Infective Endocarditis(IE) Is due to bacterial or fungal infection of the heart valves (endocardium). Characterized by: Formation of bulky, friable,easily detached and infected vegetations. Damage to heart Valves and Chorda tendinae perforation, ulceration, destruction (causes valve dysfunction)

1. 1
Vegetations

2. 2
Infective Endocarditis
(IE)
• Is due to bacterial or fungal infection of the
heart valves (endocardium).
• Characterized by:
1. Formation of bulky, friable,easily detached
and infected vegetations.
2. Damage to heart Valves and Chorda tendinae
• perforation, ulceration, destruction
(causes valve dysfunction)

3. 3
Infective Endocarditis
• Classification: based on clinical course
– Acute infective endocarditis:
• Is infection of a normal valve
• Caused by virulent organisms e.g. S. aureus.
• Affected valve rapidly destroyed
– Subacute infective endocarditis:
• Is less fulminant disease
• Caused by less virulent organisms e.g.Strep.
viridans
• Infects structurally abnormal valve

4. 4
Infective Endocarditis
Predisposing conditions
1. Transient bacteremia:
due to
– Dental and surgical
procedures
– Urinary
catheterization
– GI endoscopy
• *Prophylactic
antibiotic
recommended
2. Intrvenous drug abuse
(IVDA)
3. Prosthetic heart valve
4. Injury to colon, Ca colon
5. Indwelling venous
catheter
6. Congenital heart disease
with jet streams
7. Chronic RHD
8. Mitral valve prolapse

5. 5
Infective Endocarditis
• Etiology:
– Streptococcus viridans
• MC overall cause of IE
– Staph.aureus
• MCC of IE in IVDA
– Staph.epidermidis:
• MC cause of IE due to prosthetic devices
– Strep.bovis:
• MC cause of IE in ulcerative colitis or
colorectal cancer

6. 6
Infective Endocarditis
• Pathogenesis:
– Bacteremia  seeding of a normal or damaged
valves  inflammation  injury  platelets+
fibrin accumulate  VEGETATIONS.
– S. aureus
• infects normal or damaged valves
– Strep. viridans
• infects damaged valves

7. 7
Infective Endocarditis
• Valves involved
– Mitral valve:
• Most common overall valve involved
in IE
– Tricuspid valve and aortic valve:
• MC valves involved in IE due to
IVDA

8. 8

9. 9
Valvular destruction

10. 10
Infective Endocarditis: Clinical
findings
1. Large, friable vegetations can embolize
– Producing abscess and infarctions in distant
sites (e.g. embolic stroke, splenic and kidney
infarcts etc.)
2. Valve destruction leads to
– regurgitation murmurs and CHF.
3. Extension of infection into heart ( abscess)
4. Fever:
– Is the most consistent sign
5. Splenomegaly.

11. 11
Roth’s spot

12. 12
Splinter hemorrhages

13. 13
Janeway lesion
Osler’s node
Osler’s node
Osler’s node

14. 14
Infective Endocarditis: Clinical findings
• Immune complex vasculitis
– Roth’s spot (hemorrhages) in retina
– Splinter hemorrhages in nail beds
– Osler’s node (painful) on hands and feet
– Janeway lesions hand and feet (painless)
– Glomerulonephritis
• Hematuria and RBC casts
• Lab:
– positive blood culture in majority of cases

15. 15
Mitral valve from a patient with +ve ANA

16. 16
Libman-Sacks endocarditis
• Associated with SLE
• Involves mitral valve
• Sterile vegetations with fibrinoid necrosis.
– Do not embolize
• Vegetations located all over the valve unlike in
rheumatic fever
• Usually not clinically significant
• Can cause valve deformity and MR.

17. 17
Aortic valve: Patient had
adenocarcinoma of colon
Mitral valve: Patient had
adenocarcinoma of pancreas

18. 18
Nonbacterial thrombotic endocarditis
(NBTE)
(aka: Marantic Endocarditis)
• Is a paraneoplastic syndrome.
• Characterized by
– Sterile, nondestructive vegetations on the
mitral valve
• Procoagulant effect of circulating mucin
from mucin producing cancers of colon and
pancreas
• Complications:
– Embolization***
– May be secondarily infected

19. 19
Diseases of Myocardium

20. 20
Myocarditis
• Inflammation of myocardium associated with
myocyte necrosis and degeneration.
• MC seen in children (1-10 years age).
• Etiology:
1. Microbial pathogens
1. Coxsackievirus B (MCC)****
2. Trypanosoma cruzi (Chagas disease)
– Leishmanial form infects cardiac muscle
• Borrelia burgdorferi, Diptheria etc
– Non infectious causes:
• Acute RF, drugs (doxorubicin), SLE etc

21. 21
Lymphocytes
Myocytes

22. 22

23. 23
Myocarditis
• Pathology:
– Endocardial biopsy done if infection is
suspected
• Focal myocyte necrosis
• A lymphocytic infiltrate is highly predictive
of coxsackievirus**
• Clinical findings:
– Asymptomatic or may have symptoms
• Fever, chest pain, arrhythmias.
– Most eventually develop CHF
• Labs:Increased troponins and CK-MB.

24. 24
Cardiomyopathy

25. 25
Cardiomyopathy
• Definition:
• Group of non-inflammatory diseases that
primarily involve the myocardium and
produce myocardial dysfunction.
• Usually present with heart failure and
arrhythmias.
• Treatment: cardiac transplant.
• Three types of cardiomyopathies:
1. Dilated (congestive) (MC type)
2. Hypertrophic
3. Restrictive

26. 26
Cardiomyopathy
Due to infiltration of myocardium by different
substances.
Results in impaired ventricular filling.
Causes: amyloidosis and hemochromatosis.
Restrictive
Characterized by: Asymmetric interventricular
septal hypertrophy
Resulting in: left ventricular outflow obstruction.
Hypertrophic
All four chambers are dilated, and there is also
hypertrophy.
Causes: chronic alcoholism, previous viral
myocarditis, pregnancy etc.
Dilated
(Congestive)
FindingsType of CMP

27. 27

28. 28
Dilated Cardiomyopathy (DCM)
• Is the most common cardiomyopathy*
• Is characterized by gradual four chamber
dilation resulting in systolic failure  CHF
• Etiology:
– Idiopathic (in most cases)
– Alcohol toxicity: direct toxic effect or
thiamine deficiency
– Previous myocarditis (Coxsackie MCC)
– Drugs: Doxorubicin, cocaine
– Postpartum state

29. 29
Dilated Cardiomyopathy
• Pathophysiology:
– Decreased contractility with a decreased
Ejection fraction (EF) (<40%)
• Clinical findings:
– Global enlargement of heart
• All chambers are dilated
• Echo shows poor contractility
• X ray shows : cardiomegaly
– Present with
• Progressive Left and right heart failure
– Complications:
• Bundle branch block and atrial and
ventricular arrhythmias

30. 30

31. 31
1
3
2
4

32. 32
Hypertrophic cardiomyopathy (HCM)
• Synonyms:
– Asymmetrical septal hypertrophy,
– Idiopathic hypertrophic subaortic stenosis.
• Characterized by:
– Asymmetrical cardiac hypertrophy
– Most prominent in the interventricular septum
• Epidemiology:
– Most common cause of sudden death in young
athletes**

33. 33
Hypertrophic cardiomyopathy (HCM)
• Etiology:
– Familial form:
• Autosomal dominant (>50%)
• Occurs in young individuals
• Due to mutation in genes coding for
– beta myosin heavy chain**
– Myosin binding protein
– Troponin T.
– Sporadic form:
• Occurs in elderly

34. 34
Left ventricular
hypertrophy
Asymmetrical
septal
hypertrophy
Myofiber disarray

35. 35
Hypertrophic cardiomyopathy (HCM)
• Gross:
– Asymmetrical cardiac hypertrophy
– Most prominent in the interventricular
septum
• Micro:
– cardiac microfiber hypertrophy and
disarray
– (normally myofibers have parallel
arrangement).

36. 36
Hypertrophic cardiomyopathy (HCM)
• Pathophysiology:
– Obstruction of blood flow is below aortic valve
• Anterior leaflet of mitral valve is drawn against
the asymmetrically hypertrophied septum as
blood exits LV  decreased CO
– Aberrant myofibers and conduction system in IVS
• Conduction disturbances*** are responsible for
sudden death.
– Decreased diastolic filling
• Muscle thickening restricts filling
• Management:
– Anything that increases preload improves
symptoms
– Ex: Lying down, Beta blockers, Ca channel blocker

37. 37
Restrictive cardiomyopathy
• Characterized by restricted ventricular filling leading
to reduced CO.
• Etiology:
– Infiltrative disease
• Pompe’s glycogenosis* , amyloidosis*
,hemochromatosis*,
– Endocardial fibroelastosis in a child *
• thick fibroelastic tissue in the endocardium
• MC disease causing restrictive CDM in children
• Need a heart transplant.
– Tropical endomyocardial fibrosis
• Most common cause worldwide

38. 38
Fibrous thickening of the endocardium.
Endocardial Fibroelastosis

39. 39
Amyloidosis

40. 40
Hemochromatosis
Normal myocardium Pompe’s disease
Myocardial fibers
full of glycogen

41. 41
Restrictive cardiomyopathy
• Pathophysiology
– Decreased ventricular compliance
• Non compliant heart- can not fill properly.
• Clinical findings:
– Arrhythmias (conduction defect), CHF

42. 42
Pericardial disorders

43. 43
Pericardial disorders
• Normal pericardium:
– lubricates the surface of heart
– Prevents deformation/dislocation
– Acts as barrier to spread of infection.
• Pericardial cavity:
– contains 50 ml of fluid.
• Three pericardial disorders:
1. Acute pericarditis
2. Pericardial effusion
3. Constrictive pericarditis

44. 44
Acute Pericarditis
• Inflammation of pericardium.
• Etiology:
– Secondary to
• MI*, Acute RF* ,Surgery*, infections.
• Coxsackie MC overall cause*.
– Other causes:
• Diptheria toxin, drugs (doxorubicin), SLE*
• Acute pericarditis is very often associated with
pericardial effusion*

45. 45
Acute Pericarditis
• Depending on nature of fluid accumulated acute
pericarditis can be classified into:
– Fibrinous pericarditis (MC type)*
• MI, Acute RF, uremia
– Serous pericarditis
• SLE, viral infection
– Purulent pericarditis
• Bacterial infections
– Hemorrhagic pericarditis
• Tumors, bacterial infections

46. 46
Pericarditis
Fibrinous pericarditis: characterized by
– Accumulation of exudate rich in fibrin
– Aka Bread and butter pericarditis
– Often associated with pericardial effusion
– Healing with fibrous tissue and calcification
can cause adhesions leading to constrictive
pericarditis.

47. 47

48. 48
Acute Pericarditis
• Clinical findings:
– Precordial chest pain:
• Pain relieved – leaning forward
• Pain increases – inspiration
– Pericardial friction rub
• Scratchy sound.
– Pericardial effusion
• Muffled heart sound
• Cardiac tamponade
– Raised JVP
– Increased neck vein distension during inspiration
(Kussmaul’s sign)
– Reduced cardiac output

49. 49
Constrictive pericarditis
• Is chronic fibrosing disease of the pericardium
– Compresses the heart and restricts inflow
• Pathology:
– It results due to healing process after acute
pericardial injury.
– Pericardium becomes thick, fibrous and
calcified.
– Pericardial space obliterated and layers of
pericardium fuse.
• Etiology:
– TB is MCC worldwide
– In US most cases are idiopathic

50. 50
Constrictive pericarditis
The pericardial space:
obliterated
Heart : encased in a fibrotic
, thickened pericardium

51. 51
Constrictive pericarditis
• Pathophysiology:
– Incomplete filling of cardiac chambers
• Due to thickening of parietal pericardium
• Decreased CO
– Pericardial knock
• Due to ventricles hitting the thickened
parietal pericardium

52. 52
Tumors of the heart

53. 53
Tumors of the heart
• Epidemiology:
– Metastasis to heart is more common than
primary tumors
• Example: cancer lung, breast, malignant
melanoma*.
– Pericardium is the most common site for
metastasis
• Leads to pericarditis and effusions

54. 54

55. 55
Primary tumors of heart
1. Cardiac myxomas
2. Rhabdomyomas

56. 56
Atrial
Myxoma

57. 57
Cardiac myxomas
• Most common primary heart tumor in adults*
• Pathology:
– Benign primary mesenchymal tumor
– ~ 90% arise from the left atrium*
– Sessile or pedunculated
– “Ball-valve” effect*
• Due to blockage of mitral valve orifice
• Blocks diastolic filling of left ventricle, simulating
mitral valve stenosis
• Clinical findings:
– Fever, fatigue,malaise,anemia
• Complications:
– Embolization, syncopal episodes

58. 58
Cardiac Rhabdomyoma
• MC primary tumor of heart in infants and
children*
– Major association with tuberous sclerosis*
• Arise from heart muscle