The Heart Valves

1. The Heart Valves Mohammad Saifur Rohman MD. PhD. Consultant of Interventional cardiology Department of Cardiology and Vascular Medicine Faculty of Medicine Brawijaya University

3. more on valves

4. Heart sounds • Called S1 and S2 • S1 is the closing of AV (Mitral and Tricuspid) valves at the start of ventricular systole • S2 is the closing of the semilunar (Aortic and Pulmonic) valves at the end of ventricular systole • Separation easy to hear on inspiration therefore S2 referred to as A2 and P2 • Murmurs: the sound of flow • Can be normal • Can be abnormal

5. Places to auscultate

6. Function of semilunar valves (Aortic and pulmonic valves)

7. Function of AV valves

8. Normal Valve Function • Maintain forward flow and prevent reversal of flow. • Valves open and close in response to pressure differences (gradients) between cardiac chambers.

9. Abnormal Valve Function • Valve Stenosis • Obstruction to valve flow during that phase of the cardiac cycle when the valve is normally open. • Hemodynamic hallmark -“pressure gradient” • Valve Regurgitation, Insufficiency, Incompetence • Inadequate valve closure  back leakage • A single valve can be both stenotic and regurgitant; but both lesions cannot be severe • Combinations of valve lesions can coexist • Single disease process • Different disease processes • One valve lesion may cause another • Certain combinations are particularly burdensome (AS & MR)

10. Aortic Stenosis Degenerative calcific (senile) Congenital – Uni or bicuspid Rheumatic Prosthetic Acute Aortic Insufficiency Infective endocarditis Acute Aortic Dissection Marfan’s Syndrome Chest trauma Chronic Aortic Insufficiency Aortic leaflet disease Infective endocarditis Rheumatic Bicuspid Aortic valve Prolapse & congenital VSD Prosthetic Aortic root disease Aortic aneurysm/dissection Marfan’s syndrome Connective tissue disorders Syphilis HTN Annulo-aortic ectasia Aortic Valve Disease: Etiology

11. Aortic Stenosis Overview: • Normal Aortic Valve Area: 3-4 cm2 • Symptoms: Occur when valve area is 1/4th of normal area. • Types: • Supravalvular • Subvalvular • Valvular

12. Etiology of Aortic Stenosis • Congenital • Rheumatic • Degenerative/Calcification Patients under 70: >50% have a congenital cause Patients over 70: 50% due to degenerative

16. Aortic Stenosis - Pathophysiology • Normal AVA 2.5-3.0cm2 • Severe AS <1.0cm2 • Critical AS <0.7cm2; <0.5cm2/m2 • Hemodynamic Hallmark • Systolic pressure gradient • AV grad ~ AV flow//AVA • AV flow = CO/SEP (systolic ejection period) • 50-100mmHg gradients are common in severe AS

17. Pathophysiology of Aortic Stenosis- LVPO • Chronic LV Pressure Overload Concentric LVH • “Stiff” noncompliant LV • Increased LVEDP • Increased LV mass Increased MVO2 • Well tolerated for decades • LV fails CHF • Atrial fibrillation • Poorly tolerated • Loss of atrial “kick” • Rapid HR • Acute pulmonary edema and hypotension.

18. Pathophysiology of Aortic Stenosis • A pressure gradient develops between the left ventricle and the aorta. (increased afterload) • LV function initially maintained by compensatory pressure hypertrophy • When compensatory mechanisms exhausted, LV function declines.

19. Asymptomatic for many years Symptoms develop when valve is critically narrowed and LV function deteriorates Bicuspid AV 5th - 6th decade Senile AS 7th-8th decades Classic Symptom Triad Angina pectoris – 5 years CHF 1-2 years Syncope 2-3 years Sudden Death Natural History Studies- Pts grad 25mmHg –20% chance of intervention in 15 years Pts with asymptomatic severe AS require close f/u Gradient progression 6-10mmHg/yr Risk Factors Age > 70 CAD, hyperlipidemia Chronic renal failure Aortic Stenosis: Natural History & Clinical Symptoms

20. Natural History • Mild AS to Severe AS: • 8% in 10 years • 22% in 22 years • 38% in 25 years • The onset of symptoms is a poor prognostic indicator.

22. Aortic Stenosis: Physical Findings

23. Evaluation of AS • Echocardiography is the most valuable test for diagnosis, quantification and follow-up of patients with AS. • Two measurements obtained are: • Left ventricular size and function: LVH, Dilation, and EF • Doppler derived gradient and valve area (AVA)

24. Echo Surveillance • Mild: Every 5 years • Moderate: Every 2 years • Severe: Every 6 months to 1 year

25. Management of AS • General- IE prophylaxis in dental procedures with a prosthetic AV or history of endocarditis. • Medical - limited role since AS is a mechanical problem. Vasodilators are relatively contraindicated in severe AS • Aortic Balloon Valvotomy- shows little benefit. • Surgical Replacement: Definitive treatment

26. Balloon Aortic Valvuloplasty • Indications for BAV in critical Aortic Stenosis • Younger patients with congenital AS and predominant commissural fusion • Bridge to eventual AVR • Moderate to severe heart failure/cardiogenic shock • Extremely high risk for AVR • Urgent/emergent need for noncardiac surgery • Patient with limited lifespan – cardiac or noncardiac • Patient refuses surgery

27. Simplified Indications for Surgery in Aortic Stenosis • Any SYMPTOMATIC patient with severe AS (includes symptoms with exercise) • Any patient with decreasing EF • Any patient undergoing CABG with moderate or severe AS

28. Aortic Regurgitation Overview • Definition: Leakage of blood into LV during diastole due to ineffective coaptation of the aortic cusps

31. Etiology of Acute AR • Endocarditis • Aortic Dissection • Physical Findings: • Wide pulse pressure • Diastolic murmur • Florid pulmonary edema

32. Etiology of Chronic AR • Bicuspid aortic valve • Rheumatic • Infective endocarditis

33. Acute vs Chronic AR Pathophysiology and Clinical Presentation • Acute Aortic Regurgitation • Sudden AoV incompetence • Noncompliant LV • Acute Pulmonary Edema • Emergency AVR • Chronic Aortic Regurgitation • Long asymptomatic phase • Progressive LV dilatation • DOE, orthopnea, PND • Frequent PVC’s

34. Aortic Regurgitation- Pathophysiology • 10 abnormality – LVVO • Severity of LVVO • Size of regurgitant orifice • Diastolic pressure gradient between Ao & LV • HR or duration of diastole • Compensatory Mechanisms • LV dilatation & eccentric LVH • Increased LV diastolic compliance • Peripheral vasodilation

35. LV Volume vs Pressure Overload

36. Natural History of AR • Asymptomatic until 4th or 5th decade • Rate of Progression: 4-6% per year • Progressive Symptoms include: - Dyspnea: exertional, orthopnea, and paroxsymal nocturnal dyspnea • Nocturnal angina: due to slowing of heart rate and reduction of diastolic blood pressure • Palpitations: due to increased force of contraction

37. Chronic Aortic Regurgitation: Physical Findings • Widened Pulse Pressure > 70mmHg (170/60) • Low diastolic pressure <60mmHg • Hyperdynamic LV – • DeMusset’s signs • Corrigan’s pulse • Quincke’s pulsations, • Durozier’s murmur • Auscultation: • Diminished A2 • Descrescendo diastolic blowing murmur @ LSB • Austin-Flint murmur – diastolic flow rumble @ apex • Due to interference with trans-mitral filling by impignement from aortic regurgitant jet. • DDx - mitral stenosis(increases intensity with amyl nitrite)

38. The Evaluation of AR • CXR: enlarged cardiac silhouette and aortic root enlargement • ECHO: Evaluation of the AV and aortic root with measurements of LV dimensions and function (cornerstone for decision making and follow up evaluation) • Aortography: Used to confirm the severity of disease

39. Management of AR • General: IE prophylaxis in dental procedures with a prosthetic AV or history of endocarditis. • Medical: Vasodilators (ACEI’s), Nifedipine improve stroke volume and reduce regurgitation only if pt symptomatic or HTN. • Serial Echocardiograms: to monitor progression. • Surgical Treatment: Definitive Tx

40. Treatment of Acute AR • True Surgical Emergency: • Positive inotrope: (eg, dopamine, dobutamine) • Vasodilators: (eg, nitroprusside) • Avoid beta-blockers • Do not even consider a balloon pump

42. Simplified Indications for Surgical Treatment of AR • ANY Symptoms at rest or exercise • Asymptomatic treatment if: • EF drops below 50% or LV becomes dilated

43. Mitral Valve Competence: • Integrated function of several anatomic elements • Posterior LA wall • Anterior & Posterior valve leaflets • Chordae tendineae • Papillary muscles • Left ventricular wall where the papillary muscles attach

44. Mitral Stenosis Rheumatic - 99.9%!!! Congenital Prosthetic valve stenosis Mitral Annular Calcification Left Atrial Myxoma Acute Mitral Regurgitation Infective endocarditis Ischemic Heart disease Papillary ms rupture Mitral valve prolapse Chordal rupture Chest trauma Chronic Mitral Regurgitation Ischemic Heart disease Papillary ms dysfunction Inferior & posterior MI Mitral Valve prolapse Infective endocarditis Rheumatic Prosthetic Mitral annular calcification Cardiomyopathy LV dilatation IHSS Mitral Valve Disease: Etiology

45. Mitral Stenosis Overview • Definition: Obstruction of LV inflow that prevents proper filling during diastole • Normal MV Area: 4-6 cm2 • Transmitral gradients and symptoms begin at areas less than 2 cm2 • Rheumatic carditis is the predominant cause • Prevalence and incidence: decreasing due to a reduction of rheumatic heart disease.

48. Etiology of Mitral Stenosis • Rheumatic heart disease: 77-99% of all cases • Infective endocarditis: 3.3% • Mitral annular calcification: 2.7%

49. MS Pathophysiology • Progressive Dyspnea (70%): LA dilation  pulmonary congestion (reduced emptying) • worse with exercise, fever, tachycardia, and pregnancy • Increased Transmitral Pressures: Leads to left atrial enlargement and atrial fibrillation. • Right heart failure symptoms: due to Pulmonary venous HTN • Hemoptysis: due to rupture of bronchial vessels due to elevated pulmonary pressure

50. Mitral Stenosis -Pathophysiology • Restriction of blood flow from LALV during diastole. • Normal MVA 4-6cm2. • Mild MS 2-4cm2. • Severe MS < 1.0cm2. • MV Pressure gradient – • MV grad ~ MV flow//MVA. • Flow = CO/DFP (diastolic filling period). • As HR increases, diastole shortens disproportionately and MV gradient increases.