Valvular heart disease assessment of lesion severity


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  • Figure 1. Example of a Jet of Aortic Regurgitation, as Shown by Color-Flow Imaging.
    The three components of the regurgitant flow (flow convergence above the orifice, vena contracta through the orifice, and the jet below the orifice) are shown. The width of the vena contracta (as indicated by crosses) can be measured as a surrogate for the regurgitant orifice.
  • Table 1. Classification of the Severity of Aortic Regurgitation.
  • Figure 2. Example of Quantitation of Aortic Regurgitation by the Convergence of the Proximal Flow.
    Panel A is a color-flow image of the aortic valve; the measured radius of the proximal flow convergence (R) is 0.74 cm, and the regurgitant flow is calculated as 138 ml per second. The "aliasing" velocity of 0.40 m per second (modified by baseline displacement) is the blood velocity at the junction of the orange and blue flows. Panel B shows a continuous-wave Doppler measurement of regurgitant blood velocity, at 455 cm per second (arrow). The effective regurgitant orifice area is determined by dividing the flow by the velocity, which in this case is 0.30 cm2.
  • Valvular heart disease assessment of lesion severity

    1. 1. Valvular Heart DiseaseValvular Heart Disease Assessment of Lesion severityAssessment of Lesion severity Dr Awadhesh kumar sharma DM Cardiology PGIMER &Dr RML Hospital,New Delhi
    2. 2.  In managing the patient with valvular heart disease (VHD) three major issues must be addressed:-  Assessment of the severity of disease,  The effect the disease is having or is likely to have on the patient and his/her cardiovascular system  The timing and type of intervention to be used to correct the lesion. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 8th ed. Philadelphia, PA: WB Saunders; 2007:1625-1712.
    3. 3.  The distinction between mild, moderate and severe disease is thought crucial since it is believed that, in most cases, mild and moderate disease are tolerated indefinitely (unless severity worsens) and only severe disease (as defined) causes symptoms and cardiac dysfunction. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 8th ed. Philadelphia, PA: WB Saunders; 2007:1625-1712.
    4. 4.  Classification of the severity of valve lesions should be based on multiple criteria, including the initial findings on the physical examination, which should then be correlated with data from a comprehensive TTE.  Intervention should primarily be performed on patients with severe VHD Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 8th ed. Philadelphia, PA: WB Saunders; 2007:1625-1712.
    5. 5. Classification of progression of VHD J Am Coll Cardiol. March 2014.Online first.
    6. 6. OBJECTIVE ASSESSMENT OF DISEASE SEVERITY  The physical examination  In this age of high-tech diagnostic modalities, the physical examination, and the skill applied when performing it, seem to be diminishing.  However, the importance of the physical exam cannot be overemphasized because it lays the Bayesian foundation for all tests that follow.
    7. 7. Mitral stenosis (MS) Etiology  Most commonly rheumatic fever ——rheumatic heart disease ( RHD )  Symptoms commence mostly in 2nd~4th decade  2/3 of all patients are female  25% of all patients with RHD have pure MS  40% have combined MS and mitral regurgitation (MR) J Am Coll Cardiol. 1994;24:152-8.
    8. 8. Clinical features s/o severe MS  PND  Pulmonary edema  Orthopnea  Atrial fibrillation  Ortner syndrome  Short A2-OS interval  Long duration of diastolic murmur J Am Coll Cardiol. 1994;24:152-8.
    9. 9. Laboratory examination Electrocardiography (ECG) Left atrial enlargement Mitral valve P wave P-wave duration in lead II > 0.12 s Large terminal negative P force in lead V1 Right ventricular hypertrophy Arrhythmia Premature atrial contraction → atrial fibrillation
    10. 10. Radiological findings “Mitral valve heart” Marked enlargement of LA Enlargement of RV Dilatation of PA Pulmonary congestion Interstitial edema (manifested as Kerley B lines)
    11. 11. Echocardiography The most valuable technique for diagnosing MS, and determining its severity M-mode echoM-mode echo :: Thickened, calcified leaflets open poorly, close slowly (EF slope↓) The double peaks disappear Both leaflets move anteriorly during early diastole Two-dimensional echo:Two-dimensional echo: Fusion, thickening, doming of the valve leaflets, and poor leaflet separation in diastole; mitral orifice area↓ Eur J Echocardiogr. 2009;10:1-25.
    12. 12. Mitral stenosis Moderate MS Severe MS
    13. 13. Hemodynamic changes MS involves mainly LA and RV 1. Effect of MS on left atrioventricular pressure gradient and left atrial pressure (LAP) MVA transvalvular gradient LAP Normal 4 ~ 6cm2 Mild MS > 1.5cm2 <5 mmHg ↑ Moderate 1.0 ~ 1.5cm2 5-10mmHg ↑↑ Severe < 1.0cm2 ≥10mmHg 25mmHg Eur J Echocardiogr. 2009;10:1-25.
    14. 14. Mitral stenosis
    15. 15. Doppler echoDoppler echo :: Most accurate noninvasive technique for quantifying the severity of MS Spectrum Doppler: measure transvalvular gradient, MVA Color Doppler: display high velocity color jet Provide other important information Cardiac chamber size (LA, RV) Left ventricular contractility Pulmonary arterial pressure Other coexisted valvular or congenital abnormalities Mural thrombi Eur J Echocardiogr. 2009;10:1-25.
    16. 16. Cardiac catheterization Its value in assessment of patients with MS or suspected MS has been largely superseded by echocardiography If surgery is planned, coronary angiography is performed to ascertain whether or not bypass grafting is indicated in patients at risk of having coexisting coronary artery disease J Am Coll Cardiol. 1994;24:152-8.
    17. 17. 2014 AHA/ACC Valvular Heart Disease Guidelines J Am Coll Cardiol. March 2014.Online first.
    18. 18. Mitral regurgitation (MR) Etiology Mitral valve apparatus and/or LV structural and functional abnormality RHD: common(1/3); + MS and/ or aortic valve disease Mitral valve prolapse (MVP) myxomatous degeneration, floppy and redundancy Ischemic heart disease (or CAD) papillary muscle dysfunction Mitral annular calcification
    19. 19. Severe dilatation of LV result in dilatation of the mitral annulus and lateral movement of papillary muscle Infective endocarditis valve leaflets destruction, perforation, retraction; valve closure interfered by vegetation Other causes: Rupture of the chordae congenital abnormalities obstructive hypertrophic cardiomyopathy
    20. 20. Hemodynamic changes MR involves mainly LA and LV Chronic MR Compensation: MR→ LV volume↑→LV, LA↑→ LVEDV↑→ SV↑→ CO↑, EF↑ Decompensation: Left HF, LAP and LVEDP↑ → pulmonary congestion, pulmonary hypertension, right HF (hepatomegaly, edema, and ascites) CO↓ Acute MR MR →LA, LV volume↑→LVEDP↑→LAP↑→ ↓ pulmonary congestion, pulmonary edema SV and CO↓
    21. 21. Clinical manifestations Symptoms Chronic MR Mild— no symptom Severe— left-sided heart failure Weakness, fatigue (CO↓) Dyspnea (pulmonary congestion) RHD: symptoms occur late, once present, LV dysfunction is usually irreversible MVP: asymptomatic, or atypical chest pain, palpitation, fatigue; in severe MR, left HF occur at late stage Acute Mild— mild exertional dyspnea Severe— acute left HF, pulmonary edema, or cardiac shock Circulation. 2003;108:2432-2438.
    22. 22. Physical examination Cardiac impulse at apex Hyperdynamic Displaced laterally, inferiorly (Chronic) Changes of heart sounds S1↓(RHD) or normal (MVP, CAD) S3 (severe MR): prominent Mid or late systolic click ( MVP ) ( Acute: P2↑ , S4 ) Circulation. 2003;108:2432-2438.
    23. 23. Systolic murmur RHD : Pansystolic, blowing, high-pitched murmurPansystolic, blowing, high-pitched murmur maximal at the apex Anterior valve lesion, radiate to the axilla and back Posterior leaflet abnormality, radiate to the base MVP : mid- to late-systolic murmur Dysfunction of papillary muscles: Variable (early, mid, late or holosystolic) Rupture of the chordae: musical (Acute MR: not pansystolic murmur, but lower-pitched, decrescendo, and softer than the murmur of chronic MR) Circulation. 2003;108:2432-2438.
    24. 24. Severe MR  Hyperdynamic LV type apex  Systolic thrill over apex  S3  Functional flow mid diastolic murmur Circulation. 2003;108:2432-2438.
    25. 25. Laboratory examination ECG Chronic (severe) MR: LA dilation, Atrial fibrillation LV enlargement and non-specific ST-T changes Acute MR: sinus tachycardia Radiological findings Chronic (severe) MR: Cardiomegaly with LA, LV↑; pulmonary congestion, interstitial edema with Kerley B lines (left HF) C-shaped calcification of mitral annulus Acute MR: Normal cardiac silhouette or mild LA dilation overt pulmonary congestion, edema J Am Coll Cardiol. 1999;34:1137-44.
    26. 26. Echocardiography 1 、 Display anatomy of the mitral valve apparatus Useful in determining the etiology of MR (2D) 2 、 Confirm the existence of MR Doppler (color, spectrum): reveal high-velocity jet into LA during systole Sensitivity~100% Estimate the severity of MR < 4 cm2 Mild ( Color flow jet area ) 4~8 cm2 Moderate > 8 cm2 Severe 3 、 Measure cardiac chamber sizes, evaluate LV function, pulmonary artery pressure, provide data concerning other valvular lesions J Am Coll Cardiol. 1999;34:1137-44.
    27. 27. Calculating (PISA)  Apical 4Ch view  Narrow sector width  Minimise depth  Zoom  Adjust Colour Doppler alaising velocity (20-40 cm/s)
    28. 28. PISA  Measure the radius of the hemisphere. (red/blue interface) – PISA radius =2πr2 (cm2 ) • Mild MR: <0.4 • Severe MR:>1.0
    29. 29. Colour Doppler Indicators of Mitral Regurgitation Severity Mild Moderate Severe Colour Doppler Jet area (cm2 ) Nyquist 50-60cm/s <4 >10 Ratio of jet area to left atrial area (%) <20 >40 Vena contracta width (cm) <0.3 >0.7 PISA radius (cm) at Nyquist 40cm/s <0.4 >1.0
    30. 30. Continuous wave and Pulse wave Doppler  Continuous wave spectral Strength – Apical 4Ch view CW of regurgitant jet • Faint in mild mitral regurgitation • Denser in moderate and severe regurgitation.
    31. 31. Peak Mitral Valve E velocity  Increased mitral valve E velocity (>1.2m/s) may indicate significant regurgitation. – Assumes ejection fraction is>40%)  Decreased mitral valve DT (<150msec) may indicate significant regurgitation. – Assumes normal diastolic LV function.
    32. 32. Pulmonary Vein Systolic Flow Reversal  PW doppler 1cm into the pulmonary veins – Systolic S (systolic) wave is normally larger than the D (diastolic) wave. – If D wave is larger there is blunting of forward flow. – S wave inversion demonstrates systolic flow reversal (indicative of severe MR).
    33. 33. Limitation  Eccentric jets may affect pulmonary vein flow
    34. 34. Determination of Pulmonary Artery Pressures at Rest and Exercise
    35. 35. Multimodality Indicators of Mitral Regurgitation Severity Mild Moderate Severe Multimodality Regurgitant volume (mL/beat) <30 30-59 >60 Regurgitant fraction (%) <30 30-49 >50 Effective regurgitant orifice area (cm2 ) <0.20 0.20-0.39 >0.40
    36. 36. Regurgitant Volume, Regurgitant Fraction and ERO  Regurgitant volume  Step 1 – A4ch view measure diameter of the mitral annulus. • CSAMV=0.785 X (mitral annulus diameter)2
    37. 37. Regurgitant volume  Step 2 – Apical 4Ch view measure the VTI of the mitral inflow (using PWD) – Commonly at valve tip level. • VTIMV in cm  Step 3. Stroke Volume – SVMV(mL/beat) =CSAMV X VTIMV
    38. 38. Regurgitant volume  Step 4 – In PLAx measure the diameter of the LVOT (cm). – Calculate CSA of the LVOT (cm2 ) • CSALVOT = 0.785 x (LVOT diameter)2
    39. 39. Regurgitant volume  Step 5 – In the Ap5 Ch view measure the VTI of the LVOT outflow (using PWD) • VTILVOT (cm)  Step 6. Stroke volume – SVLVOT = CSALVOT x VTILVOT
    40. 40. Regurgitant Volume/Fraction  Step 6 – Mitral regurgitant volume (RV)(mL) • RV =SVMV – SVLVOT – Mild MR:<30 Mod MR:31-59 – Severe MR:>60  Step 7 – Mitral regurgitant Fraction (MF)(cm2 ) • RF = RV / SVMV (x100) – Mild MR:<30 Mod MR:31-49 – Severe MR:>50
    41. 41. Regurgitant orifice area  Step 8 – Measure the VTI of the mitral regurgitation VTIMR (cm) (using CWD) – Calculate Regurgitant Orifice Area (ROA) in cm2 • ROA = RV / VTIMR – Mild MR:<0.20 – Mod MR:0.21-0.39 – Severe MR:>0.40
    42. 42. Regurgitant Orifice Area PISA method  Step 1. Measure the radius of the hemisphere. (red/blue interface) – PISA =2πr2 (cm2 ) – Calculate regurgitant flow rate – RFR mL/s =PISA X aliasing velocity
    43. 43. Regurgitant orifice area  Step 2. CWD of the mitral regurgitation. Measure peak velocity (VMR) in cm/s.  Calculate Regurgitant Orifice Area in cm2 . – ROA =Regurgitant flow rate / VMR
    44. 44. Common pitfalls  Measuring regurgitant jet area or VC width on colour doppler with inappropriate colour gain settings  Underestimating severity of eccentric jets on CFD.  Failure to align the doppler beam with regurgitant flow during CW doppler interrogation.  Inaccurate measurement of mitral valve orifice area or LVOT diameter when calculating RV.  Trying to calculate RV when there is coexistant aortic regurgitation.  Failure to average several readings when the patient is in AF.
    45. 45. Radionuclide angiography and MRI Evaluate LV function Estimate the severity of regurgitation The regurgitant fraction can be estimated from the ratio of LV to RV (LV/RV) stroke volume Cardiac catheterization Confirm the diagnosis of MR and estimate its severity, evaluate cardiac function and pulmonary artery pressure Coronary angiography is performed to determine presence of CAD prior to surgery J Am Coll Cardiol. 1999;34:1137-44.
    46. 46. 2014 AHA/ACC Valvular Heart Disease Guidelines J Am Coll Cardiol. March 2014.Online first.
    47. 47. 2014 AHA/ACC Valvular Heart Disease Guidelines J Am Coll Cardiol. March 2014.Online first.
    48. 48. Aortic stenosis (AS) Etiology RHD Common, + AR and mitral valve disease Degenerative calcific AS Common in the elderly, accompanied by calcification of the mitral annulus Congenital abnormalities Calcific stenosis of congenitally bicuspid aortic valve Congenital aortic stenosis
    49. 49. Hemodynamic changes Normal aortic orifice area (AOA): 3.0~4.0 cm2 AOA ≤1.0cm2, LVSP↑, with significant transvalvular gradient Compensation AS→LV pressure load↑ Concentric LVH→compliance↓→LVEDP↑→LAH Maintain systolic wall stress and CO ↑LVEDV Decompensation LVEDV↑→wall stress↑, myocardial ischemia, fibrosis → left HF
    50. 50. Classic symptom triad  Dyspnea  Angina  Syncope
    51. 51. Classic symptom triad  Once any of these classic symptoms develop, prognosis dramatically worsens.  Thus, within 5 years of the development of angina, approximately 50% of patients will die unless aortic valve replacement is performed.  For syncope, 50% survival is 3 years  For congestive heart failure, 50% survival is only 2 years unless the valve is replaced.  Angina 5yrs, Syncope 3yrs, and CHF 2yrs.
    52. 52. Severe AS  Triad of angina,dyspnoea and syncope  Heaving apex  Slow rising small volume pulse  Reverse splitting of S2  Long duration of systolic murmur  Late peaking of murmur  Presence of S4
    53. 53. Laboratory examination ECG Severe: LVH and secondary ST-T changes, LA↑ , arrhythmias Radiological findings Normal size or slightly enlarged heart Calcification of the aortic valve Poststenotic dilatation of the ascending aorta Pulmonary congestion
    54. 54. Echocardiography Establish a diagnosis, and determine the severity of AS M-mode and 2D echo Observe aortic valve opening, thickening and calcification Helpful in determining the etiology of AS Also invaluable in detecting associated mitral valve disease and in assessing LV performance, hypertrophy, and dilatation Eur J Echocardiogr. 2009;10:1-25.
    55. 55. Doppler echo Allows calculation of the aortic valve gradient Estimate the severity of the stenosis < 20 mmHg Mild AS MPG 20~40 mmHg Moderate AS > 40 mmHg Severe AS Color Doppler flow imaging is helpful in the detection and determination of the severity of any accompanying aortic regurgitation Eur J Echocardiogr. 2009;10:1-25.
    56. 56. Enriquez-Sarano, M. et al. N Engl J Med 2004;351:1539-1546 Jet of Aortic Regurgitation, as Shown by Color-Flow Imaging
    57. 57. Enriquez-Sarano, M. et al. N Engl J Med 2004;351:1539-1546 Classification of the Severity of Aortic Regurgitation
    58. 58. Enriquez-Sarano, M. et al. N Engl J Med 2004;351:1539-1546 Quantitation of Aortic Regurgitation by the Convergence of the Proximal Flow
    59. 59. Cardiac catheterization Determine the severity of AS by measuring systolic LV and aortic pressure simultaneously, and calculating the valve area An average pressure gradient of > 40mmHg or peak pressure gradient of ≥ 70mmHg represent severe AS Coronary angiography is performed in most adults to assess for concomitant coronary disease
    60. 60. Cath data  “Pull back” tracing can be used in pt with NSR but not accurate in irregular rhythms or low-out put states.  In low cardiac output, the stenosis may be severe, with a mean gradient <50mm Hg per echo.  Gorlin equation can be used to calculate AVA from pressure gradients, independent of CO.  AVA= (1000)(CO) (44)(SEP)(HR)(√∆P)
    61. 61. 2014 AHA/ACC Valvular Heart Disease Guidelines J Am Coll Cardiol. March 2014.Online first.
    62. 62. 2014 AHA/ACC Valvular Heart Disease Guidelines J Am Coll Cardiol. March 2014.Online first.
    63. 63. Aortic regurgitation (AR) Etiology Primary disease of the aortic valves and/ or aortic root
    64. 64. Aortic valve disease ① RHD : most common, about 2/3 + AS and/or mitral valve disease ② Infective endocarditis ③ Congenital deformity: bicuspid valves ④ Myxomatous degeneration of the aortic valve Aortic root dilatation ① Marfan syndrome ② Aortic dissection (involve annulus or leaflets) ③ Syphilitic aortitis Clinical practice: aortic regurgitation. N Engl J Med. 2004;351:1539-1546.
    65. 65. Valvular Abnormalities leading to AR Nodular Rheumatic Disease Aortic Root Dilation Endocarditis
    66. 66. Hemodynamic changes Chronic AR Compensation : AR→LV volume↑→ LV↑, LVEDV↑→ SV↑(CO) Decompensation: LV systolic dysfunction→ LV failure (EF↓, LVESV↑) Acute AR AR →LV volume↑→ LVDP↑→ LAP↑ ↓ ↓ CO↓ pulmonary congestion pulmonary edema Clinical practice: aortic regurgitation. N Engl J Med. 2004;351:1539-1546.
    67. 67. Clinical manifestations Symptoms Chronic AR Asymptomatic for many years Palpitation, precordial discomfort, head pounding (related to SV↑) LV failure (dyspnea, fatigue): occur at late stage Angina pectoris or chest pain: less common Acute AR mild—no symptom severe—Acute LV failure and hypotension (pulmonary edema) Clinical practice: aortic regurgitation. N Engl J Med. 2004;351:1539-1546.
    68. 68. Physical examination Chronic, severe AR ① Peripheral arterial signs: Owing to wide pulse pressure: SBP↑, DBP↓ Water-hammer pulseWater-hammer pulse (rapid rise and fall) “Pistol shot soundsPistol shot sounds” (booming systolic & diastolic sounds heard over femoral artery) Duroziez’s signDuroziez’s sign (systolic, diastolic murmur over partially compressed femoral artery) Quincke’s signQuincke’s sign (subungual capillary pulsations) de Musset’s signde Musset’s sign (head bobs with each heartbeat ) ② Apical impulse: diffuse and forceful, displaced laterally and inferiorly (hyperactive, enlarged LV) ③ Heart sound: An S3 gallop is common with LV failure Clinical practice: aortic regurgitation. N Engl J Med. 2004;351:1539-1546.
    69. 69. ④ Heart murmurs Aortic diastolic murmur:Aortic diastolic murmur: High-pitched, blowing, decrescendo pattern When AR is due to primary valvular disease, the diastolic murmur is best heard along the left sternal border in the 3rd and 4th intercostal spaces However, when it is due mainly to dilatation of the ascending aorta, the murmur is often more readily audible along the right upper sternal border Austin-Flint murmur: apical mid or late diastolic low-pitched murmur: common in severe AR, owing to partial closure of MV by the regurgitant jet Circulation. 2005;112(1):125-134.
    70. 70. Ejection systolic murmur: common harsh at the base of the heart accompanied by a systolic thrill Acute AR S1 soft or absent , P2↑ , S3 and S4 AR murmur: lower pitched and shorter than that of chronic AR Austin-Flint murmur: brief Circulation. 2005;112(1):125-134.
    71. 71. Laboratory examination ECG Acute: sinus tachycardia; nonspecific ST-T changes Chronic: LV enlargement and hypertrophy, arrhythmias Circulation. 2005;112(1):125-134.
    72. 72. Radiological findings Acute AR: cardiac size normal or slightly enlarge,signs of pulmonary congestion, pulmonary edema Chronic: LV enlargement, associated with dilatation of the ascending aorta Severe, aneurysmal dilatation of the aorta suggests aortic root disease Marfan syndrome) Pulmonary congestion ( LV heart failure ) Chronic Acute LVE with normal pulmonary vasculature Normal size LV with pulmonary vascular congestion
    73. 73. Echocardiography Confirm diagnosis, estimate severity, identify the cause 2-D echo: Structural changes of the valve leaflets and/or aortic root M mode echo: Diastolic fluttering of the anterior leaflet of the mitral valve is an important echocardiographic finding in AR Serial assessments of LV size and function Doppler echo: Sensitive, accurate noninvasive technique for detecting AR LVOT diastolic regurgitant jet, estimate the severity of AR Cardiac catheterization Quantify the severity of AR Evaluate the coronary and aortic root anatomy J Am Soc Echocardiogr.2003;16:777-802.
    74. 74. AMVL fluttering Color Flow – top mild, bottom moderate
    75. 75. Regurgitant jet width/LVOT diameter ratio greater than or equal to 60 percent
    76. 76. Vena contracta greater than 6 mm
    77. 77. Regurgitant jet area/LVOT area ratio greater than or equal to 60 percent
    78. 78. Holodiastolic flow reversal in the descending thoracic or abdominal aorta
    79. 79. Assessing Severity of AR  Assess severity by impact on peripheral signs and LV-  Duration of murmur >2/3 of diastole  Bisferiens pulse  Hills sign>60 mmHg  Apical impulse down & out  Austin flint murmur  Marked peripheral sign Circulation. 2005;112(1):125-134.
    80. 80. Features AS > AR AR > AS Symptoms: Anginal pain, blackout Palpitation +++ + + +++ Pulse Low volume Bisferians pulse High volume Corrigan’s pulse Pulse pressure Normal to low Wide Peripheral signs +/- + Apex Heaving Hyperdynamic Thril Always systolic Rarely S3 Absent May be present S4 May be present Absent Ejection click Present Rare Diastolic murmur Very short Classic murmur of AR Systolic murmur Classic murmur of AS Function systolic murmur +/- Chest X-Ray Calcification + Cardiomegaly ECG Pressure overload Volume overload
    81. 81.
    82. 82. 2014 AHA/ACC Valvular Heart Disease Guidelines J Am Coll Cardiol. March 2014.Online first.
    83. 83. 2014 AHA/ACC Valvular Heart Disease Guidelines J Am Coll Cardiol. March 2014.Online first.
    84. 84. Tricuspid stenosis  Uncommom valvular lesion  Rheumatic heart disease  Congenital TS  Carcinoid syndrome
    85. 85. Severe TS  Giant a wave in JVP  Duration of diastolic murmur over tricuspid valve  Signs of right heart failure N Engl J Med. 1997;337:32-41.
    86. 86.  ECG-  Absence of evidence of RVH  Right atrial abnormality  Chest X ray  Prominence of right atrium and SVC N Engl J Med. 1997;337:32-41.
    87. 87. 2014 AHA/ACC Valvular Heart Disease Guidelines J Am Coll Cardiol. March 2014.Online first.
    88. 88. Tricuspid regurgitation  Primary disorders of the tricuspid apparatus  Rheumatic disease  Prolapse  Congenital disease (Ebstein’s)  IE  Radiation  Carcinoid  Blunt chest wall trauma  RV endomyocardial biopsy related trauma  Intra-annular RV pacemaker or implantable cardioverter- defibrillator leads. N Engl J Med. 1997;337:32-41.
    89. 89.  Approximately 80% of cases of significant TR are functional in nature and related to tricuspid annular dilation and leaflet tethering in the setting of RV remodeling due to pressure and/or volume overload. J Am Soc Echocardiogr.2003;16:777-802.
    90. 90. Tricuspid stenosis
    91. 91. 2014 AHA/ACC Valvular Heart Disease Guidelines J Am Coll Cardiol. March 2014.Online first.
    92. 92. 2014 AHA/ACC Valvular Heart Disease Guidelines J Am Coll Cardiol. March 2014.Online first.
    93. 93. Pulmonary stenosis  Pulmonic stenosis is essentially a congenital disorder.  Less common etiologies include carcinoid and obstructing vegetations or tumors.  Assessment with TTE alone is usually sufficient for diagnosis and clinical decision making. N Engl J Med. 1997;337:32-41.
    94. 94. Pulmonary stenosis
    95. 95. 2014 AHA/ACC Valvular Heart Disease Guidelines J Am Coll Cardiol. March 2014.Online first.
    96. 96. Pulmonary regurgitation  Mild-to-moderate PR seen on echocardiography is common and does not require further follow-up or intervention if asymptomatic with normal RV size and function.  Significant PR in patients is uncommon.  Primary PR that follows in the wake of childhood surgery for tetralogy of Fallot or other congenital lesions may progress insidiously J Am Soc Echocardiogr.2003;16:777-802.
    97. 97. 2014 AHA/ACC Valvular Heart Disease Guidelines J Am Coll Cardiol. March 2014.Online first.
    98. 98.  We urgently need research on almost every aspect of VHD to ensure that patients who already have VHD receive optimal therapy and to prevent VHD in those at risk.  Approaches to improving outcomes in patients with VHD include – 1) National and international registries and RCTs 2) Continuous evaluation of outcomes data at each Heart Valve Center of Excellence 3) Focus on patient-centric care with involvement of the patient in the decision-making process.
    99. 99. THANK YOU