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Cardiovascular System
Heart
• Heart is a muscular pump that ejects
blood into vascular tree with sufficient
pressure to maintain optimal circulation.
• Heart is lined by three layers
• Pericardium-outermost layer
• Myocardium-middle (muscular layer)
• Endocardium-innermost layer
Atherosclerosis
• It is an thickening/hardening of large and medium sized muscular
arteries,primarily due to involvement of tunica intima and characterised by
fibrofatty plaques /atheroma
• Athero-Porridge(soft lipid rich material in the centre of atheroma)
• Sclerosis-Scarring(connective tissue in the plaques)
• Most commonly affected- Aorta
Reaction to injury hypothesis
• Endothelial injury-initial triggering event
• Two risk factors – hemodynamic stress from hypertension and chronic dyslipidemia
• Intimal smooth muscle proliferation
• Endothelial injury causes adherence, aggregation and platelet release at the site of exposed
subendothelial connective tissue and infiltration by inflammatory cells
• Proliferation of intimal smooth muscle and production of extracellular matrix is stimulated
by cytokine release
• Role of blood monocytes-play important role in formation of foam cells. Death of
foam cells by apoptosis release lipid to form lipid core of plaque
Morphological features
1. Fatty streaks and dots
• Harmless but precursor lesions of atheromatous plaques
• Grossly-flat/slightly elevated and yellow
• Small ,multiple dots in the form of elongated, beaded streaks.
• Microscopically- closely packed foam cells, lipid containing elongated smooth muscle
and few lymphoid cells
2.Gelatinous lesion-
Precursor of plaques. They are round or oval ,circumscribed grey elevations about 1 cm in
diameter.
Microscopically-gelationous lesions are foci of increased ground substance in the intima
with thinned overlying endothelium.
3.Atheromatous plaques
• A fully developed athesclerotic lesion is called atheromatous plaque/fibrous
plaque/atheroma
• Most often and most severely affected is Abdominal aorta
• Grossly-whitish to yellowish white lesion
• Cut section of the plaque reveals the luminal surface as a firm,white fibrous
cap and a central core composed of yellow to yellow-white ,soft porridge like
material
Microscopically
• Superficial luminal part of fibrous cap is covered
by endothelium, and is composed of smooth
muscle cells, dense connective tissue and
extracellular matrix.
• Cellular area under fibrous cap is comprised by
mixture of macrophage, foam cells,lymphocytes
and few smooth muscle cell.
• Deeper central core consists of extracellular lipid
material, cholestrol cleft, fibrin, necrotic debris and
lipid laden foam cells
Ischemic heart disease
• It is defined as acute or chronic form of cardiac disability arising from
imbalance between the myocardial supply and demand for oxygenated blood.
• Synonymous with Coronary Artery disease
• Leading cause of death in developed country
• Men develop IHD early than women.
Spectrum of IHD
1. Angina pectoris
2. Myocardial infarction
3. Chronic ischemic heart disease
4. Sudden cardiac death
Etiopathogenesis
• IHD is caused by disease affecting coronary arteries
1. Coronary atherosclerosis
• Results in fixed obstruction
• Most common site- Left anterior descending artery
2. Superadded changes in coronary atherosclerosis
• Acute changes in chronic atheromatous plaques such as plaque haemorrhage, fissuring
or ulceration that results in thrombosis.
Classification of atherosclerosis
Myocardial infarction
• It is an area of coagulative necrosis in heart
• Caused by acute plaque changes
• It is of two types
• Transmural-involves all 3 layers of heart.It is also known as ST elevation infarct.
• Subendothelial infarct- involves only subendothelium. It is also known as non ST
segment elevation infarct
• Most common vessel affected- Left anterior descending artery> Right cornonary
Artery ,
Morphologic changes in heart after MI
Rheumatic heart disease
• Rheumatic fever is a systemic, post streptococcal , non suppurative inflammatory
disease principally affecting heart,joints,CNS,skin and subcutaneous tissue.
• Immunologically mediated multi system disease
• Type 2 hypersensitivity reaction
• Age: 5-15 years
• Usually occurs 2-3 weeks after sore throat with beta hemolytic streptococci
• Streptococcal m protein cross reacts with glycoprotein in heart and joints.-
molecular mimicry
• Most common valve affected-mitral valve
• Least common valve affected- pulmonary valve
• In acute rheumatic fever- mitral regurgitation
• In chronic rheumatic fever- mitral stenosis
Revised Jones criteria
• Joints-Migratory polyarteritis
• Subcutaneous nodules-painless and on
the extensor surface of palms and
soles
• Erythema marginatum
• Sydenham’s chorea
• Pericarditis
•
Minor Criteria
Fever, polyarthralgia
Increased ESR,CRP and prolonged PR intervel
Morphology in RHD
• Aschoff bodies-pathognomic for RHD
• Consists of lymphocytes, plasma cells,giant cells,fibrinoid necrosis, collagen and cells
with wavy, slender,ribbon like nucleus(Antischkow cells)
• Bread and butter pericarditis
• McCallum plaques/Subendocardial jets
• In chronic rheumatic heart diease-Fish mouth stenosis and button hole stenosis seen
• Vegetations- small,warty,verrucous vegetation along the line of closure of valve leaflets
Aschoff bodies
Infective endocarditis
• It can be acute-occurs in previously normal heart valve
• .Caused by staphylococci aureus.
• Subacute- occurs in prevoiusly damaged heart valve
• Caused by streptocci
• Diagnosis;Dukes criteria
Morphological features
• Presence of typical vegetation on the valve cusps or leaflets
• Most commonly affected valve-mitral valve and aortic valve
• Large grey-tawny to greenish irregular typically friable vegetations
• Composed of outer eosinophilic zone of fibrin and platelets covering
colonies of bacteria and deeper zone of nonspecific inflammatory cells
• Thank you

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Cardiovascular System, Rheumatic Heart Disease

  • 2. Heart • Heart is a muscular pump that ejects blood into vascular tree with sufficient pressure to maintain optimal circulation. • Heart is lined by three layers • Pericardium-outermost layer • Myocardium-middle (muscular layer) • Endocardium-innermost layer
  • 3. Atherosclerosis • It is an thickening/hardening of large and medium sized muscular arteries,primarily due to involvement of tunica intima and characterised by fibrofatty plaques /atheroma • Athero-Porridge(soft lipid rich material in the centre of atheroma) • Sclerosis-Scarring(connective tissue in the plaques) • Most commonly affected- Aorta
  • 4. Reaction to injury hypothesis • Endothelial injury-initial triggering event • Two risk factors – hemodynamic stress from hypertension and chronic dyslipidemia • Intimal smooth muscle proliferation • Endothelial injury causes adherence, aggregation and platelet release at the site of exposed subendothelial connective tissue and infiltration by inflammatory cells • Proliferation of intimal smooth muscle and production of extracellular matrix is stimulated by cytokine release • Role of blood monocytes-play important role in formation of foam cells. Death of foam cells by apoptosis release lipid to form lipid core of plaque
  • 5.
  • 6. Morphological features 1. Fatty streaks and dots • Harmless but precursor lesions of atheromatous plaques • Grossly-flat/slightly elevated and yellow • Small ,multiple dots in the form of elongated, beaded streaks. • Microscopically- closely packed foam cells, lipid containing elongated smooth muscle and few lymphoid cells
  • 7. 2.Gelatinous lesion- Precursor of plaques. They are round or oval ,circumscribed grey elevations about 1 cm in diameter. Microscopically-gelationous lesions are foci of increased ground substance in the intima with thinned overlying endothelium.
  • 8. 3.Atheromatous plaques • A fully developed athesclerotic lesion is called atheromatous plaque/fibrous plaque/atheroma • Most often and most severely affected is Abdominal aorta • Grossly-whitish to yellowish white lesion • Cut section of the plaque reveals the luminal surface as a firm,white fibrous cap and a central core composed of yellow to yellow-white ,soft porridge like material
  • 9. Microscopically • Superficial luminal part of fibrous cap is covered by endothelium, and is composed of smooth muscle cells, dense connective tissue and extracellular matrix. • Cellular area under fibrous cap is comprised by mixture of macrophage, foam cells,lymphocytes and few smooth muscle cell. • Deeper central core consists of extracellular lipid material, cholestrol cleft, fibrin, necrotic debris and lipid laden foam cells
  • 10. Ischemic heart disease • It is defined as acute or chronic form of cardiac disability arising from imbalance between the myocardial supply and demand for oxygenated blood. • Synonymous with Coronary Artery disease • Leading cause of death in developed country • Men develop IHD early than women.
  • 11. Spectrum of IHD 1. Angina pectoris 2. Myocardial infarction 3. Chronic ischemic heart disease 4. Sudden cardiac death
  • 12. Etiopathogenesis • IHD is caused by disease affecting coronary arteries 1. Coronary atherosclerosis • Results in fixed obstruction • Most common site- Left anterior descending artery 2. Superadded changes in coronary atherosclerosis • Acute changes in chronic atheromatous plaques such as plaque haemorrhage, fissuring or ulceration that results in thrombosis.
  • 14. Myocardial infarction • It is an area of coagulative necrosis in heart • Caused by acute plaque changes • It is of two types • Transmural-involves all 3 layers of heart.It is also known as ST elevation infarct. • Subendothelial infarct- involves only subendothelium. It is also known as non ST segment elevation infarct • Most common vessel affected- Left anterior descending artery> Right cornonary Artery ,
  • 15. Morphologic changes in heart after MI
  • 16. Rheumatic heart disease • Rheumatic fever is a systemic, post streptococcal , non suppurative inflammatory disease principally affecting heart,joints,CNS,skin and subcutaneous tissue. • Immunologically mediated multi system disease • Type 2 hypersensitivity reaction • Age: 5-15 years • Usually occurs 2-3 weeks after sore throat with beta hemolytic streptococci • Streptococcal m protein cross reacts with glycoprotein in heart and joints.- molecular mimicry
  • 17. • Most common valve affected-mitral valve • Least common valve affected- pulmonary valve • In acute rheumatic fever- mitral regurgitation • In chronic rheumatic fever- mitral stenosis
  • 18. Revised Jones criteria • Joints-Migratory polyarteritis • Subcutaneous nodules-painless and on the extensor surface of palms and soles • Erythema marginatum • Sydenham’s chorea • Pericarditis • Minor Criteria Fever, polyarthralgia Increased ESR,CRP and prolonged PR intervel
  • 19. Morphology in RHD • Aschoff bodies-pathognomic for RHD • Consists of lymphocytes, plasma cells,giant cells,fibrinoid necrosis, collagen and cells with wavy, slender,ribbon like nucleus(Antischkow cells) • Bread and butter pericarditis • McCallum plaques/Subendocardial jets • In chronic rheumatic heart diease-Fish mouth stenosis and button hole stenosis seen • Vegetations- small,warty,verrucous vegetation along the line of closure of valve leaflets
  • 21. Infective endocarditis • It can be acute-occurs in previously normal heart valve • .Caused by staphylococci aureus. • Subacute- occurs in prevoiusly damaged heart valve • Caused by streptocci • Diagnosis;Dukes criteria
  • 22. Morphological features • Presence of typical vegetation on the valve cusps or leaflets • Most commonly affected valve-mitral valve and aortic valve • Large grey-tawny to greenish irregular typically friable vegetations • Composed of outer eosinophilic zone of fibrin and platelets covering colonies of bacteria and deeper zone of nonspecific inflammatory cells