2- ischaemic heart disease
DESCRIPTION
2- Ischaemic Heart DiseaseTRANSCRIPT
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Ischaemic Heart Disease
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Ischaemic Heart Disease (IHD)
Common Health problem.
High Mortality & Morbidity.
Etiology: common Atherosclerosis
Two major types: Angina & MI.
Risk factors :
Hypertension
Hypercholesterolemia
Diabetes
Smoking, Life style, Diet, Genetic.
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Patterns of IHD:
• Angina Pectoris:
• Acute Myocardial Infarction:
• Sudden cardiac death:
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Pathogenesis
• Obstruction to blood flow
– Atheroma, Thrombosis, Embolism
• Diminished coronary perfusion
– Ischemia – Angina
– Infarction – Necrosis
• Granulation tissue
• Fibrous scarring.
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Myocardial Infarction-MI
• “Death of heart tissue due to lack of blood supply”
• Atherosclerosis is the common cause.
• Infarction causing Coagulative necrosis (intact cell shape).
• Severe chest pain, breathlessness & sweating
• Complications: Cardiogenic shock, Heart failure or Death.
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Coronary Atherosclerosis with Thrombosis
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Recent transmural infarct
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Wavy fibers are another sign of an early infarct.
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Coagulative necrosis and a few inflammatory cells
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Coagulative necrosis, interstitial bleeding, and a few inflammatory cells.
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Complications
Cardiogenic shock, death
Arrhythmias and conduction defects
Congestive heart failure (pulmonary edema)
Mural thrombosis, or embolization
Myocardial wall rupture
Ventricular aneurysm
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Angina Pectoris
Paroxysmal attacks of chest pain
Substernal or precordial
Myocardial ischemia
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Gross - Morphology - Micro
• 1-18h: None
• 24h: Pale, edema
• 3-4D: Hemorrhage
• 1-3W: Thin, yellow
• 3-6W: Tough white
• None
• Edema, inflammation
• Necrosis, granulation
• Granulation tissue
• Dense Fibrosis
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1- Stable Angina
Pain related to exertion
Relieved by rest or vasodilators
Subendocardial ischemia
ST-segment depression
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2- Variant Angina
Classically occurs at rest
Reversible spasm
ST-segment elevation or depression
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3- Unstable Angina
Prolonged pain or pain at rest
ST-segment depression
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Sudden Cardiac Death
Unexpected death within one hour of heart attack
300,000-400,000 persons per year
Usually high grade coronary stenosis
Ventricular electrical instability
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Chronic Ischemic Heart Disease
LV Dilatation, atherosclerosis, focal scars
Myocyte hypertrophy, myocytolysis, focal small
interstitial scars
Slow progressive heart failure with or without previous
MI or angina
40% of mortality in IHD
Ischemic cardiomyopathy
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Pathology of
Hypertension
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Introduction
• Silent Killer – painless – complications
• dizziness, headache, and visual difficulties,
• It is the leading risk factor – MI, DM, Stroke
• 25% of population, ~35% unaware.
• “Sustained increase in blood pressure”
• Systolic >140, Diastolic > 90 mm of Hg*
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Etiologic Classification:
• Primary or Essential Hypertension(95%)
• Secondary Hypertension (5-10%)
–Renal – Kidney disorders.
–Other – endocrine, drugs etc.
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Pathogenesis of complications Of Hypertension
Ishchemia – MI, CNS,
Kidney, eye
Aneurism / Rupture – CNS,
Aorta,
Myocardial Hypertrophy
LVH, Cardiac failure.
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Consequences of Hypertension:
• Blood Vessels
–Atherosclerosis, Arteriolosclerosis.
• Heart
–Enlarge, Ischemia, Infarction.
• Kidney
– Ischemia, Infarction - nephrosclerosis.
• Eyes:
–Retinopathy – Ischemia, infarction.
• Brain:
– Ischemia, infarction, Haemorrhages.
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Thickening of blood vessel:
Onion Skin Thickening
Of arterioles.
Narrow Lumen
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Hypertrophy of heart:
Left Ventricular Hypertrophy
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Cardiomyopathy
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Myocarditis:
Etiology
Viral – Coxsackie A, ECHO, Influenza
Chlamydia and Rickettsia – psittaci & typhi
Bacteria – diphtheria, TB, Strep
Fungal & Protozoa – Trypanosomes, Toxo
Hypersensitivity – SLE, RHD, drugs
Physical Agents – Radiation
Idiopathic – Giant cell myocarditis
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Morphology
• Gross: dilated, flabby heart, pale patches with
hemorrhage
• Microscopic: interstitial inflammatory infiltrate with
myocyte necrosis, fibrosis
• Mononuclear cells: idiopathic or viral
• Neutrophils: bacterial
• Eosinophils: hypersensitivity
• Granulomatous: TB or sarcoid
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Dilated heart in myocarditis
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Myocarditis : T lymphocyte infiltrate and myocyte necrosis.
This is usually either viral or of unknown cause.
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Toxic myocarditis: There is some inflammation, myocyte
changes (big nucleolus). Myocyte necrosis also happens.
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Giant Cell Myocarditis
• Myocyte necrosis
• Multinucleated giant cells
• Lymphocytes, plasma cells, macrophages,
eosinophils, and neutrophils
• Rapid progression to death
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Giant Cell Myocarditis
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Cardiomyopathies
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Dilated Cardiomyopathy
• Gross: increased weight, dilatation, endocardial
fibrosis, normal valves and coronary arteries
• Microscopic: myocyte hypertrophy, myofibrillar loss
and interstitial fibrosis
• Etiology: viral, genetic, toxins
• Clinical significance: heart failure & death
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Dilated cardiomyopathy
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Cardiomyopathy – loss of myofibrils
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• Cardiomyopathy – trichrome stain showing extensive fibrosis
(blue) between the myocytes. The myocytes also vary in size, and
some have partial loss of myofibrils.
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Hypertrophic Cardiomyopathy
• Hypertrophy of ventricular septum (95%)
• Disarray of myofibers (100%)
• Volume reduction of ventricles (90%)
• Endocardial thickening of LV (75%)
• Mitral valve leaflet thickening (75%)
• Dilated atria (100%)
• Abnormal intramural coronaries (50%)
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• Etiology: hereditary, can appear sporadically
• Clinical significance: syncope, arrhythmias and
sudden death with a risk of 2-6% per year
• Cannot equate with hypertrophy alone! There is
variation in heart size without disease.
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Hypertrophic cardiomyopathy
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Hypertrophic cardiomyopathy – myofiber dysarray – not all
fibers are pulling the same direction. Thus the contraction is
ineffective.
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Restrictive Cardiomyopathy
• Endomyocardial fibrosis; subendocardial fibrosis
• Loeffler’s endocarditis – eosinophilic infiltrate
• Endocardial fibroelastosis
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Amyloidosis – notice the
pink material between the
myocytes.
Amyloidosis – Congo Red is
very, very positive.
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Amyloidosis: this heart is thickened, pale, and has a rubbery
consistency that interferes with cardiac expansion during
diastole.
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Specific Heart Muscle Diseases
• Toxic: alcohol, cocaine, Adriamycin
• Metabolic: hemochromatosis, hyperthyroidism
• Neuromuscular: muscular dystrophy
• Storage disease: glycogen
• Infiltrative: sarcoidosis
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Note the fibrosis and loss of myofibrils in some cells.
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Hemochromatosis: note the brown perinuclear deposits of
hemosiderin. It is the soluble iron.
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Hemochromatosis – iron stain (iron is blue).
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Cardiac tumors
• Primary tumors are rare (most common benign)
• Metastases far more common.
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Metastatic neoplasms
• Most common cardiac neoplasms.
– Lung
– Breast
– Melanomas
– Lymphomas
– Leukemias
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