1. Pathology of Cardiovascular System Lectures Valvular Diseases; Rheumatic Heart Disease, Endocarditis & Myocarditis
Dr. Samir Al Bashir, MD.

2. Valve Diseases Manifested by:
- Stenosis:- failure of the valve to open completely, obstructing forward blood flow.
- Insufficiency:- failure of the valve to close completely so allowing Regurgitation (reverse flow).
The disorder can be: a. pure b. mixed
The disorder can be: a. isolated b. combined.

3. Valve abnormalities produce abnormal heart sounds called murmers.
Valve abnormalities can be :-
- Congenital or – acquired.
The most common abnormalities are acquired stenosis of the mitral and aortic valves.
The stenosis is almost always due to primary cusp abnormality and is always a chronic process.
The regurgitation is either due to cusp abnormality or disease of the supporting structures like papillary muscles or the chordae tendinae and can be acute or chronic.

4. Acute Rheumatic Fever
Definition: Rheumatic fever is an acute, immunologically mediated, multi-system inflammatory disease - follows an episode of group A beta-hemolytic streptococcal pharyngitis after an interval of a few weeks.
Epidemiological studies and patient history
Serological studies: elevated levels of antibodies to streptococcal enzymes (streptolysin O and DNAse B).
Definition
Rheumatic fever is an acute, immunologically mediated, multi-system inflammatory disease that follows, after (10 days to 6 weeks), an episode of group A beta-hemolytic streptococcal pharyngitis
Occurs in only 3% of patients with group A streptococcal pharyngitis. So, genetic susceptibility that regulates the hyper sensitivity reaction is suspected.
Peak incidence: ages of 5-15 years.
The incidence has declined in the developed world because of improvement in diagnosis and treatment
But In the 3rd world countries and in crowded, economically depressed urban areas in the western world, rheumatic fever remain a major health problem.
Affects large joints causing Arthritis.
Affects the heart during its acute phase  acute rheumatic carditis
after many years may cause chronic valvular deformities

5. Acute Rheumatic Fever
Occurs in only 3% of patients with group A streptococcal pharyngitis.
Peak incidence: ages of 5-15 years.
Incidence declined over the past 30 years
Heart during acute phase  acute rheumatic carditis  after many years may cause chronic valvular deformities.
It also affects large joints causing Arthritis.
Definition
Rheumatic fever is an acute, immunologically mediated, multi-system inflammatory disease that follows, after (10 days to 6 weeks), an episode of group A beta-hemolytic streptococcal pharyngitis
Occurs in only 3% of patients with group A streptococcal pharyngitis. So, genetic susceptibility that regulates the hyper sensitivity reaction is suspected.
Peak incidence: ages of 5-15 years.
The incidence has declined in the developed world because of improvement in diagnosis and treatment
But In the 3rd world countries and in crowded, economically depressed urban areas in the western world, rheumatic fever remain a major health problem.
Affects large joints causing Arthritis.
Affects the heart during its acute phase  acute rheumatic carditis
after many years may cause chronic valvular deformities

6. Rheumatic Fever Diagnosis
Evidence of recent infection + 2 or more Jones criteria:
Migratory large joint polyarthritis
Pancarditis
Subcutaneous nodules
Erythema marginatum of skin
Sydenham’s chorea
Fever, arthralgias, ECG changes, raised CRP etc…

7. Acute Rheumatic Fever Pathogenesis
It is a hypersensitivity reaction induced by group A streptococci.
Antibodies directed against the M proteins of group A streptococci cross-react with normal proteins in the tissues, leading to tissue damage.
Alternatively, rheumatic fever may result from an immune response against the offending bacteria.
Pathogenesis
1- It is strongly suspected that acute rheumatic fever is a hypersensitivity reaction induced by group A streptococci.
2- It is presumed that antibodies directed against the M proteins of group A streptococci cross-react with normal proteins in the tissues, leading to tissue damage.
3- Alternatively it has been proposed that rheumatic fever results from an immune response against the offending bacteria.

8. Acute Rheumatic Fever Pathology
Inflam. infiltrates in many tissues: synovium, joints, skin, and heart.
Focal fibrinoid necrosis provokes inflam. response
Fibrosis is common especially in cardiac tissues.
Blood cultures are sterile.
Pathogenesis
1- It is strongly suspected that acute rheumatic fever is a hypersensitivity reaction induced by group A streptococci.
2- It is presumed that antibodies directed against the M proteins of group A streptococci cross-react with normal proteins in the tissues, leading to tissue damage.
3- Alternatively it has been proposed that rheumatic fever results from an immune response against the offending bacteria.

9. Acute Rheumatic Carditis (Pancarditis) inflam
Acute Rheumatic Carditis (Pancarditis) inflam. changes in all layers of the heart
Myocardium
Scattered multiple foci of inflammation “Aschoff Bodies” lie proximate to small vessels.
Consisting of central fibrinoid necrosis surrounded by lymphocytes, and large macrophages (basophilic cytoplasm and vesicular nuclei) known as Anitschkow cells, which may become multinucleated forming Aschoff giant cells (cardiac histiocytes).
Diffuse interstitial inflammatory infiltrates
Acute changes may resolve completely or progress to scarring and chronic valvular deformities.
Acute Rheumatic Carditis (Pancarditis): pathology
Characterized by inflammatory changes in all three layers of the heart.
Multiple foci of inflammation within the heart connective tissue called
Aschoff bodies which is
Consisting of central fibrinoid necrosis surrounded by a collection of lymphocytes, and large macrophages (with basophilic cytoplasm and vesicular nuclei) known as
Anitschow cells.
It may become multinucleated forming Aschoff giant cells (Caterpillar cells or cardiac histiocytes).
Acute changes may resolve completely or progress to scarring and chronic valvular deformities.

10. Acute Rheumatic Carditis (Pancarditis)
Endocardium
Common, may affect any valve, mostly mitral and aortic valves.
Valves are edematous and thickened with foci of fibrinoid necrosis. (Aschoff nodules uncommon).
Formation of small vegetations “fibrinous clots” along the lines of valve closure (Verrucous Endocarditis).
Pericardium
Fibrinous pericarditis, sometime associated with serous or serosanguinous pericardial effusion.
Acute Rheumatic Carditis (Pancarditis): Pathology
In Myocardium we see
1- Scattered Aschoff bodies lie in close proximity to a small vessel.
2- Diffuse interstitial inflammatory infiltrates (may lead to generalized dilation of the cardiac chambers).
In Endocardium
Acute Rheumatic Carditis is Common and may affect any valve, mostly mitral and aortic valve.
1- Valves are edematous and thickened with foci of fibrinoid necrosis. (Aschoff nodules uncommon).
2- Formation of small vegetations “fibrinous clots” along the lines of valve closure (Verrucous Endocarditis).
Pericardial involvement
Fibrinous pericarditis, sometime associated with serous or serosanguinous pericardial effusion.

11. Acute Rheumatic Carditis (Pancarditis): Clinical Manifestations
Symptoms:
Pericardial friction rubs,
Weak heart sounds,
Tachycardia (rapid beating) and
Arrhythmias.
In severe cases: myocarditis  cardiac dilation  functional mitral valve insufficiency or even congestive heart failure.
Symptoms:
Pericardial friction rubs,
Weak heart sounds,
Tachycardia (rapid beating) and
Arrhythmias (irregular heartbeat).
In severe cases: myocarditis  cardiac dilation  functional mitral valve insufficiency or even congestive heart failure.

12. Acute Rheumatic Heart Disease Pathogenesis and Key Morphologic Changes

13. Small vegetations (verrucae) are visible along the line of closure of the mitral valve leaflet.

14. Verrucous Endocarditis in Acute Rheumatic Fever

15. Aschoff Body in Acute Rheumatic Carditis

16. Aschoff Body with “Caterpillar” Nuclei

17. Fibrinous Pericarditis in Acute Rheumatic Fever

18. Chronic Rheumatic Heart Disease
Characterized by irreversible deformity of one or more cardiac valves. Usually mitral valve is abnormal (alone in 70% of cases).
Combined aortic and mitral valve disease is present in another 25% of cases. Aortic valve alone is rarely affected.
Tricuspid and Pulmonic valves are extremely rare to be affected.
Pathological changes:
Chronic scarring and calcification of the valve leaflets, → stiff and thickened structure → stenotic valve orifice and improper closure (regurgitation).
Shortening, thickening and fusion of the chordae tendineae.
Chronic Rheumatic Heart Disease is Characterized by irreversible deformity of one or more cardiac valves.
1- Mitral valve is abnormal in 95% of cases.
2- Combined oartic and mitral valve disease is present in 25% of cases. Aortic valve alone is rarely affected.
3- Pulmonary and Tricuspid valves are extremely rare to be affected.
Clinical manifestations: depend on which valve is involved
1- Cardiac murmurs, Arrhythmia,
2- Hypertrophy, Dilation, Congestive heart failure,
3-Thromboembolic complications and infective endocarditis
Pathological changes:
1- Chronic scarring and calcification of the valve leaflets, which invert the valve into stiff and thickened structure which may lead to:
Valve orifice becomes stenotic
improper closure (regurgitation).
2- Shortening and fusion of the chordae tendineae.

19. Chronic Rheumatic mitral valvulitis
The most common cause of mitral stenosis, it causes stenosis > regurgitation. Females > males.
Mitral Stenosis:
Leaflets are thick, rigid, and inter-adherent. And the orifice is narrowed “fish mouth” deformity.
Dilatation and hypertrophy of left atrium.
Endocardium is thickened above posterior mitral leaflet .
Mitral Regurgitation:
Valve leaflets are retracted.
Left ventricular dilation and hypertrophy (added volume load)
Chronic Rheumatic mitral valvulitis is the most common cause of mitral stenosis
It causes stenosis > regurgitation, and occurs in females > males.
In Mitral Stenosis:
Leaflets are thick, rigid, and inter-adherent.
Mitral orifice is narrowed “fish mouth” deformity.
Dilatation and hypertrophy of left atrium.
Endocardium is thickened above posterior mitral leaflet .
Mural thrombi may be present
Lungs: firm and heavy (result of chronic passive congestion).
In Mitral Regurgitation:
Valve leaflets are retracted
Left ventricular dilatation and hypertrophy.

20. Mitral valve, rheumatic mitral stenosis - diffuse fibrous thickening & distortion of valve leaflets, commissural fusion (arrow) "fish mouth" shape.

21. Chronic Aortic Valvulitis
Males > females and usually associated with mitral valvulitis.
May occur in congenital bicuspid aortic valve (2%)
Aortic stenosis:
Valve cusps are thickened, firm and adherent to each other  the aortic valve orifice is reduced to a rigid triangular channel.
Aortic stenosis increases the pressure load on left ventricle causing hypertrophy.
Subsequent left ventricular failure is associated with dilation of the chamber.
Chronic Aortic Valvulitis Occurs in Males > females and usually associated with mitral valvulitis.
Aortic stenosis:
Valve cusps are thickened, firm and adherent to each other  the aortic valve orifice is reduced to a rigid triangular channel.
Aortic stenosis increases the pressure load on left ventricular causing hypertrophy.
Subsequent left ventricular failure is associated with dilation of the chamber.

22. Surgically removed specimen of rheumatic aortic stenosis demonstrating thickening and distortion of the cusps with commissural fusion (rigid triangular channel)

23. Calcific Aortic Stenosis (degenerative calcific aortic stenosis)
Degenerative changes in the cardiac valves are part of normal aging process, but it can develop into pathologic stenosis.
Leaflets are rigid and deformed by fibrosis and calcified masses, leading to valve sclerosis.
It differs from rheumatic aortic stenosis by:
The calcium deposits lie behind the valve cusps.
The free edges of the cusps are usually not affected.
Calcific stenosis does not fuse the cusps.
Symptom: severe cases may cause angina, syncope (fainting), congestive heart failure, L.V. hypertrophy, and sudden death due to arrhythmia.
Calcific Aortic Stenosis or (degenerative calcific aortic stenosis DCAS)
1- Part of normal aging process is degenerative changes in the cardiac valves but it can develop to cause pathologic stenosis.
2- The aortic valve leaflets are rigid and deformed by calcified masses, so fibrosis and calcification of the valve cusps lead to valve sclerosis.
3- The calcium deposits lie behind the valve cusps (at the bases of the cusps).
4- The free edges of the cusps are usually not affected.
5- Calcific stenosis does not fuse the cusps.
Symptom: severe cases may cause angina, syncope (fainting), congestive heart failure, L.V. hypertrophy, sudden death due to arrhythmia.

24. Degenerative calcific aortic stenosis of a normal valve having three cusps. Nodular masses of calcium are heaped up within the sinuses of Valsalva (arrow). The commissures are not fused.

25. Mitral Valve Prolapse
Primary form of myxomatous degeneration of mitral valve
Common cardiac disorder (up to 3% of adult population).
It is usually an isolated problem but it may arise as a complication of certain connective tissue disorders (e.g. Marfan’s syndrome).
Most patients are asymptomatic, some have palpitations and fatigue, or atypical chest pain, and mid-systolic click with a late systolic murmur.
Mitral Valve Prolapse is a common cardiac disorder (occurs in 3-5% of adult population, mainly females, ages years).
It is usually an isolated problem but it may arise as a complication of certain connective tissue disorders (e.g. Marfan syndrome).
It has been reported as an isolated autosomal dominant condition that maps to chromosome 16p. Less commonly, as an x-linked recessive disorders.
Symptoms: Most patients are asymptomatic, some have palpitations and fatigue, or atypical chest pain, and mid-systolic click with a late systolic murmur.

26. Mitral Valve Prolapse
The valve leaflets (posterior cusp) are soft and enlarged → balloon intruding into left atrium during systole.
Chordae tendineae are elongated, fragile and may rupture in severe cases.
Microscopic examination
Excessive amounts of loose, edematous, faintly basophilic tissue within the middle layer of the valve leaflets (spongiosa) and chordae.
Complications
Mitral regurgitation and congestive heart failure.
Sudden death caused by ventricular arrhythmias.
Infective endocarditis.
Pathology
1- The valve leaflets (posterior cusp) are soft and enlarged causing a characteristic ballooning of the valve leaflets into the left atrium during systole.
2- The chordae tendineae, which are often elongated and fragile, may rupture in severe cases.
3- The valve annulus may be dilated.
Microscopic examination: Reveals excessive amounts of loose, edematous, faintly basophilic tissue within the middle layer (spongiosa) of the valve leaflets and chordae.which causes the valve to become floppy and incompetent during systole.
Complications:
Mitral regurgitation and congestive heart failure.
Sudden death caused by ventricular arrhythmias.
Infective endocarditis

27. Left ventricle demonstrates ballooning with prolapse of the posterior mitral leaflet into the left atrium.

28. Infective Endocarditis (IE)
Infection of the cardiac valves or the endocardium, which results in the formation of vegetation on valve (s), mostly aortic and mitral valves.
Infective Endocarditis is divided into two forms:
Acute Infective Endocarditis
Subacute Infective Endocarditis
Infective Endocarditis
Definition:
1- Infection of the cardiac valves or the surface of endocardium, resulting in the formation of vegetation (an adherent mass of thrombotic debris and organisms).
2- Vegetations may be single or multiple, involve one or more valve (s). Mostly, aortic and mitral valves (right side valves in i. v. users).
Divided into two forms:
1- Acute Endocarditis: high virulent organisms (staphylococcus aureus), infect even normal valves, causing rapidly progressive infection, with little local host reaction. Leads to death of more than 50% of patients.
2- Subacute Endocarditis: infection of previously abnormal valves by organisms of low virulence (-hemolytic streptococci), progress slowly, and induce local inflammatory reaction. Most patients recover with antibiotics , the lesion tends to be less destructive

29. Infective Endocarditis
Acute
Subacute
Organism
High virulence (staphylococcus aureus)
Low virulence
(α hemolytic streptococcus)
Valve
Normal and deformed
Deformed
Response
Necrosis and ulceration
Local inflammatory reaction
Progression
Rapid and destructive
Slow and less destructive
Resolution
Death (50%)
Recovery (antibiotic)

30. Acute infective endocarditis - serious destruction in the aortic valve
Acute infective endocarditis - serious destruction in the aortic valve. Irregular reddish tan vegetations overlie valve cusps that are being destroyed.

31. Endocarditis of the mitral valve (subacute, caused by streptococcus viridans)

32. IE.: Etiology, Pathogenesis
Bacteremia: Causative Organisms
-Hemolytic streptococci (viridans) attacks deformed valves (50-60%).
Staphylococcus aureus attacks healthy or deformed valves (intravenous drug abusers) (10-20%).
Coagulase-negative staphylococci (S. epidermidis) attacks prosthetic valve.

33. IE.: Etiology, Pathogenesis
High risk group
Obvious hematogenous infection as with:
Cardiac abnormalities: as chronic valvular diseases and high pressure shunts within the heart (small ventricular septal defects).
Intravenous drug abusers (right side of the heart).
Prosthetic heart valves.
Previous dental, surgical or interventional procedure (e.g. urinary catheterization).
Occult source of bacteremia
small injuries to skin or mucosal surfaces such as brushing the teeth.

34. IE.: Pathology Acute Endocarditis Gross:
Vegetations may obstruct valve orifice and cause rupture of the leaflets, cordae tendineae, or papillary muscles.
Vegetations may erode into myocardium to produce abscess in perivalvular tissue (ring abscess).
Friable vegetations may become systemic emboli  infarcts (brain, kidneys, myocardium) and abscesses.
Micro: vegetations consist of large number of organisms, fibrin and blood cells.
Infective Endocarditis: Pathology
1- Acute Endocarditis
Gross:
1- vegetations may obstruct valve orifice and cause rupture of (the leaflets, cordae tendineae, or papillary muscles),
2- May cause abscess in perivalvular tissue (ring abscess).
3- Vegetations may become systemic emboli  infarcts (brain, kidneys, myocardium) and abscesses.
Micro: vegetations consist of large number of organisms, fibrin and blood cells.
2- Subacute Endocarditis:
Gross: vegetations are firmer and less destructive (ring abscess uncommon).
Systemic emboli may develop and cause infarcts, without abscesses
Micro:
1- granulation tissue is seen at the base of the vegetations.
2- Later: fibrosis, calcifications and chronic inflammatory infiltrates.

35. IE.: Pathology Subacute Endocarditis:
Gross: vegetations are firmer and less destructive (ring abscess uncommon).
Systemic emboli may develop and cause infarcts, without abscesses.
Micro: granulation tissue is seen at the base of the vegetations.
Later: fibrosis, calcifications and chronic inflammatory infiltrates.
Infective Endocarditis: Pathology
1- Acute Endocarditis
Gross:
1- vegetations may obstruct valve orifice and cause rupture of (the leaflets, cordae tendineae, or papillary muscles),
2- May cause abscess in perivalvular tissue (ring abscess).
3- Vegetations may become systemic emboli  infarcts (brain, kidneys, myocardium) and abscesses.
Micro: vegetations consist of large number of organisms, fibrin and blood cells.
2- Subacute Endocarditis:
Gross: vegetations are firmer and less destructive (ring abscess uncommon).
Systemic emboli may develop and cause infarcts, without abscesses
Micro:
1- granulation tissue is seen at the base of the vegetations.
2- Later: fibrosis, calcifications and chronic inflammatory infiltrates.

36. IE.: Clinical Onset: gradual or explosive (organisms).
Organism of low virulence cause low-grade fever, malaise, weight loss, and flulike syndrome .
Organism of high virulence cause high fever, shaking chills, and weakness.
Cardiac murmurs.
Blood culture is important (only minority of cases remain negative).
Infective Endocarditis: Clinical
1- Onset: gradual or explosive (organisms).
Organism of low virulence cause low-grade fever, malaise, weight loss.
Organism of high virulence cause high fever, shaking chills.
2- Cardiac murmurs.
3- Enlargement of spleen, clubbing of digits (particularly in subacute cases).
4- Petechiae.
5- Blood culture is important (only minority of cases remain negative).
Complications:
Regurgitation leading to congestive heart failure.
Myocardial abscess (ring abscess).
Extension of infection to root of aorta (mycotic aneurysm).
Systemic emboli, also pulmonary emboli in right-sided endocarditis.
Renal complications (glomerulonephritis and Infarction)

37. IE.: Complications Regurgitation leading to congestive heart failure.
Myocardial abscess (ring abscess).
Extension of infection to the root of aorta (mycotic aneurysm).
Systemic emboli, also pulmonary emboli in right-sided endocarditis.
Enlargement of spleen, and clubbing of digits (particularly in subacute cases).
Petechiae, nail-bed splinter hemorrhage.
Renal complications (glomerulonephritis and Infarction)
Infective Endocarditis: Clinical
1- Onset: gradual or explosive (organisms).
Organism of low virulence cause low-grade fever, malaise, weight loss.
Organism of high virulence cause high fever, shaking chills.
2- Cardiac murmurs.
3- Enlargement of spleen, clubbing of digits (particularly in subacute cases).
4- Petechiae.
5- Blood culture is important (only minority of cases remain negative).
Complications:
Regurgitation leading to congestive heart failure.
Myocardial abscess (ring abscess).
Extension of infection to root of aorta (mycotic aneurysm).
Systemic emboli, also pulmonary emboli in right-sided endocarditis.
Renal complications (glomerulonephritis and Infarction)

38. Bacterial Endocarditis Remote Embolic Effects

39. Nonbacterial Thrombotic Endocarditis (NBTE) Marantic Endocarditis
Characterized by small sterile vegetations (less than 5 mm), on the valve leaflets along the line of closure.
Vegetations contain fibrin, platelets and other blood components.
The valve leaflets are normal, no inflammation or fibrosis
Mitral valve is the most common site, followed by aortic valve
Hypercoagulable state are the usual precursor to NBTE Chronic DIC, hyperestrogenic states, malignancy (mucinous adenocarcinoma).

40. Nonbacterial Thrombotic Endocarditis (NBTE)
Nonbacterial Thrombotic Endocarditis (NBTE). Nearly complete row of thrombotic vegetations along the line of closure of the mitral valve leaflets.

41. Libman-Sacks Endocarditis (LSE)
Small sterile vegetations on ventricular or both surfaces of mitral & tricuspid valves in some patients with Systemic Lupus Erythematosus.

42. RHD: row of small vegetations along the lines of closure of the valve leaflets. IE: large, irregular masses on the valve cusps that extend onto the cords. NBTE: small, bland vegetations, usually attached at the line of closure. LSE: has small or medium-sized vegetations on either or both sides of the valve leaflets.
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 warty, small 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 cords (see Fig. 13–18 A). NBTE (nonbacterial thrombotic endocarditis) typically exhibits small, bland vegetations, usually attached at the line of closure. One or many may be present (see Fig. 13–20). LSE (Libman-Sacks endocarditis) has small or medium-sized vegetations on either or both sides of the valve leaflets.

43. Myocardial Diseases
A group of diseases intrinsic to myocardial fibers, including mainly:
Myocarditis
Cardiomyopathies: primary non-infectious abnormalities in the myocardium.

44. Myocarditis
A group of Inflammatory conditions of the myocardium that result in injury to cardiac myocytes.
The heart is dilated, and the myocardium is flabby and pale, contains small areas of hemorrhage.
Clinical features range from an asymptomatic state to severe congestive heart failure at late stage.
Lethal ventricular arrhythmias accounts for most sudden cardiac deaths.

45. Myocarditis: Major Causes
Infections
Viruses: the most common cause in USA (e.g., coxsackievirus A and B, HIV and echoviruses).
Chlamydia (e.g., C. psittaci)
Rickettsia (e.g., R. typhi [typhus fever])
Bacteria:
Corynebacterium [diphtheria],
Neisseria [meningococcus],
Borrelia [Lyme disease]
Fungi (e.g., Candida)
Protozoa (e.g., Trypanosoma cruzi [Chagas disease], the most common cause in South America)
Helminths (e.g., trichinosis)

46. Myocarditis: Major Causes
Immune-Mediated Reactions
Postviral
Poststreptococcal (rheumatic fever)
Systemic lupus erythematosus
Drug hypersensitivity (e.g., methyldopa, sulfonamides)
Transplant rejection
Unknown : Sarcoidosis, and Giant cell myocarditis

47. Myocarditis: Microscopically
Viruses: edema, inflammatory infiltrate dominated by lymphocytes, and myocyte degeneration and necrosis.
Chronic cases: ventricular dilation, inflammation is less obvious, myocardial fibrosis becomes more prominent
Parasites: the organism is demonstrable histologically, (Chagas disease, trypanosomes directly infect cardiac muscle fibers).
Bacteria: neutrophilic infiltrate, and abscess.
Cardiac transplant rejection: interstitial lymphocytes and myocyte degeneration.
Giant cell myocarditis is characterized by an inflammatory infiltrate in which multinucleated giant cells are prominent.

48. Lymphocytic Myocarditis: Dense mononuclear inflammatory cell infiltrate.

49. Hypersensitivity Myocarditis

50. Giant cell myocarditis

51. Myocarditis caused by Trypanosoma cruzi (Chagas disease)
Myocarditis caused by Trypanosoma cruzi (Chagas disease). Intracellular organisms inside a myocyte