1. VALVULAR HEART DISEASES
Col. Samina Waqar

2. VALVULAR HEART DISEASES
Normal Anatomy:

3. VALVULAR HEART DISEASES
Stenosis/ Regurgitation: intrinsic disease damage to the supporting structure
Congenital:
Acquired:
Stenosis of aotic or mitral valve
2/3- valvular diseases
Functional regurgitation:
Abnormality of supporting structures
Dilation- right/left ventricle, dilated- pulmonary artery/aorta

4. VALVULAR HEART DISEASES
Clinical consequences:
Depends upon:
Valve involved
Degree of impairment
Rate of impairment
Rate and quality of compensatory mechanism
e.g Infective endocarditis produces severe, rapid and fatal aortic regurgitation. Rheumatic mitral stenosis is indolent and well tolerated. Pregnancy complicates valvular disease by increasing demands on heart.

5. VALVULAR HEART DISEASES
Valve degeneration associated with calcification:
Calcific aortic stenosis
Bicuspid valve stenosis(congenital)
Mitral valve prolapes
RHD (Rheumatic Heart Disease)
Endocarditis:
IEC (Infective endocarditis)
NBTE (Non bacterial thrombotic endocarditis)
LSE (Libman Sacks endocarditis

6. VALVULAR HEART DISEASES
Aortic stenosis:
Senile calcific aortic stenosis
Bicuspid aortic valve
Mitral annular calcification

7. CALCIFIC AORTIC STENOSIS
Age related: 7th, 8th decade senile calcific aortic stenosis
Stenotic bicuspid valve: 5th- 7th decade
Functional area decreases
Non Rheumatic, Rheumatic
Left ventricular hypertrophy

8. Calcific aortic stenosis
Pathogenesis:
Accumulation of hydroxyapatite
Wear and tear
Chronic injury due to hyperlipidemias, hypertention and/or inflammation
Osteoblast like cells- synthesize –bone matrix protein.
Causes outflow obstruction

9. MITRAL LEAFLET PROLAPSE
Myxomatous degeneration of mitral leaflets
Attenuation of outer fibrosa core
Increase in inner spongiosa core
Etiology? Marfans syndrome: fibrillin mutation leading to dysregulation of TGF-b
Valve surgical correction
Complication- mitral insufficiency, IE, stroke

10. VALVULAR HEART DISEASES
RHEUMATIC HD:

11. RHEUMATIC FEVER & RHEUMATIC HEART DISEASE (RHD)
DEFINITION
“ACUTE IMMUNOLOGICALLY MEDIATED MULTISYSTEM INFLAMMATORY DISEASE THAT OCCURS A FEW WEEKS AFTER AN EPISODE OF GROUP- A, ß – HAEMOLYTIC STREPTOCOCCAL PHARYNGITIS AND OFTEN INVOLVES HEART”

12. PATHOLOGY OF RHEUMATIC HEART DISEASE
AETIOLOGY
INFECTIVE ELEMENT
PERSONAL SUSCEPTIBILITY
SOCIAL DISTRIBUTION

13. MAJOR MANIFESTATIONS MIGRATORY POLYARTHRITIS-LARGE JOINTS CARDITIS
SUBCUTANEOUS NODDULES
ERYTHEMA MARGINATUM – SKIN
SYDENHAM’S CHOREA

14. MINOR MANIFESTATIONS FEVER ARTHRALGIA INCREASED ESR LEUKOCYTOSIS
C – REACTIVE PROTEIN
ECG CHANGES: PROLONGED P- R INTERVAL

15. JONE’S CRITERIA FOR DIAGNOSIS OF RF
REQUIRES TWO MAJOR FEATURES OR ONE MAJOR AND TWO MINOR FEATURES PLUS RAISED ANTI-STREPTOCOCCAL ANTIBODY LEVELS (ANTI-STREPTOLYSIN O TITRE) OR POSITIVE THROAT CULTURE FOR GROUP A, ß-HEMOLYTIC STREPTOCOCCUS

16. PATHOGENESIS EXACT- UNKNOWN IMMUNE REACTION
HYPERSENSITIVITY REACTION TO GROUP A, ß-HEMOLYTIC STREPTOCOCCUS
ABSENCE OF STREPTOCOCCI –LESIONS
ANTIBODIES AGAINST M-PROTEINS
CROSS REACTION WITH TISSUE GLYCOPROTEINS
AUTOIMMUNITY
GENETIC SUSCEPTIBILITY

17. P A T H O G E N E S I S - R H E U M A T I C H E A R T D I S E A S E

18. PATHOLOGY OF RHEUMATTIC HEART DIEASE
ACUTE R.H.D – HEART (Pancarditis)
PERICARDIUM
MYOCARDIUM
ENDOCARDIUM

19. MORPHOLOGY ACUTE RHEUMATIC FEVER MYOCARDITIS
ASCHOFF BODIES – FIBRINOID NECROSIS, T-LYMPHOS, PLASMA CELLS, MACROPHAGES AND GIANT CELLS.
ANTISCHKOW CELLS (CATERPILLAR) ASCHOFF giant cells
PERICARDITIS – BREAD AND BUTTER

20. MORPHOLOGY (Contd) ENDOCARDITIS LEFT ATRIUM MacCALLUM PLACQUES
SMALL VEGETATIONS ALONG LINE OF CLOSURE – VALVES
LEFT ATRIUM MacCALLUM PLACQUES

21. RHEUMATIC HEART DISEASE (RHD)
ACTIVE LESION
EXUDATIVE LESION
COLLAGEN DEGENERATION
OEDEMA
CELLULAR INFILTRATE
ASCHOFF BODY
HEALED LESION
FIBROSIS
MYXOMATOUS CHANGES
CALCIFICATION

22. MORPHOLOGY-CHRONIC RHD
SOLITARY MITRAL VALVE (65-70%)
LEAFLETS THICKENING, COMMISSURAL FUSIONS AND SHORTENING, THICKENING AND FUSION OF TENDINOUS CORDS (FISH-MOUTH APPEARANCE)
AORTIC/MITRAL VALVE (20-25%)
TRICUSPID & PULM. VALVE (RARE)
DILATATION OF LEFT ATRIUM
MURAL THROMBUS

23. CLINICAL FEATURES 10-42 DAYS AFTER PHARYNGITIS
MOSTLY CHILDREN (5-15 YEARS)
MIDDLE AGED 20%
MIGRATORY POLYARTHRITIS
TACHYCARDIA, ARRHYTHMIA
PERICARDIAL RUB
RAISED ASOT

24. EFFECTS / COMPLICATIONS
VALVULAR STENOSIS / DEFORMITY
LEFT ATRIAL DILATATION / HYPERTROPHY
ATRIAL FIBRILLATION
MURAL THROMBUS – EMBOLISM
CHRONIC CONGESTION OF LUNG
RIGHT VENTRICULAR HYPERTROPHY & CHF
INCREASED RISK OF IE
ADHESIVE PERICARDITIS

25. CAUSES OF DEATH IN RHEUMATIC HEART DISEASE
CARDIAC FAILURE
BACTERIAL ENDOCARDITIS
EMBOLISM

26. VALVULAR HEART DISEASES
BACTERIAL ENDOCARDITIS:

27. Figure Diagrammatic comparison of the lesions in the four major forms of vegetative endocarditis. The rheumatic fever phase of RHD (rheumatic heart disease) is marked by a row of small, warty vegetations along the lines of closure of the valve leaflets. IE (infective endocarditis) is characterized by large, irregular masses on the valve cusps that can extend onto the chordae (see Fig ). NBTE (nonbacterial thrombotic endocarditis) typically exhibits small, bland vegetations, usually attached at the line of closure. One or many may be present (see Fig ). LSE (Libman-Sacks endocarditis) has small or medium-sized vegetations on either or both sides of the valve leaflets.
Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 27 October :48 AM)
© 2005 Elsevier 27

28. VEGETATIVE ENDOCARDITIS
INFECTIVE ENDOCARDITIS
NON INFECTIVE ENDOCARDITIS
NON BACTERIAL THROMBOTIC
ENDOCARDITIS
ENDOCARDITIS ASSOCIATED WITH SYSTEMIC LUPUS ERYTHEMATOSUS

29. INFECTIVE ENDOCARDITIS (IE)
DEFINITION
“ Characterized by colonization or invasion of the heart valves, the mural endocardium or other cardiovascular sites by a microbiologic agent, leading to the formation of bulky, friable vegetations composed of thrombotic debris and organisms, often associated with destruction of the underlying cardiac tissues.”

30. INFECTIVE ENDOCARDITIS (IE) (Contd)
TYPES
ACUTE INFECTIVE ENDOCARDITIS HIGHLY VIRULENT ORGANISMS, NORMAL HEART
SUBACUTE INFECTIVE ENDOCARDITIS LOW VIRULENT ORGANISMS, ABNORMAL HEART

31. CAUSES AND PATHOGENESIS -IE
PREDISPOSING FACTORS
RHEUMATIC HEART DISEASE
CONGENITAL HEART DISEASES
MYXOMATOUS MITRAL VALVE
DEGENERATIVE CALCIFIC VALVULAR STENOSIS
BICUSPID AORTIC VALVE
PROSTHETIC VALVE
VASCULAR GRAFTS

32. OTHER RISK FACTORS-IE NEUTROPENIA IMMUNODEFICIENCY DIABETES MELLITUS
ALCOHOL
INTRARENOUS DRUG ABUSE
INDWELLING VASCULAR CATHETERS

33. CAUSATIVE ORGANISMS-IE
STREPTOCOCCUS VIRIDANS (alpha-HAEMOLYTICUS) - 50 to 60 %
STAPHYLOCOCCUS AUREUS -10 to 20 %
STAPHYLOCOCCUS EPIDERMIDUS – PROSTHETIC VALVE
HAEMOPHILUS INFLUNENZAE, ACTINOBACILLUS, CARDIOBACTERIUM, EIKENELLA, KINGELLA - (HACEK)
FUNGI
CHLAMYDIA
RICKETTSIA

34. SOURCE OF INFECTION-IE
DENTAL/SURGICAL PROCEDURES
CONTAMINATED INJECTIONS
OCCULT SOURCE: GUT, ORAL CAVITY, TRIVIAL INJURIES & INFECTED SITES

35. CULTURE NEGATIVE ENDOCARDITIS (10%)
PRIOR ANTIBIOTICS THERAPY
IMPROPER TIMINGS – BLOOD SAMPLING
DIFFICULTIES IN ISOLATION
DEEPLY EMBEDDED ORGANISMS

36. MOROPHOLOGY -IE
ACUTE IE - BULKY, FRIABLE, IRREGULAR VEGETATIONS ON VALVE CUSPS AND CORDS
SUBACUTE IE - SMALLER VEGETATIONS

37. MOROPHOLOGY –IE (Contd)
NONVALVULAR IE - VEGETATIONS DOWNSTREAM
WITH PROSTHETIC VALVES - RING ABSCESSES
WITH I/V DRUG ABUSE – RIGHT SIDED VALVE

38. CLINICAL FEATURES-IE FEVER, CHILLS FATIGUE LOSS OF WEIGHT MURMURS(90%)
PETECHIAE
SUBUNGUAL HAEMORRHAGES
ROTH SPOTS-EYES

39. COMPLICATIONS-IE CARDIAC COMPLICATIONS
VAVULAR INSUFFICIENCY / STENOSIS
MYOCARDIAL RING ABSCESS
PERFORATION-AORTA & INTERVENTRICULAR SEPTUM
SUPPURATIVE PERICARDITIS
DEHISCENCE WITH PARAVALVULAR LEAKS

40. EMBOLIC COMPLICATIONS - IE
LEFT SIDED LESIONS
CEREBRAL INFARCT, BRAIN ABSCESS, MENINGITIS, MI, SPLENIC ABSCESS & RENAL ABSCESS
RIGHT SIDED LESIONS PULMONARY INFARCT, LUNG ABSCESS AND PNEUMONIA

41. RENAL COMPLICATIONS -IE
RENAL INFARCT
FOCAL AND DIFFUSE GLOMERULONEPHRITIS
MULTIPLE RENAL ABSCESSES