Vulvular heart diseases


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Vulvular heart diseases

  1. 1. Diseases of the heart valves
  2. 2. Causes of valve diseaseValve regurgitation Valve stenosis Congenital  Congenital Acute rheumatic  rheumatic carditis carditis  Senile degeneration Chronic rheumatic carditis Infective endocarditis Syphilitic aortitis Valve ring dilatation
  3. 3. Rheumatic Heart DiseaseAcute rheumatic feverChronic rheumatic heart disease
  4. 4. Rheumatic heart diseaseAcute rheumatic fever(ARF)Incidence Children Young adults Rare in western Europe & Northen America Endemic; parts of Asia Africa South America100/100,000
  5. 5. Pathogenesis Immune-mediated delayed response to infection with specific strain of group A streptococci that possess antigen which cross-react with cardiac myosin & sarcolemmal membrane protein Ab against the streptococcal Ag mediate inflammation in endocardium,myocardium,pericardium,joint & skin Fibrinoid degeneration in the collagen of connective tissues Aschoff nodules –only in the heart
  6. 6. Clinical features Streptococcal pharyngitis Fever,anorexia,lethargy,joint pain 2-3 wks after initial attack of pharyngitis Arthritis Rashes Carditis Neurological changes
  7. 7. Jones criteria for the diagnosis of acute Rheumatic fever Major manifestations Carditis Erythema marginatum Polyarthritis Subcutaneous nodules Chorea Minor manifestations Fever Raised ESR or CRP Arthralgia Leucocytosis Previous rheumatic fever First degree AV blockPlus Supporting evidence of streptococcal infection;recent scarlet fever, raised ASO or other streptococcal antibody titre, positive throat swab culture
  8. 8. Investigations Positive blood culture Raised antistreptolysin O(ASO)without evidence of recent streptococcal infection Isolated chorea pancarditis
  9. 9. Carditis Pancarditis Declines with increasing age (90% at 3yrs-30% in adolescent) Breathlessness Palpitation Chest pain Tachycardia Cardiac enlargement New or changed cardiac murmur
  10. 10. Carditis Soft MDM(Carey coombs murmur) AR 90% TV & PV rarely involved Pericarditis Cardiac failure ECG –conduction defect,ST-T changes
  11. 11. Arthritis Early feature Acute,painful,asymmetric and migratory joint inflammation of the large joints Red, tender & swollen b/t a day & upto 4 wks Characteristically response to aspirin
  12. 12. Skin lesionsErythema marginatum Subcutaneous nodules <5%  5-7% Red macules which fade  0.5-2 cm in the centre  Firm & painless Remain red at the edges  Extensor surface of Trunk & proximities but bone or tendon not the face  3 wks after onset of May coalesce or overlap other menifestations
  13. 13. Sydenham’s chorea(st Vitusdance) Late neurological manifestation 3/12 after episode of ARF 1/3 of cases More common in females Emotional lability Purposeless choreiform movements of the hands,feet or face Explosive & halting speech Spontaneous recovery within a few months 1/4 of pts with Sydenham’s chorea –chronic rheumatic ht disease
  14. 14. Investigations Evidence of a systemic illness(non-specific) Raised WBC,ESR,CRP Evidence of preceding streptococcal infection(specific) Throat swab culture(pt& family contact) ( + ) in 10-25% of cases ASO titre >200(adults) ,>300(children) 1/5 of cases & most cases of chorea
  15. 15. Investigations Evidence of carditis CXR cardiomegaly,pulmonary congestion ECG Features of pericarditis,1st & 2nd Degree ht block, low QRS voltage Echo; Cardiac dilatation,Valve abnormalities, Pericardial effusion
  16. 16. Treatment of acute attack A single dose of benzyl penicillin 1.2 MU im Oral phenoxymethyl penicillin 250mg 6hrly for 10 d Erythromycin or cephlosporin Limiting cardiac damage and relieving symptoms
  17. 17. Bed rest & supportive therapy Bed rest Avoid strenuous exercise Treat cardiac failure Valve replacement if not respond to medical treatment Pacemaker insertion in cases with progressive AV block
  18. 18. Aspirin 60mg/kg /day 6 dividing doses 100mg/kg/d in adults or Maximum 8g/d Nausea,tinitus,deafness Vomiting tachypnoea Acidosis Should be continued until ESR has fallen & then gradually tailed off
  19. 19. Corticosteroids More rapid symptomatic relief > aspirin Carditis Severe arthritis Prednisolone 1-2mg/kg/d in divided doses Should be continued until the ESR is normal & then gradually tailed off
  20. 20. Secondary preventionLong term prophylaxis IM benzyl penicillin 1. 2 million U monthly Oral phynoxymethyl penicillin 250mg 12hrly Sulphadiazine or erythromycin in pts allergic to penicillin At the age of 21 it should be stopped
  21. 21. Secondary preventionTreatment s/b extended if an attack has occurred in the last 5 years Pts live in an area of highly prevalence Has an occupation with high exposure to streptococcal infectionIn those with residual heart disease s/continue until 10yrs after last episode or 40yrs of age**Not protect infective endocarditis
  22. 22. Chronic Rheumatic Heart Disease Chronic rheumatic heart disease  In at least half of the those affected by rheumatic fever with carditis  Two third of cases – women  Only possible to elicit a history of RF or chorea in about half of all patients with chronic rheumatic heart disease  Symptomatic during fulminant forms of ARF  Asymptomatic for many years
  23. 23. Chronic rheumatic heart disease Mitral valve – more than 90 % Aortic valve Tricuspid valve Pulmonary valve Isolated mitral stenosis-25% Mixed mitral stenosis & regurgitation
  24. 24. Pathology Progressive fibrosis Predominantly involved heart valves Involvement of pericardium & myocardium m/contribute to heart failure & conduction disorder Fusion of the mitral valve commissures & shortening of the cordae tendinae –mitral stenosis+/- mitral regurgitation Similar changes in other valves
  25. 25. Mitral Valve Disease
  26. 26. Mitral valve diseaseMitral stenosiscauses Almost always rheumatic in origin Heavy calcification in elderly Congenital
  27. 27. Pathophysiology In rheumatic MS progressive calcification of fusion of cups fibrosis the valve leaflet & subvalvular apparatus Mitralvalve orifice restricted flow from LA to LV pulmonary venous congestion (enlarged LA & LV filling mainly on LA contraction)
  28. 28. Pathophysiology Increase in heart rate shortens diastole Further rise in LA pressureDemand an increase in cardiac outputFurther increase in left atrial pressure
  29. 29. Pathophysiology MV orifice 5cm2 1cm2 or less in severe MS Remain asymptomatic until MV orifice 2cm2 At first,symptoms occur only on exercise Severe stenosis ; breathlessness at rest Reduced lung compliance due to chronic pulmonary congestion Low cardiac output ;fatigue
  30. 30. Pathophysiology Progressive dilatation of the LA Atrial fibrillationTachycardia Loss of atrial contractionMarked Haemodynamic deterioration with rapid rise in LA pressure Pulmonary oedema
  31. 31. Pathophysiology More gradual rise in LA pressureAn increase pulmonary vascular resistance Pulmonary hypertension Right ventricular hypertropy & dilation Tricuspid regurgitation Rt heart failure
  32. 32. Pathophysiology In sinus rhythm < 20% Small LA Severe pulmonary hypertensionAll pts with MS particularly in those with AF LA thrombosis systemic thromboembolism
  33. 33. Clinical featuresSymptoms Signs Breathlessness  AF Fatigue  Mitral facies Oedema  Auscultation; Ascites loud 1st heart sound Palpitation opening snap Haemoptysis Mid-diastolic murmur Cough  Signs of raised pulmonary Chest pain capillary pressure Symptoms of crepitations,pulmonary thromboembolic oedema,effusions complications  Signs of pulmonary hypertension RV heave,loud P2
  34. 34. InvestigationsECG Doppler LAH(If not in AF)  Pressure gradient RVH across the mitral valveCXR  Pulmonary arterial Enlarged LA Signs of pulmonary venous pressure congestion  LV functionEcho Cardiac catherization Thickened immobile cusps  Assessment of Reduced valve area coexisting coronary Reduced rate of diastolic artery disease filling of LV &mitral regurgitation
  35. 35. ManagementMedical treatment Pts with minor symptomsDefinitive treatment Pts remain symptomatic with medical treatment Balloon valvuloplasty Mitral valvotomy Mitral valve replacement
  36. 36. Medical treatmentAtrial fibrillation Anticoagulant Digoxin B blockers Rate limiting calcium antagonistHeart failure DiureticsProphylaxis of infective endocarditis Antibiotics
  37. 37. Specific managementMitral balloon valvuloplasty Treatment of choiceCriteria significant symptoms isolated MS no or trivial MR mobile non-calcified valve/subvalve apparatus on echo LA free of thrombus
  38. 38. Specific managementClosed or open mitral valvotomy No facilities or expertise for balloon valvuloplasty s/receive prophylactic antibiotics for IE Follow up 1-2 yrlyMitral valve replacement substantial mitral reflux rigid or calcified
  39. 39. Mitral regurgitationCauses Rheumatic disease Mitral valve prolapse After mitral valvotomy or valvuloplasty Dilation of LV and mitral valve ring Damage to valve cusps and cordae Damage to papillary muscle Myocardial infarction
  40. 40. Pathophysiology Chronic Mitral regurgitation Gradual dilation of the LAwith little in pressure gradual  LVdiastolic pressure& LA pressure No symptoms Breathlessness & pulmonary oedema
  41. 41. Pathophysiology Acute mitral regurgitation Rapid rise in LA pressureMarked symptomatic deterioration
  42. 42. Mitral valve prolapse Floppy mitral valve Congenital Degenerative myxoematous changes A features of connective tissue disorders
  43. 43. Pathophysiology (MVP)Mildest form Regurgitation haemodynamically significantCompetent valveduring systole Infective endocarditisBulge back to LAMid-systolic click click followed by Antibiotics( no murmur) late systolic murmur
  44. 44. Clinical featuresSymptoms Signs Breathlessness  AF/flutter/cardiomegaly Fatigue  Auscultation; apical pansystolic Palpitation murmur Oedema ±thrill Ascites soft S1,apical S3  Signs of raised pulmonary venous congestion (crepitations,pulmonary oedema,effusions)  Signs of pulmonary hypertension & RHF RV heave,loud P2
  45. 45. InvestigationsECG Echo LAH(If not in AF)  Thickened immobile cusps LVH  Reduced valve areaCXR  Reduced rate of diastolic Enlarged LA filling of LV Enlarged LV Doppler Signs of pulmonary venous  Detects & quantifies congestion regurgitation Pulmonary oedema Cardiac catheterization  Dilated LA,LV,MR  Pulmonary hypertension  Assessment of coexisting coronary artery disease
  46. 46. TreatmentMedical treatment Moderate severityDefinitive treatment Pts remain symptomatic with medical treatment Progressive radiological cardiac enlargement or echo cardiac evidence of deteriorating LV function Mitral valve replacement/repair
  47. 47. TreatmentAtrial fibrillation Anticoagulant DigoxinHeart failure Diuretics Vasodilators e.g ACEIProphylaxis of infective endocarditis Antibiotics
  48. 48. TreatmentMitral valve repair MVP More advantage > MV replacement Prevent irreversible LV damage Those with CAD-CABG + MV repair by inserting annuloplasty ring to overcome annular dilation & to bring the valve leaflets closer together
  49. 49. Aortic valve disease disease Aortic valve
  50. 50. Aortic stenosis 2nd most frequently affected by rheumatic fever Commonly both mitral & aortic valves are affected In elderly structurally normal TV; similar process of arthrosclerosis in arterial wall Haemodynamically significant AS develops slowly Age 30-60 rheumatic fever 50-60 bicuspid AV 70-90 degenerative AS
  51. 51. Aortic stenosis(AS)CausesInfants,children,adolscents Congenital AS Congenital subvalvular AS Congenital supravalvular ASYoung adults and middle-aged Calcifications and fibrosis congenital bicuspid aortic valve Rheumatic ASMiddle-aged to elderly Senile degenerative aortic stenosis Calcifications of bicuspid aortic valve Rheumatic AS
  52. 52. PathophysiologySteadily increase pressure gradient across the AV LV increasingly hypertrophied Inadequate coronary blood flow Angina
  53. 53. Pathophysiology Fixed outflow obstruction limit the increase in CO required by exercise Effort related hypotension SyncopeLV can no longer overcome outflow obstruction Pulmonary oedema
  54. 54. Clinical featuresSymptoms SignsMild to moderate-  Slow rising carotid pulse asymptomatic  Narrow pulse pressure Exertional dyspnoea  Thrusting apex beat(LV Angina overload) Exertional syncope  Harsh ejection systolic Sudden death murmur Episodes of acute  Soft S2 pulmonary oedema  Signs of pulmonary venous congestion(crepitations,pul monary oedema)
  55. 55. InvestigationsECG Doppler  Severity of stenosis LVH LBBB  Detection ofCXR associated aortic Normal regurgitation Enlarged LV Cardiac catheterization Dilated ascending aorta(PA )  Assessment of coexisting Calcified valve(lateral) coronary artery disease  Pressure gradient b/t LV &Echo aorta calcified valve with CT/MRI restricted opening  Degree of valve Hypertrophied LV calcification & stenosis
  56. 56. ManagementAsymptomatic Under reviewSymptomatic –prompt surgery Moderately severe/ severe stenosis yearly doppler echo Pts remain symptomatic with medical treatmentElderly –relatively benign prognosis-medical treatment
  57. 57. ManagementAV replacement Severe stenosis with symptoms Asymptomatic - careful exercise test;symptoms on moderate exertionValloon valvuloplasty congenital AS no long term value in elderly pts with calcified ASAnticoagulants AF Coexisting mitral valve disease Valve replacement with mechnical prosthesis
  58. 58. Aortic stenosis in old patients Most common form Syncope,angina,heart failure Low pulse pressure Surgery –successful in those aged 80 without co-morbid condition higher operative mortality Prognosis without surgery is poor if pt has symptoms Valve replacement –bioprosthetic valve
  59. 59. Aortic regurgitationAetiology Congenital Bicuspid or disproportionate cuspsAcquired Rheumatic disease Infective endocarditis Trauma Aortic dilatation(marfan’s syndrome,aneurysm,dissectionsyphillis,ankylosing spondylitis
  60. 60. Clinical featuresSymptomsMild- moderate AR Often asymptomatic Awareness of heart beatSevere AR Breathlessness Angina
  61. 61. Clinical featuresSigns Murmur Pulse  Early diastolic murmur Large or collapsing pulse  Systolic murmur(stroke Low diastolic pressure&  volume) pulse pressure ,Bounding  Austin flint murmur(soft peripheral pulses mid-diastolic murmur Capillary pulsations in nail Other signs beds Displaced,heaving apex Femoral bruit(pistol shot)- beat duroziez’s sign pre-systolic impulse Head nodding with pulse 4th heart sound De Musset ‘s sign pulmonary venous congestion
  62. 62. InvestigationsECG Doppler Initially normal  detects reflux Later LVH T wave inversion Cardiac catheterization  Dilated LVCXR  Aortic regurgitation Cardiac dilation  Dilated aortic root Features of left heart  Presence of coexisting CAD failureEcho Dilated LV Hyperdynamic LV Fluttering anterior mitral leaflet
  63. 63. ManagementTreat the underlying conditions Aortic valve replacement ± aortic root replacement & CABG symptomaticChronic AR without symptoms s/report if symptoms are developed Annually f/up with echocardiogramAVR if evidence of increasing ventricular size If systolic dimension ≥55mmLV dilationControl BP Nefidipine/ACEI
  64. 64. Tricuspid valve diseaseTricuspid valve Disease
  65. 65. Tricuspid stenosis Rheumatic in origin <5% Always association with mitral & aortic valve disease Isolated TV stenosis very rare TS & TR features of carcinoid syndrome
  66. 66. Clinical features and investigations Symptoms of associated mitral & aortic valve disease Symptoms of right heart failure Raised JVP with a prominent a wave A slow y descent due to loss of normal rapid RV filling A mid-diastolic murmur at LLSE or RLSE High pitch > murmur of MS Increased by inspiration Hepatomegaly Presystolic pulsation (large a wave) Peripheral oedema Echo & Doppler ;similar appearance of mitral stenosis
  67. 67. Tricuspid regurgitationCausesPrimary Rheumatic heart disease Endocarditis Ebstein’s congenital anomalySecondaryRv dilatation( chronic LHFRV infarctionPulmonary hypertension( corpulmonale)
  68. 68. Clinical features Non-specific symptoms Tiredness Venous congestion A large systolic phase in JVP A cv wave replace normal x descent PSM at LSE Systolic pulsation of the liver
  69. 69. InvestigationsEchocardiogram Dilation of the RV Thickened valve Vegetations in endocarditis Ebstein’s anomaly TV displaced towards the RV apex with consequent enlargement of the RA associated with TR
  70. 70. Management Correct RV overload Normal pulmonary artery tolerate tricuspid reflux well valve damage dut to IE not always needs valve replacement repair of the valve with annuloplasty to bring the leaflets together in patients undergoing MVR those with rheumatic damage m/require Tricuspid valve replacement
  71. 71. Pulmonary Valve disease Pulmonary valve Disease
  72. 72. Pulmonary stenosisCauses Carcinoid syndrome Usually congenital Isolated or associated with other abnormalities e.g TOF
  73. 73. Clinical features ESM at left upper sternum Radiation to left shoulder Thrill Preceded ejection click Wide split S2 Loud harsh murmur inaudible P2  RV heave Prominent a wave in JVP
  74. 74. InvestigationsECG RVHCXR Post-stenotic dilation in the pulmonary arteryDoppler echo
  75. 75. Management Mild to moderate isolated pulmonary stenosis Not usually progress Not required treatment Low risk for IE Severe Pulmonary stenosis ( resting gradient >50mmHg with normal CO) Percutaneous pulmonary balloon valvuloplasty Not available;surgical valvotomy Long term results very good Post operative pulmonary regurgitation is common Benign
  76. 76. Pulmonary regurgitation Rarely an isolated phenomenon Usually associated with pulmonary artery dilatation due to pulmonary hypertension EDM at LSE in MS( Graham steel murmur) Pulmonary hypertension 2 to other disease of left heart primary pulmonary vascular disease Eisenmenger’s syndrome Trivial PR frequent doppler finding in normal individuals
  77. 77. Sample Questions