MITRAL STENOSIS - UG Final by Dr JTR.pptx

Mitral stenosis is an important topic for MBBS Students. Clinical features, diagnosis and management covered in this PPT.

1. Education arises from some ingenious balance between challenges & Support Support Mentors need to support their mentees, but challenge them too Challenges

2. MITRAL STENOSIS Dr. JALAGAM THIRUPATHI RAO PROFESSOR OF GENERAL MEDICINE

3. INTRODUCTION Mitral stenosis (MS), known in the literature since at least the 1669 MS characterized by narrowing of the mitral valve, causing obstructed blood flow from the left atrium to the ventricle

4. Mitral valve anatomy 2 Mitral leaflets (Anterior and Posterior) 2 C ommissures - anteromedial and posterolateral Valve Annulus-Fibrous ring Chordae tendineae Papillary muscles Adjacent LV myocardium

5. EPIDEMIOLOGY Rheumatic Mitral Stenosis largely concentrated among the low and middle income countries that are endemic for group A Streptococcus (GAS) pharyngitis and acute rheumatic fever Non-rheumatic Mitral Stenosis Degenerative MS is most common in the Western world and is mainly mitral annular calcification related

6. ETIOLOGY 1) Rheumatic fever 2) Congenital (parachute valve, cor triatriatum ) 3) Severe mitral annular calcification extending to leaflets 4) SLE , RA 5) LA Myxoma 6) IE with large vegetations 7) Malignant carcinoid 8) Mucopolysaccharoidoses – hunter hurley type 9) Amyloid deposits 10) Drugs - Methysergide therapy

7. The developed world eliminated Rheumatic heart disease It continues to be a major cause of heart disease, morbidity, and mortality in the low and middle income countries Pure or Predominant MS in 40 % of RHD

8. PATHOLOGY Acute rheumatic fever Exaggerated immune response Inflammatory process of valve leaflets due to cross reactivity Valvulitis with mitral regurgitation Chronic inflammation + fibrosis Diffuse thickening of valve leaflets Mitral commisure fused,Chordae tendinae shortens, valvular cusps rigid Narrowing at apex – fish mouth appearance Calcification – I mmobilisation of valve leaflet

9. Fused commissures are the hallmark of rheumatic MS. Fusion starts along the valve tips and progresses to limit the opening from both ends .

10. The proximal and mid parts of the leaflets preserve some flexibility which results in the hockey stick appearance of the anterior leaflet in diastole More severe disease extends into the subvalvular apparatus creating a dense fused and shortened chordae that adds an additional level of resistance

11. Mitral orifice 4 to 6 cm 2 Anterior leaflet is thicker Posterior leaflet is more prone for prolapse Postero -medial papillary muscle is more commonly involved in acute myocardial infarction as it has only single vessel supply, supplied by RCA

12. In normal diastole Left atrial pressure (LAP) = left ventricular diastolic pressure(LVDP ) No diastolic gradiant across mitral valve LAP = LVEDP = PCWP = PAEDP PCWP : Pulomary Capillary Wedge Pressure PAEDP : Pulmonary Artery End Diastolic Pressure HEMODYNAMICS

13. Consequences of LA Pressure Pulmonary venous hypertension Pulmonary capillary hypertension Pulmonary arterial hypertension RV Dilatation & failure Secondary TR

14. MITRAL STENOSIS

15. Why AF in MS Left atrial dilatation Fibrosis of LA Wall Disorganisation of Atrial muscle fibers After established AF Hemodynamic deterioration Impaired LA contractility Decreased CO Thrombus formation

16. Pulmonary hypertension (1) Passive backward transmission of the elevated LA pressure (2) Pulmonary arteriolar constriction (the so-called “second stenosis ”), which presumably is triggered by LA and pulmonary venous hypertension (Reactive pulmonary hypertension) (3) Interstitial edema in the walls of the small pulmonary vessels (4) At end stage, organic obliterative changes in the pulmonary vascular bed.

17. Symptoms of Mitral Stenosis Latent period between the initial rheumatic carditis and the development of symptoms due to MS is two decades Dyspnea and cough Orthopnea and PND Hemoptysis Oedema, Ascites , Hepatomegaly (RVF), Hydrothorax Fatigue and decreased exercise tolerance Recurrent pulmonary emboli Winter bronchitis : Pulmonary infections, i.e. , bronchitis, bronchopneumonia, and Lobar pneumonia

18. Clinical features- symptoms Duration: Initial attack of rheumatic carditis to MS symptoms → 20 years Smaller interval around 10 years in tropical & developing countries Common presentation in fourth decade of life Dyspnea Precipitated by exertion ↑ severity of MS → Easier precipitation , Orthopnea , PND develops ( adrenergic drive & Resp. drive, Fluid shift )

19. Hemoptysis : Due to LAP , Pulmonary venous hypertension Due to rupture of thin walled dilated bronchial veins Sudden hemorrhage due to rupture of thin walled dilated bronchial veins ( Pulomary apoplexy ) Pulmonary edema with rupture of pulmonary alveolar capillaries ( Pink frothy sputum ) Anti coagulation for AF

20. Recurrent pulmonary emboli & infarcts Important cause of morbidity and mortality Pulmonary changes: Fibrosis of capillary & alveoli walls ↓ Vital capacity, TLC, O2 uptake, compliance (with ↑capillary pressure)

21. Thrombo-embolism: Thrombi formed in LA, especially in enlarged atrial appendage 10-20% incidence High risk in patient with AF, age > 65, ↓ cardiac output Important cause of morbidity & mortality H oarseness in MS patients ( Ortner’s syndrome )- due to compression of recurrent laryngeal nerve by a greatly dilated left atrium, enlarged tracheobronchial lymph nodes, and dilated pulmonary artery . Swelling Increased systemic vein pressure Chest pain – Severe RV HTN, RV Ischemia , Pulm . HTN, Pulm ., Coronary embolisation , Embolism (ASD) Palpitations – AF (LAE)

22. Large left atrium causes Atrial fibrillation Compression bronchi causing persistant cough Compression of recurrent laryngeal nerve, hoarseness Esophagus , dysphagia Left atrial appendage clots Mitral facies pinkish purple patches on cheeks due to decreased cardiac output produces vasoconstriction

23. Triggers of MS Exercise Anaemia Pregnancy Thyrotoxicosis Infections Atrial Fibrillation

24. Natural History

25. Arterial Pulse in mitral stenosis The factors influencing the arterial pulse in mitral stenosis are Rhythm Severity of mitral stenosis Aortic valve disease, Systemic HTN, Anaemia Age of the patient Right ventricular failure and functional TR Presence absence of systemic embolism

26. The arterial pulse in mitral stenosis has a normal or decreased pulse volume and a normal contour Pulses In atrial fibrillation - Irregularly irregular with a variable pulse volume . Typical low volume pulse occurs with severe MS, severe PAH and RVF High volume pulse in MS occurs with associated AR, Anaemia or Systemic HTN Arterial Pulse in mitral stenosis

27. Jugular Venous Pulse Sinus rhythm , PAH + RVH -> Prominent a wave RV Failure + TR -> Raised JVP AF -> Absent a wave

28. Jugular Venous Pulse Depends on severity of MS, Degree of PAH, arterial HTN, associated tricuspid valve disease, diuretic therapy, rhythm ( AF or sinus rhythm ) and presence or absence of RVF Most impressive JVP features are seen with severe MS, severe PAH, severe functional TR and RVF The earlobe may move with each v wave and pulsatile exophthalmos may be seen in some patients with severe TR Tricuspid regurgitation, a common complication, will result in a large systolic CV wave

29. Jugular venous pulse in mitral stenosis Features Level Wave pattern a wave X descent Findings Normal and elevated Mechanisms/significance Normal or prominent Elevated with Right ventricular failure Associated organic tricuspid disease Associated atrial septal defect ( Lutembacher syndrome) Prominent a wave with
Tight MS with severe PAH
Associated TS
Associated ASD Absent with Atrial fibrillation Severe TR Normal or obliterated

30. Prominent with Right ventricular failure TR Rapid with right ventricular
failure, TR Slow with associated TS Normal or prominent Normal or rapid or slow V wave Y decent

31. Cardiac impulse in mitral stenosis The factors influencing the cardiac impulse in MS Severity of mitral stenosis Presence and severity of pulmonary arterial hypertension Right ventricular failure and functional TR Associated conditions : Mitral regurgitation, Aortic valve disease, Tricuspid valve disease, ASD OR Systemic HTN Complications : Calcification of mitral valve, Rhythm

32. Classical features of the cardiac impulse in MS The apical impulse is diffuse and is formed by right ventricle Diastolic thrill at apex Sustained left parasternal impulse Palpable pulmonary arterial pulsations Palpable pulmonary sound

33. Left Ventricular Impulse . The left ventricle in pure mitral stenosis typically is under filled and, therefore, does not produce a forceful apical impulse. It is essential to locate the LV apex beat to assist in optimal auscultation of the mitral diastolic rumble. This is best done in the left recumbent position

34. Right Ventricular Impulse A gentle, low amplitude RV lift detectable at the 3rd to 5th left interspace adjacent to the sternum To detect parasternal motion, it is desirable to use firm pressure with the heel of the hand during held-expiration A parasternal lift indicates increased right ventricular hypertrophy or dilatation, possibly augmented by the enlarged left atrium displacing the right ventricle in an anterior direction

35. Heart Sounds

36. Characteristics of S1 The first heart sound is typically discrete and loud and has a slapping quality S1 is audible throughout the precordium and is heard maximally between the lower sternal edge and the apex . The loud S1 is often palpable . It is important to recognize the palpable shock of S1 and differentiate it from the left ventricular apex impulse, which usually is feeble is mitral stenosis

37. Mechanism of loud first heart sound Open mitral valve at end diastole Wide open valve cusps Delayed closure of mitral valve Mitral valve closure at higher pressure of left ventricle - (IVC) Rate of raise LV Pressure – dp / dt Morphology - Thickened but mobile mitral valve Tachycardia ---> Short PR Interval – Closes with a high velocity large excursion The thickened leaflets and high pressure in the left atrium are the central features .

38. Causes of soft first heart sound Heavily calcified mitral valve Calcification results in loss of pliability Severe sub valvular fusion Associated mitral regurgitation Associated severe aortic regurgitation Masked left ventricular events due to severe right ventricular hypertrophy Active Rheumatic carditis (Due to prolonged PR interval) Left atrial failure (LAF)

39. S2 In mild or moderate MS – Normal split In severe MS with severe PAH Close split or single Intensity of pulmonic sound correlates well with the severity of PAH Wide split S2 in MS – Associated ASD considered

40. Opening Snap in MS Due to thickening of the valve with a doming motion towards the left ventricle due to high pressure in the left atrium Sudden tensing of valve cusps

41. Opening Snap The opening snap (OS) is one of the classic findings in cardiac physical diagnosis This sound results from the maximal opening excursion of the mitral valve cusps into the left ventricular cavity in early diastole after LV pressure falls below that in the left atrium The OS coincides precisely with the maximal opening movement of the anterior leaflet of the mitral valve

42. The opening snap is typically a medium to high frequency sound, quite distinct and sharp, which initiates the mitral diastolic rumble The OS is best heard inside or medial to the LV apex in the mid- precordial area . The opening snap should be sought by using firm pressure with the diaphragm of the stethoscope in both the supine and left lateral recumbent positions. Mild exercise or handgrip will augment the intensity of the snap

43. OS present means mitral valve is not significantly rigid and calcified

44. OS Loudest apex S2 Best heard at base

45. S2 –OS vs A2-P2 gap Venous return to heart decreases Amount of blood entering right atrium decreases A2-P2 gap narrows LA-LV pressure gradient decreases Delayed opening of mitral valve S2 – OS gap increases Pulmonary valve closes early Venous return to heart decreases Amount of blood entering right ventricle is less

46. Timing (A2-0S Interval) A n indicator of the severity of mitral stenosis . In general a narrow A2-0S interval indicates severe stenosis , and a long interval suggests mild disease With a high LA pressure, a, the mitral valve opens much earlier than normal. In mild to moderate mitral stenosis , LA pressure is less elevated and the LV-LA pressure crossover, as well as mitral valve opening, occurs somewhat later in diastole

47. Missing opening snap in mitral stenosis Severely calcified mitral valve Mitral regurgitation ( significant) Aortic regurgitation (severe) Aortic stenosis (severe) Coronary artery disease with left ventricular dysfunction Any condition with associated left ventricular failure Very close S2-OS (<30 msec ) Auscultatory incompetence OS heard but mistaken for wide split second heart sound

48. Location the zone of auscultation is often quite small, localized to the apex impulse in the left recumbent position. The murmur may be inaudible even 1 to 2 cm away from this area. Radiation low intensity mitral stenosis murmur is well localized and does not radiate appreciably. When the murmur is very loud, it may be heard toward the lower left sternal border Intensity The intensity of the murmur of mitral stenosis is directly related to the velocity of blood flow across the mitral valve and the severity of the stenosis . MDM of mitral stenosis

49. Mechanisms influencing length of the murmur Cardiac output Heart rate Left atrial pressure Left ventricular end-diastolic pressure Heart rhythm

50. Absent MDM in MS Severe silent MS Severe cardiac failure Emphysema Obesity

51. Loud P2 and palpable P2 Prominent parasternal heave : right ventricular hypertrophy Tricuspid regurgitation murmur, Pansystolic - best heard along lower left sternal border : caravallo’s sign Hepatomegaly , edema, ascitis Prominent epigastric suprsternal space pulsations JVP – a wave and v wave--  Prominent FEATURES OF PULMONARY HYPERTENTION

52. MS + Sev . Pul . HTN H igh-pitched , diastolic, decrescendo blowing murmur along the left sternal border ( Graham Steell mumur of PR)

53. Non valvular pulmonary ejection sound – Dilatation of PA Diminished during inspiration

54. MDM other than MS Carey coombs murmur – Acute rhuematic fever Austin flint murmur – Severe AR Atrial myxoma Large VSD, PDA, Severe MR – Increased flow across non stenotic mitral valve Large ASD, Severe TR – Increased flow across non stenotic Tricuspid valve

55. Why there is MDM in Mitral stenosis The valve will open only after the isovolumetric relaxation phase

56. Questions need to be answered at the end of physical examination Is it MS or condition simulating it If MS, what is the severity Is the valve pliable or calcified Is there sub valvular fusion What is rhythm Is there PAH, what is the severity Is there RHF Are there associated lesions Is there a discrepancy between symptoms and physical signs Is there a peripheral embolism Is left atrial myxoma , a possibility

57. Before OR after - Theory OR Practical exams

58. STRATEGIC TIMEOUT If you could eliminate one thing from your daily routine, what would it be and why?

59. INVESTIGATIONS

60. ELECTROCARDIOGRAPHIC FINDINGS : In severe MS & sinus rhythm – P waves usually suggest LA enlargement (90%) P-WAVE : Tall peaked in lead ll upright in V1 [ when severe pulmonary HTN or TS complicate MS & RA enlargment QRS – normal [ with severe pulmonary HTN - right axis deviation , RV hypertrophy ]

61. ECG ECG: P wave suggests LA enlargement If Pul . HTN develops: RA enlargement RV hypertrophy & Rt. Axis deviation may be seen

62. CHEST RADIOGRAPHY FINDINGS : Early stages : straightening of upper left heart border Due to enlarged LA Backward displacement of esophagus (in lateral view ) Double shadow Splaying of carina – left main bronchus is lifted up Prominent upper zones pulmonary veins [ inverted moustache/ Antler’s horn sign/ cephalization of pulmonary blood flow

63. Kerley -B lines I ndicates fluid collection in interlobular septa & lymphatics when resting mean LA pressure exceed 20 mm of hg Castrophrenic angles – Most often seen Fine , dense , opaque short horizontal lines More pominent in lower & mid lung fields

64. Kerly A lines In severe long standing MS Straight dense lines – Run towards hilum Kerley C lines Reticular opacities at the lung base Represent end on view of Kerley B lines

65. Kerley’s A lines (arrows) Kerley B lines (white arrowheads) Kerley C lines (black arrowheads) Kerley A  lines - linear opacities extending from the periphery to the hila caused by distention of anastomotic channels between peripheral and central lymphatics Kerley B  lines are small, horizontal, peripheral straight lines demonstrated at the lung bases that represent thickened interlobular septa on CXR. They represent edema of the interlobular septa Kerley C  lines are reticular opacities at the lung base, representing Kerley’s B lines end on (‘ en face’) .

66. ECHOCARDIGRAM : Transthoracic echo with color flow &spectral doppler imaging shows Measurements of mitral inflow velocity during early[ E-waves ] & late [A-waves] in pts with sinus rhythm – diastolic filling Estimates transvlavular peak , mean gradients, & mitral area orifice Severity of any association of MR

67. Extent of leaflet calcification & restriction Degree of distortion of subvalvular apparatus Anatomy for percutaneous mitral balloon commissurotomy also assessment of LV,RV function chamber size Estimation of PA systolic pressure based on tricuspid regurgitation velocity Pressure & severity of associated valvular leions [AS/&AR]

68. A)Long axis view-both leaflets are thickend with pliable anterior leaflet B)Short axis view-fusion of both commissures C) A coptation defect of mitral can be detected with severely dilated LA. D) colour flow mapping showing severe MR

69. When TTE is inadeqate TEE – Superior images Especially indicated for exclusion of left atrial thrombus prior to PMBC Transesophageal echocardiography

70. CARDIAC CATHETERIZATION Rotinely not necessary Useful in discrepency between clincal & non invasive findings (TEE , exercise echo ) Also helpful in assessing associated AS , AR & in pt.s with recurring worsening symptoms after MV Intervention LA and LV Pressures Mean trans valvular pressure gradient Measuring trans mitral volume/flow rate Valve area – Gorlin formula

71. Gorlin formula Cardiac output (ml/min) DFP x HR x 0.85 x 44.3 x mean grad (mm of hg) MVA =

72. CT-CORONARY ANGIOGRAPHY Screen pre-operatively for presence of CAD in appropriate pt.s prior to valve surgery / transcather treatment

73. Stages of Mitral Stenosis (MS)

74. Diagnostic testing of Rheumatic MS

75. Prevention of recurrent Rheumatic fever Prevent and treatment complications of MS

76. Secondary prevention of Rheumatic fever Antibiotic for prevention Dosage Penicillin G benzathine 1.2 million U intramuscularly every 4 week Penicillin V Potassium 200 mg orally twice daily Sulfadiazine 1 g orally once daily Macrolide or azalide antibiotic (For patients allergic to penicillin and sulfadizine ) Varies

77. Duration of secondary prophylaxis of Rheumatic fever Type Duration after last attack Rheumatic fever with carditis and residual heart disease (Persistent VHD) 10 yr OR until patient is 40 yrs of age (whichever is longer) Rheumatic fever with carditis but no residual heart disease (No valvular disease ) 10 yr OR until patient is 21 yrs of age (whichever is longer) Rheumatic fever without carditis 5 yr OR until patient is 21 yrs of age (whichever is longer)

78. Heart rate reduction –mandatory with BETA blockers BB, Verapamil , Diltiazem Reduce volume – Diuretics / Salt restriction

79. Indications for Anti coagulation AF Any prior embolic event LA Thrombus Warfarin [INR 2-3 ]

80. If AF is relatively new onset & pt.s whose MS Iis not so severe enough to warrant PMBC/ surgery ; reversal is by pharmocological or cardioversion CARDIOVERSION : usually if pts had atleast 3 consecutive weeks of anticoagulation. if more urgent , IV heparin intiated & TEE to rule out LA thrombus Rarely successful in severe MS ; Significant LA enlargement ; AF > 1year ; or conditions that favour LA myopathy

81. PBMV – Preserve native valve MV Repair – OMV / CMV TMVR

82. PBMV Pliability of valve Loud S1, Sharp (crisp) OS 2 D echo

83. : INDICATIONS [AHA] Symptomatic pt.s [NYHA II , lll , lV ] ; Severe Rheumatic MS ; favorable MV morphology & No clot in LA / Less than moderate MR Favourable valve morphology wilkins < 8 Less than moderate MR < 2 + TEE prior to BMV Avoid BMV in commissural calcification PERCUTANOUS MITRAL BALLON VALVOTOMY

84. Tri leaflet Valve

85. Mechanical vs Tissue Mitral valves

86. Surgical valvotomy Closed Mitral Valvotomy Open Mitral Valvotomy Mitral Valve Replacement Indications for surgery 1) No candidate for PMBC 2) Failed previous PMBC

87. TMVR Procedure

88. SUMMARY

89. Mentor shows the door of success & Helps mentee open it “There is no lack of knowledge out there …. Just a shortage of asking for HELP” TEACH Praise Inspire Encourage Instruct Influence Guide

90. THANK YOU

91. Features of murmur of mitral stenosis

92. Opening Snap in the Absence of Mitral Stenosis Mitral Valve Origin Mitral regurgitation
Patent ductus arteriosus
Ventricular septal defect Thyrotoxicosis Heart blocks 2 & 3 degree Hypertrophic cardiomyopathy Tetralogy of Fallot after shunt operation Tricuspid Valve Origin Atrial septal defect
Tricuspid regurgitation Ebstein’s anomaly

93. LA Pressure Higher transmitral -gradient Decrease in diastolic filling time

94. A2-OS gap Length of murmur Presystolic accentuation AF PHT MVA = 220/PHT

95. Factors That May Affect the A2-0S Interval in Mitral Stenosis Associated Condition Effect on A2·.OS Interval Systemic hypertension Increase Mitral regurgitation Decrease Aortic regurgitation Decrease or increase Aortic stenosis Increase Calcified mitral valve Increase LV dysfunction Increase Old age Increase

96. In MS, increased resistance to blood flow leads to diastolic gradient Increase in left atrial pressure to maintain cardiac output It increases pulmonary venous and capillary pressure Exertional dyspnea Reflex pulmonary artery constriction : Decreases amount of blood flow through pulmonary vasculature Theory of second Stenosis Relieving of symptoms