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  2. MITRAL VALVE • Mitral valve connects the left atrium and left ventricle. • The normal function of the mitral valve depends on its 6 components, MITRAL VALVE APPARATUS which are (1) the left atrial wall, (2) the annulus, (3) the leaflets, (4) the chordae tendineae, (5) the papillary muscles, and (6) the left ventricular wall.
  3. Mitral Valve apparatus : Left Atrial wall Annulus Leaflets Chordae Tendineae Papillary Muscles Left ventricular wall
  4. Mitral Annulus: Anatomical structure that separates the LV & LA Caption
  5. 2. MITRAL LEAFLETS • Mitral Leaflets : Thin and pliable leaflets that contain scallops which represent segmental markers. • 2 Leaflets with 3 Scallops ◦ Anterior Leaflet (AML): larger & thicker Dome-shaped Scallops: A1 (lateral), A2 (central), A3 (medial) ◦ Posterior Leaflet (PML): thinner & more flexible Crescent shaped Scallops: P1 (lateral), P2 (central), P3 (medial) • Leaflets thin & pliable • Scallops serve as segmental markers of Leaflets
  6. 3. COMMISSURES Commissures: 2 specific sites where the leaflets insert and join into mitral annulus • Anterolateral Commissure • Posteromedial Commissure
  7. 4. CHORDAE TENDINAE Chordae Tendinae: Fibrous strings that attach specific portions of mitral leaflets to papillary muscle tips • Normal average length is around 20mm • Normal average thickness is 1- 2mm • Key items to look for: thickening, fusion, calcification, elongation, rupture
  8. 5. PAPILLARY MUSCLES Papillary Muscles: Large trabeculae muscles that branch from 1/3rd of LV, connecting chordae to mitral leaflets 2 papillary muscles: • Anterolateral (APM): ◦ Dual blood supply (LAD & Cx) • Posteromedial (PPM): ◦ Single blood supply (Either RCA or LCX) ◦ Prone to injury from MI due to single blood supply
  10. • In normal adults, the area of the mitral valve orifice is 4-6 cm2. • In mitral stenosis, the area of valve orifice decreases. • Minimal MS - >2.5 cm2 • Mild MS - 1.6- 2.5 cm2 • Moderate MS – 1- 1.5 cm2 • Severe MS(tight/critical) - <1 cm2
  11. • In normal adults, the area of the mitral valve orifice is 4–6 cm2. • In the presence of significant obstruction, i.e., when the orifice area is reduced to <~2 cm2, blood can flow from the LA to the left ventricle (LV) only if propelled by an abnormally elevated left atrioventricular pressure gradient, the hemodynamic hallmark of MS. • When the mitral valve opening is reduced to <1.5 cm2, referred to as “severe” MS, an LA pressure of ~25 mmHg is required to maintain a normal cardiac output (CO).
  12. Major Causes of Mitral Stenosis •Rheumatic fever •Congenital (parachute valve, cor triatriatum) •Severe mitral annular calcification with leaflet involvement •SLE, RA •Myxoma • IE with large vegetations
  13. PATHOPHYSIOLOGY • Rheumatic fever is the most common cause of MS. • In rheumatic MS, chronic inflammation leads to diffuse thickening of the valve leaflets with formation of fibrous tissue and/or calcific deposits. • The mitral commissures fuse, the chordae tendineae fuse and shorten, the valvular cusps become rigid. • These changes, in turn, lead to narrowing at the apex of the valve. • Calcification of the stenotic mitral valve immobilizes the leaflets and narrows the orifice further.
  14. Mitral Stenosis: Natural History • Progressive, lifelong disease, • Usually slow & stable in the early years. • Progressive acceleration in the later years • 20-40 year latency from rheumatic fever to symptom onset. • Additional 10 years before disabling symptoms
  15. CLINICAL PRESENTATION • Symptoms d/t pulmonary hypertension- 1. Dyspnoea, orthopnea, PND 2. Recurrent pulmonary infections, i.e., bronchitis, bronchopneumonia and lobar pneumonia especially during the winter months. 3. Hemoptysis results from rupture of pulmonary- bronchial venous connections. 4. Cough 5. Fatigue 6. Lower limb swelling, pain rt hypochondrium.
  16. • Palpitations can develop in case if A.fib develops •Recurrent pulmonary emboli sometimes with infarction, are an important cause of morbidity and mortality late in the course of MS. •Systemic embolization may be the presenting feature in otherwise asymptomatic patients with only mild MS.
  17. PHYSICAL EXAMINATION MITRAL FACIES Plethoric cheeks with bluish patches due to Cutaneous vasodilatation in severe MS causing Low CO
  18. • Pulse - irregularly irregular if AF is present. • JVP • -If RV failure develops, jugular veins will be distended • - If pulmonary hypertension develops, “a” wave will be prominent. • Parasternal heave can be there d/t RVH. • Tapping type of apex beat (palpable 1st heart sound) is there, normal in position, can go outwards if RVH present. • A diastolic thrill may rarely be present at the cardiac apex, with the patient in the left lateral recumbent position.
  19. • On auscultation -S1 will be loud if mitral valve is pliable. It will be muffled in calcified MS. Due to wider excursion of the leaflets while closure, since elevated LAP has kept the leaflets relatively wide apart In addition, stiff noncompliant leaflets and chordae tendineae appear to resonate with increased amplitude
  20. • LOUD P2 AND S2 CLOSELY SPILT • OPENING SNAP followed by A2 • The pulmonic component of the second heart sound (P2) is often accentuated with elevated PA pressure.(PHTN) • -Opening snap i.e. mitral valve opens suddenly with the force of increased left atrial pressure. • -Low pitched rough rumbling mid diastolic murmur with pre systolic accentuation and opening snap with bell of stethoscope at the end of expiration best heard at the apex in left recumbent position which increases on isometric exercises
  21. • If the patient is in sinus rhythm, murmur becomes louder at the end of diastole d/t atrial contraction i.e. PRESYSTOLIC ACCENTUATION. • Presystolic accentuation will be absent in case of AF, Left atrial failure and big left atrial thrombus.
  22. SEVERITY OF MS? • The time interval between A2 and OS varies inversely with the severity of the MS. Normally, it is 0.05- 0.12 s. The smaller the gap, the more severe is the MS. • Longer the duration of mid diastolic murmur, the more severe is the MS. • As the valve cusps become immobile, -Loud S1 softens -opening snap disappears • When pulmonary hypertension appears, -P2 gets loud
  23. • With severe pulmonary hypertension, a pansystolic murmur produced by functional TR may be audible along the left sternal border. This murmur is usually louder during inspiration and diminishes during forced expiration (Carvallo’s sign). • The Graham Steell murmur of PR, a high-pitched, diastolic, decrescendo blowing murmur along the left sternal border, results from dilation of the pulmonary valve ring and occurs in patients with mitral valve disease and severe pulmonary hypertension
  24. INVESTIGATIONS • Chest X-ray • Electrocardiogram • Echocardiogram • Cardiac MRI • Cardiac cathetrisation
  25. • MITRALISATION of heart straightening of the left border of heart & is due to(from above downwards) 1. Small aortic knuckle due to low CO 2. Convexity due to dilated pulmonary artery due to pulmonary hypertension 3. Left atrial appendages prominence 4. Left border of LV • Double contour of right border of heart (shadow within shadow)
  26. • Dilated pulmonary aretries at hilum with peripheral pruning (pulmonary hypertension) • Bat’s wing appearance from parahilar region to periphery and Kerly’s B lines indicating pulmonary edema • Elevation of left upper lobe bronchus which becomes horizontal due to LA enlargement • Calcified mitral valve can be seen on lateral view. • Chest Xray (RAO view) with barium filled esophagus shows sickling of esophagus by enlarged LA
  27. ECG IN MITRAL STENOSIS • LA enlargement – Wide i.e. >0.12s (3 small sq) and notched P wave with the interpeak duration of >0.04s (1 small sq) i.e. P mitrale in lead v1 & II.
  28. • P wave may become tall and peaked (>2.5 small sq) in lead II & V1 when severe pulmonary hypertension or TS complicates MS and right atrial (RA) enlargement occurs i.e. P pulmonale • Atrial fibrillation may be present.
  29. • RVH- RAD and tall R wave in lead V1(>7mm)
  30. ECHO IN MITRAL STENOSIS • To see chamber enlargement , left atrial thrombus, valve pathology, valve movement, mitral orifice, diameter. • In MS there are thickened immobile cusps, reduced valve area, LA enlargement and reduced rate of diastolic filling of LV. • TEE provides superior images and should be used when TTE is inadequate for guiding management decisions. TEE is especially indicated to exclude the presence of LA thrombus prior to percutaneous mitral balloon valvotomy (PMBV).
  31. CARDIAC CATHETRIZATION IN MS • Left and right heart catheterisation can be useful when there is a discrepancy between the clinical and noninvasive findings, including those from TEE and exercise echocardiographic testing when appropriate • CT Coronary angiography is advisable preoperatively to identify patients with critical coronary obstructions that should be bypassed at the time of operation. • Catheterisation can also be helpful in assessing a/w lesions, such as AR and AS and in patients with recurring or worsening symptoms later after mitral valve intervention
  32. COMPLICATIONS OF MS • Left atrial enlargement, acute left atrial failure and acute pulmonary edema • Pulmonary hypertension • Right ventricular failure • A fib, A flutter • Embolic manifestations • Infective endocarditis • Recurrent broncho-pulmonary infections • Compression of RLN (Ortner’s syndrome) • Dysphagia
  33. TREATMENT OF MS • Penicillin prophylaxis of group A β-hemolytic streptococcal infections for secondary prevention of rheumatic fever is important for at-risk patients with rheumatic MS. • Recommendations for infective endocarditis prophylaxis are similar to those for other valve lesions and are restricted to patients at high risk for complications from infection, including patients with a history of endocarditis. • In symptomatic patients, some improvement usually occurs with restriction of sodium intake and small doses of oral diuretics. • Beta blockers, nondihydropyridine calcium channel blockers (e.g., verapamil or diltiazem), and digitalis glycosides are useful in slowing the ventricular rate of patients with AF. •
  34. •Warfarin therapy targeted to an INR of 2–3 should be administered indefinitely to patients with MS who have AF or a history of thromboembolism. •The routine use of warfarin in patients in sinus rhythm with LA enlargement (maximal dimension >5.5 cm) with or without spontaneous echo contrast is more controversial. • Direct oral anticoagulants (e.g., apixaban, rivaroxaban) are not approved for use in patients with rheumatic MS.
  35. Mitral commissurotomy symptomatic (New York Heart Association [NYHA] Functional Class II–IV) patients with isolated severe MS, whose effective orifice (valve area) is < ~1 cm2/m2 body surface area, or <1.5 cm2 in normalsized adults. Mitral commissurotomy can be carried out either percutaneously or surgically.
  36. After trans septal puncture,the deflated balloon catheter is advanced across the interatrial septum, then across the mitral valve and into the left ventricle.
  37. The balloon is then inflated stepwise within the mitral orifice.
  38. Successful commissurotomy • 50% reduction in the mean mitral gradient • Doubling of the mitral valve area • Striking symptomatic and hemodynamic improvement
  39. INDICATIONS OF MITRAL VALVE REPLACEMENT • Presence of MR • Badly diseased or badly calcified stenotic valve • Severly distorted valve by previous trans catheter or operative manipulation • Moderate or severe MS with thrombus in LA despite anticoagulation
  40. Recommendations for Mitral Valve Repair for Mitral Stenosis – Patients with NYHA functional Class III-IV symptoms, moderate or severe MS (mitral valve area <1.5 cm 2 ),*and valve morphology favorable for repair if percutaneous mitral balloon valvotomy is not available – Patients with NYHA functional Class III-IV symptoms, moderate or severe MS (mitral valve area <1.5 cm 2 ),*and valve morphology favorable for repair if a left atrial thrombus is present despite anticoagulation – Patients with NYHA functional Class III-IV symptoms, moderate or severe MS (mitral valve area <1.5 cm 2 ),* and a non-pliable or calcified valve with the decision to proceed with either repair or replacement made at the time of the operation.