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

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Presentation on theme: "1 Valvular Heart Disease Jay L. Rubenstone, D.O., F.A.C.C."— Presentation transcript:

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

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

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

4 4 Stenotic Pathology Etiology & Pathology Commissural30% Cuspal15% Chordal10% MixedRemaining – Valve becomes funnel shaped or fish mouthed – Thickened immobile leaflets or chordal structures

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

6 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 7 Pathophysiology Pulmonary HTN – Passive Backward Transmission Of Incr. LA pressure Pulmonary Arteriolar Constriction Organic Obliterative Changes in Pulmonary Vascular Bed RV Failure

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

9 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 10 Physical Exam Auscultation O.S. Diastolic Rumble Assoc Murmur of MR Loud S 1 -thickened leaflets Increased P 2 -pulmonary hypertension Decreased B/P if C.O. decreased Prominent a wave if sinus rhythm present

11 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 12 Diagnosis ECG – Left Atrial Abnormality P wave becomes bifid and greater than 0.12 sec in duration in V 1 and Lead II – RVH- right axis deviation – R wave > S wave in V 1

13 13 Diagnosis Chest X-ray – 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 14 Diagnosis – Cardiac Catherization Gorlin Equation

15 15

16 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 17 Natural History Presurgical Survival Rates – NYHA Class II 80%-10yrs – Class III 38%-10yrs, 62% 5yrs – Class IV 15%-5yrs

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

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

20 20 Valve Replacement Indications – 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 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 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 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 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 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 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 27 History Medical Treatment Survival – 80% 5yr – 60% 10yr – 30-45% 5yr if MR severe

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

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

30 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 31 Management of Acute MR Surgical Intervention – Progressive LV Failure or Hemodynamic Deterioration – CHF – Hypertension – Valve Disruption

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

33 33 Management of Chronic MR Surgical – Indications Asymptomatic Class I – EF 45mm Severe MR Class II, III, or IV – generally considered for surgery unless EF <30% – Valve Repair vs. Replacement

34 34 Mitral Valve Prolapse Systolic Click-Murmur Syndrome Barlows Syndrome Billowing Mitral Valve Syndrome Floppy Valve Syndrome Myxomatous Valve Syndrome Parachute Valve

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

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

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

38 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 39 Physical Examination Body type – 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 40 Physical Examination Auscultation – Murmur- mid to late crescendo progressing to holosystolic if MR becomes severe – Click and murmur move closer to S 1 during strain phase of valsalva, sudden standing, and Amyl Nitrate

41 41 Diagnosis ECG and Chest X-ray – Normally unremarkable Echo – 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 42 Natural History Progressive MR in 15% over 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 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 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 45 Aortic Stenosis Etiology and Pathology Valvular Supravalvular Subvalvular Hyperthrophic Cardiomyopathy

46 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 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 48 Is this atherosclerotic disease? Degenerative A.S. accelerated in diabetes and hyperlipidemia. Associated with tobacco use and HTN. Potentially treated with HMGcoA agents?

49 49

50 50 Hemodynamics Critical (Surgical) 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 51 History Long latent period of increasing obstruction Symptoms usually begin in 5 th or 6 th 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 52 History Syncope – 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 53 Diagnosis Physical Examination – Systolic Murmur Diamond-Shaped, harsh, left sternal boarder to right intercostal spaces, neck and apex Late peak, obliteration of S 2, consistent with bedside Dx of Critical AS – Pulses Parvus Delayed and Prolonged Carotid Impulse

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

55 55 Diagnosis Cardiac Catherization – Gorlin Equation

56 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 57 Medical Management Endocarditis Prophylaxis Limit Physical Activity Watch Beta Blockers and Diuretics *Treatment of Critical AS in viable candidates is surgery

58 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 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 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 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 62 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 4 th or 5 th Decade

63 63

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

65 65 Physical Examination de Mussetts Sign (head bobbing) Corrigans Pulse water hammer – Abrupt Distention with Quick Collapse Bisferiens-pulse – 2 peaks Traubes Sign – Pistol shot sounds over femoral pulse Duroziezs Sign – Murmur over femoral pulse with compression

66 66 Physical Examination Quinckes Sign – Capillary pulsations Mullers Sign – Systolic pulsations of uvula Hills Sign – Popliteal pulse exceed brachial pulse by > 60mmHg

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

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

69 69 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

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

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

72 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 73 Surgical Treatment Mortality – 3-8% perioperative – 5-10% late mortality with significant preop LV dysfunction

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