Valvular Heart Disease and auscultation

1. Valvular Heart Diseaseand auscultation Jay L. Rubenstone, D.O., F.A.C.C Fall 2012

2. Normal StructureMitral Valve • Cross sectional Area 4-6cm2 • Anterior and Posterior Leaflets • Chordae Tendineae  Papillary Muscles

3. Mitral StenosisEtiology & Pathology • Rheumatic Fever- 99% • Other • Congenital • Carcinoid • Lupus • Amyloid • Infective Endocarditis • Mucopolysaccharide Disease

4. 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)

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

6. History • Exertional Dyspnea • Cough/Wheezing • Orthopnea/PND/CHF • Hemoptysis-Rupture of Pulm Vein-Brochial Vein Shunts

7. 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

8. Diagnosis • Cardiac Catherization • Gorlin Equation

9. 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

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

11. Management-Medical • Endocarditis Prophylaxis • Activity Limitation • Diruetics- Decrease Na Intake • Heart Rate Control for A-fib or Sinus Rhythm • Anticoagulation

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

13. 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

14. 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

15. 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

16. 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

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

18. 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.

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

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

21. Management of Chronic MR • Medical • Digoxin • Diruetics* • Afterload Reduction • Anticoagulation in A-fib • Endocarditis Prophylaxis

22. 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

23. Mitral Valve Prolapse • Systolic Click-Murmur Syndrome • Barlow’s Syndrome • Billowing Mitral Valve Syndrome • Floppy Valve Syndrome • Myxomatous Valve Syndrome • Parachute Valve

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

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

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

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

28. 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

29. 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)

30. 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*

31. 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

32. Aortic Stenosis Etiology and Pathology • Valvular • Supravalvular • Subvalvular • Hyperthrophic Cardiomyopathy

33. 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

34. 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

35. 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

36. 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

37. 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

38. 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

39. 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

40. 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%

41. 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

42. 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

43. 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

44. 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

45. 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

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

47. 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

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

49. Cardiac Auscultation Jay L. Rubenstone, D.O., F.A.C.C. October 2012

50. Techniques of Examination • Order of Exam • Aortic Area • Pulmonic Area • Tricuspid Area • Mitral Area