic Moderate-Severe AR
Limit exertional activity Aggressively treat B/P Diuretics Salt Restriction Digoxin Vasodilators (Nifedipine?)

72 Surgical Treatment Indications
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

73 Surgical Treatment Mortality 3-8% perioperative
5-10% late mortality with significant preop LV dysfunction

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