1. Cardiac Diseases Dr. Samar Al H akeem Department of pathology
بسم الله الرحمن الرحيم
Cardiac Diseases Dr. Samar Al H akeem
Department of pathology
Faculty of Medicine
University of Mosul

2. Congestive Heart Failure
Cardiac output not adequate for body needs
Mainly due to inability of the heart to eject the blood that receives from the venous system (pumping failure)
Less frequently due to
Blood loss
Low venous return
Increase demands in tissue as in pregnancy

3. 1/ Left heart failure: Causes of CHF (Congestive heart failure)
1- Ischemic heart disease
2- Hypertension
3- Aortic & mitral valve disease
4- Myocardial disease

4. Manifestations of heart failure
1/ LHF
1- Dyspnea: exertional, orthopnia, paroxysmal nocturnal dyspnea due to congestion & edema of the lungs
2- Hypoxic/ ischemic encephalopathy: due to CNS hypoxia

5. 2/ Right heart failure: 1- LHF
2-Primary disease of pulmonary vasculature
3- Pulmonary or tricuspid valve disease
4- Cardiomyopathies & myocarditis
5- Primary lung diseases

6. Manifestations of heart failure
1/ RHF
Peripheral edema
Effusion in body cavities (ascitis, pleural effusion)
Dusky face, engorged veins of the neck
Chronic liver congestion & congestive splenomegaly

7. CONGENITAL HEART DISEASES
most common types of heart diseases among children
occur in about 1% of live births, higher incidence in prematures and stillborns

8. clinical features -left to right shunt -right to left shunt
-flow obstruction
shunt is an abnormal communication
between chambers or blood vessels

9. left to right shunt -Non cyanotic heart disease
-cyanosis appears later on due to
reversing of shunt from right to left and development of (Eisenmenger syndrome)
-conditions
.atrial septal defect (ASD)
.ventricular septal defect (VSD)
.patent ductus arteriosus (PDA)
.atrioventricular septal defect

11. Ventricular septal defect

12. Right to left shunt
cyanosis, chronic cyanosis causing clubbing of the fingers and toes (hypertrophic osteo-arthropathy) and polycythemia
conditions .tetralogy of fallot .transposition of the great arteries .persistent truncus arteriosus .tricuspid atresia .total anomalous pulmonary venous connection

14. Congenital heart disease, transposition of the great arteries

15. obstructive congenital heart diseases examples
obstructive congenital heart diseases examples .coarctation of the aorta .aortic valvular stenosis .pulmonary valvular stenosis

17. Ischemic Heart disease (IHD)

18. Ischemic Heart Disease (IHD)
A group of closely related syndromes caused by an imbalance between the myocardial oxygen demands & blood supply
Most common underlying cause is atherosclerosis of coronary arteries
Clinical syndrome of IHD includes:
Angina pectoris
Myocardial infarction
Sudden cardiac death
Chronic IHD & CHF

19. Acute coronary syndromes

20. Pathogenesis of ischemic heart disease

21. 1/ Acute change in plaque morphology:
Symptomatic IHD is typically associated with a critical stenosis (75% or more) reduction in the lumen of 1 or more coronary arteries by atherosclerotic plaque
Other that play in IHD
1/ Acute change in plaque morphology:
Fissuring, hemorrhage & rupture
embolization of debris into distal coronary artery
Increase platelet aggregation
increase risk of thrombosis
Platelet aggregation causes
mechanical occlusion
vasospasm
coronary artery thrombosis

22. 2/Non atherosclerotic lesion of coronary artery
Emboli from vegetation on valves
Vasaculitis
Severe hypotension
Spasm of coronary artery
3/increase myocardial demands
Hypertrophy
Cardiomyopathies

23. Angina Pectoris

24. Angina Pectoris
A clinical syndrome characterized by paroxysmal attacks of chest pain usually situated retrosternal, radiating to precordium & left upper limb & other sites caused by transient, (15 seconds- 15 minutes) myocardial ischemia
1/ Classical AP
2/ Vasopastic (prinzmetal’s) angina

25. 3/ Unstable angina (preinfarction angina)
More frequent
Provoked by less effort or emotion
Lasts longer
Nitroglycerine is required more & less effective
Carries a bad prognostic implication
Caused by acute plaque lesion with superimposed partial thrombosis

26. Myocardial Infarction

27. Acute Myocardial Infarction
An area of ischemic necrosis
Acute MI is the most common cause of death in West 1.5 mil of MI / yr in USA with ½ mil deaths. Large number of which don’t reach hospital
2 types of MI
1/Transmural MI: full thickness infarction caused by severe atheroma with acute plaque changes leading to complete occlusion
2/Subendocardial MI: limited to inner 1/3rd or ½ of wall thickness caused by global ischemia due to atheroma with increased demand often super-imposed on chronic non-critical coronary stenosis

29. Progression of myocardial necrosis following coronary artery occlusion

30. Distribution of myocardial infarction in relation to coronary artery occlusion

31. Morphology of MI Gross pathology:
MI fewer than 12 hr old are usually unapparent on gross examination. However; it is possible to outline the area of necrosis after 2-3 hr by impression tissue slices in solution of triphenile tetrazlium, the dye impart a brick-red color to non infarct area

32. Transmural myocardial infarction, staining by tripheniletetrazolium chloride solution

33. Histology: Necrosis start after 20-40 min of ischemia
Coagulative necrosis become apparent microscopically by about 4-12 hrs

34. Myocardial Infarction
Time
1-2 hr
4-12 hr
12-24 hr
4-7 days
7-10 days
7-10 weeks
Histology
Grossly
Few wavy fibers at the margin of infarct
Early coagulative necrosis, edema, occasional polymorph
Established coagulative necrosis, heavy polymorph
Macrophages appear, disintegration of muscle fibers & phagocytosis, granulation tissue at border
Granulation tissue maximum
Fibrosis
Slight pallor area
Central pallor with hyperemic border
Yellow soft shrunken center with purple border
Firm gray fibrous tissue

35. Myocardial infarction, 1 day, 3-4 days, 7-10 days, granulation tissue, scar

36. Infarction modification after reperfusion
Reperfusion sufficiently early (within the first min) may prevent all necrosis
If delay after min might limit the size of infarction & induced some changes includes:
Hemorrhage into ischemic area due to vascular injury
Contraction band necrosis in fibers at periphery of infarct caused by hypercontraction of myofibrils in dying cells which induced by influx of calcium from plasma into the cells after the damage of cell membrane by free radicals formed by reperfusion

37. Reperfusion injury

38. Laboratory Diagnosis of MI
Cardiac enzymes & proteins
Creatinine kinase-MB: rise within 2-4 hr, peak at 18 hr & disappear after 48 hr
lactic dehydrogenase(Ld1): rises within 24 hr, peaks at 72 hr & persist for 1 week
Troponines (I & T): most specific, appear similar to CK but remain 7-10 days
c-reactive protein serves as a marker to predict the risk of MI in patients with angina and the risk of new infarcts in patients who recover from infarcts
ECG changes: q wave, ST elevation & T inversion

39. Consequences and complications of MI
Half of the deaths occur within one hour
of onset of symptoms
Factors associated with poor prognosis;
-advanced age
-female gender
-diabetes mellitus
-previous MI

40. Complication of MI
After infarction about 25% of patients experience sudden death due to fetal arrhythmias
If patient survive the acute event, 80-90% develop complications
1-Arrhythmias (75-95%)
2- CHF (60%)
3- Cardiogenic shock (10%) if > 40% of LV infarction
4- Rarely papillary muscle infarction with or without rupture leading to mitral valve dysfunction

41. 5- Mural thrombosis with thromboembolic phenomena (15-40%)
6- Ventricular rupture (1-5%)
During the 1st 10 days, maximum (4-5) days
Free wall rupture causing pericardial hemorrhage & cardiac temponade
IVS rupture causing left to right shunt & right ventricular overload
7-Venticular aneurysm
8- Fibrinous or hemorrhagic pericarditis

45. Complications of myocardial infarction, rupture, pericarditis, expansion, aneurysm

46. Sudden Cardiac Death
Unexpected death from cardiac cause within 1 hour of onset of symptoms
Majority are complication of IHD
75-95% have marked atheromas
Other causes
Marked aortic stenosis
Abnormalities of conductive system
Myocarditis
Mitral valve prolapsed
Cardiomyopathies
Ruptured aortic aneurysm

47. Left ventricular hypertrophy

48. Hypertensive heart disease, systemic, pulmonary

49. Rheumatic Fever & Rheumatic Heart Disease

50. Major Criteria: Minor Criteria:
R F is an acute recurrent immunological mediated multisystemic inflammatory disease mainly affecting children following pharyngitis with group A beta hemolytic streptococci & characterized by Jones Criteria
Major Criteria:
1-Pancarditis
2-migratory polyarthritis
3-Subcutaneous nodules
4-Sydenham’s chorea
5-Erythema marginatum of the skin
Minor Criteria:
1-Fever
2-Arthralgia
3-Elevated Antistreptolysin O(ASOT)
4-Elevated acute phase reactant C protein
5-Prolongation of PR intervals

51. Etiology & Pathogenesis of RF
RF is an immune reaction secondary to streptococcus infection
Antibodies against strept. antigen cross react with tissue antigens including cardiac antigens

52. Morphology of RF

53. 1/ Acute attack The pathognomic lesion is a disseminated focal inflammatory foci known as Aschoff bodies
Aschoff body:
focus of fibrinoid necrosis surr. by a collagen, lymphocytes, macrophages & few plasma cells plus modified histiocytes known as Antischow cells & multinucleated cells known as Aschoff giant cells.
Typically seen in myocardium esp. around blood vessels

54. 2/ Chronic attack Fibrosis & deformities of the heart esp. the valves
Mitral valve most commonly affected followed by aortic valve, tricuspid valve & lastly pulmonary valve

55. Endocarditis:
Small nodular or warty vegetations (platelets & fibrin) along lines of closure of the valve cusps, chorda tendeni & mural endocardium (verrucous or rheumatic endocarditis)
Healing either by minimal fibrosis or may end in severe valve deformity

56. Chronic Rheumatic Heart Disease
More likely to occurs in:
1-First attack in early childhood
2-Severe initial attack of RF
3-Recurrent attacks
Mitral valve alone most commonly involved in % of cases, then mitral & aortic valves in combination in 25 %, less affection is aortic valve alone
Pulmonary & tricuspid valves are rarely affected

57. Chronic Rheumatic Heart Disease
Mitral Valve:
1-Fibrous thickening & calcification of leaflets
2-Fusion of commissaries result in fish mouth or button hole deformity & stenosis
3-Chorda tendeni are thickened, fused & shortened
4-Mitral stenosis or combined stenosis & incompetence
5- More common in female
Aortic Valve:
1-Similar to MV with prominent nodular calcification in the sinuses-bind the leaflets
2-Aortic stenosis or combined stenosis & incompetence
3-More common in male

59. Complication of acute & chronic RHD
1-Mural thrombi & thromboembolism
2-Infective endocarditis superimposed deformed valve
3-Heart failure
4-Cardiac arrhythmia

60. Endocarditis

61. Endocarditis: Inflammation of valves &/or mural endocardium It classified into:
1/ Infective endocarditis:
Bacterial
Viral
fungal
Chlymadial
Recticeal (Q fever)
2/ Non-infective endocarditis:
Rheumatic endocarditis
Non-bacterial thrombotic endocarditis (Marantic endocarditis)
Libman-Sacks endocarditis (SLE ass endocarditis)

62. 1/ Infective endocarditis:
Infection & colonization of cardiac valves or mural endocardium by microbiological agents leading to formation of bulky friable & destructive vegetation
Most are caused by bacteria (bacterial endocarditis
It is classified into acute & subacute endocarditis depending on clinical course of the disease & virulence of microorganism & the underlying valve status

63. Etiology & pathogenesis:
Colonization of the valves by bacteria in episodes of bacteremia both obvious & occult
Intravenous drug abuse
Source of infection in the body
Surgical or oral procedures
Predisposing factors in IE:
Rheumatics heart disease
Congenital heart disease
Mitral valve prolapsed
Artificial valve
Neutropenia, immunodeficiency & immunosuppression

64. Causative bacterial organisms
Streptococcus viridians
Staphylococcus aureus
Oral commensals (HACEK) Haemophilus species, Aggregatibacter species, Cardiobacterium hominis, Eikenella corrodens, and Kingella species
Coagulase negative staphylococcus. (staphylococcus epidermidis)

68. Non bacterial thrombotic endocarditis (Marantic)
Precipitation of small masses of fibrin, platelets & other blood elements on valve leaflets
usually single, resemble the vegetations of rheumatic endocarditis (small non destructive, non inflammatory, sterile)
most cases seen in patients died of debilitating disease as in cancer, sepses, extensive burn
Hypercoagulable state
causing embolic phenomena
no local effect

70. Valvular Heart Diseases

71. Valvular Heart Diseases
It may congenital or acquired
Most frequent acquired stenosis of mitral & aortic valves which account for 2/3rd of all valve lesion
Incompetence may appear either
Acutely as in IF & ruptured cords
Chronically as in leaflet scaring
Valvular stenosis almost always a chronic process

72. Mitral stenosis Mitral regurgitation Causes: Complication Causes:
Rheumatic heart disease
Congenital
Large vegetation of IE
Complication
Thrombosis in LA
Systemic embolization
Arrhythmias
Causes:
Abnormalities of the leaflets
Rheumatic heart disease IE
Mitral valve prolapsed
Abnormalities of tensor apparatus
Ruptured of papillary muscle or chordae tendenea
Fibrosis of papillary muscle
Abnormalities of the LV cavity
LV enlargement
Calcification of mitral ring

73. Mitral valve prolapsed (Floppy mitral valve)
A congenital disorder characterized by ballooning of the valve leaflets, particularly the posterior leading to functional incompetence
A common condition, more in females yr of age affect 3% of population
May be a feature of Marfans syndrome

74. Aortic stenosis Causes: Aortic regurgitation Causes:
Rheumatic heart disease
Calcification
Congenital
Causes:
Intrinsic valvular diseases
Rheumatic heart disease IE
Disease of Aorta:
Syphilitic aortitis
Ankylosing spondylitis
Rheumatoid arthritis
Marfans syndrome

75. Calcific Aortic stenosis
Degenerative, age related lesions occurring more frequently & earlier (6th-7th decades) in congenital bicuspid valves
Heaped up calcified masses within the sinus of valsalva + thickening & fibrosis of the aortic cusps with narrowing of the orifice

77. Myocarditis

78. Myocarditis
Inflammation of the myocardium in which the inflammatory cells are associated with myocyte necrosis & degeneration

79. Causes of myocarditis
1- Infectious: viral, bacterial, fungal (candida), protozoal (Toxoplasmosis & Trypanosome cruzi), helminthes (Trichinosis)
2- Non infectious: rheumatic fever, SLE, drug hypersensitivity
3- Others: Sarcodosis, giant cell myocarditis
Most common is viral & esp. Coxackie-B& A viruses, other are HIV & CMV
Bacterial by Corynebacterium diphtheria & Neisseria meningococcus)

80. Cardiomyopathies Heart muscle disease of unknown cause
Pathophysiologic categories of CMP
Dilated (congested) CMP
Hypertrophic (obstructive) CMP
Restrictive (infiltrative) CMP

81. Dilated (congestive) CMP
Occurs at any age esp. between yr
Slowly developing CHF
Causes
Unknown (idiopathic)
Pregnancy induced
Alcoholism & drugs
Myocarditis
Genetic in 20-30%
Heart is always increase in weight, dilation may mask hypertrophy
Causes of death
CHF
Embolic phenomena
Fatal arrhythmias

82. Hypertrophic (obstructive) CMP (idiopathic Hypertrophic subaortic stenosis)
Characterized by
increased wall thickness, mainly LV esp. the interventicular septum particularly upper portion
Reduced compliance
Reduced volume capacity of LV
Low stroke volume

83. Hypertrophic (obstructive) CMP (idiopathic Hypertrophic subaortic stenosis)
More than ½ of pt transmitted the disease by autosomal dominant gene affected gene code for sacromer protein
Clinically: young adults or old with dyspnea, angina, near syncope & CHF. Could be asymptomatic
Marked cardiomegally due to hypertrophy
Asymmetric bulging of interventicular septum converting LV cavity into banana shaped structure
There is diastolic dysfunction

84. Hypertrophic (obstructive) CMP (idiopathic Hypertrophic subaortic stenosis)
Major complication
Atrial fibrillation
Mural thrombi with embolization
Sudden cardiac death

85. Restrictive (infiltrative) CMP
Least common type, characterized by restriction of ventricular filling during diastole & thus reduced cardiac output due to decrease compliance of ventricle
Diastolic dysfunction
Causes
Amyloidosis, both systemic or localized
Radiation, sarcoidosis
Metastatic tr
Endomyocardial fibrosis
Loffler’s endocarditis
Endocardial fibroelastosis: diffuse cartilage-like fibroelastic thickening of the endocardium most commonly seen in children
Death is usually due to emboli or CHF

86. Pericarditis Causes Infectious: viral, pyogenic bacterial, Tb, fungal
Immune mediated: RF, SLE, scleroderma
Miscellaneous: MI, uremia, malignancies
Types
Serous
Fibrinous & serofibrinous
Most common type
Purulent (suppurative) pericarditis
Bacterial, fungal and parasitic
Hemorrhagic pericarditis
Tb, malignancy
Caseous pericarditis Tb
Constrictive pericarditis

87. TUMORS OF THE HEART Primary tumors are rare.
Myxoma: most common primary tumor, benign, mostly located in the atria as solitary sessile or pedunculated mass of 1-10cm.
Rhabdomyoma: Benign tumor seen in children
Metastatic tumors to the heart occur in about 5% of patients dying of cancer