Ischaemic Heart Disease

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.

Patterns of IHD:

• Angina Pectoris:

• Acute Myocardial Infarction:

• Sudden cardiac death:

Pathogenesis

• Obstruction to blood flow

– Atheroma, Thrombosis, Embolism

• Diminished coronary perfusion

– Ischemia – Angina

– Infarction – Necrosis

• Granulation tissue

• Fibrous scarring.

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.

Coronary Atherosclerosis with Thrombosis

Recent transmural infarct

Wavy fibers are another sign of an early infarct.

Coagulative necrosis and a few inflammatory cells

Coagulative necrosis, interstitial bleeding, and a few inflammatory cells.

Complications

Cardiogenic shock, death

Arrhythmias and conduction defects

Congestive heart failure (pulmonary edema)

Mural thrombosis, or embolization

Myocardial wall rupture

Ventricular aneurysm

Angina Pectoris

Paroxysmal attacks of chest pain

Substernal or precordial

Myocardial ischemia

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

1- Stable Angina

Pain related to exertion

Relieved by rest or vasodilators

Subendocardial ischemia

ST-segment depression

2- Variant Angina

Classically occurs at rest

Reversible spasm

ST-segment elevation or depression

3- Unstable Angina

Prolonged pain or pain at rest

ST-segment depression

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

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

Pathology of

Hypertension

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*

Etiologic Classification:

• Primary or Essential Hypertension(95%)

• Secondary Hypertension (5-10%)

–Renal – Kidney disorders.

–Other – endocrine, drugs etc.

Pathogenesis of complications Of Hypertension

Ishchemia – MI, CNS,

Kidney, eye

Aneurism / Rupture – CNS,

Aorta,

Myocardial Hypertrophy

LVH, Cardiac failure.

Consequences of Hypertension:

• Blood Vessels

–Atherosclerosis, Arteriolosclerosis.

• Heart

–Enlarge, Ischemia, Infarction.

• Kidney

– Ischemia, Infarction - nephrosclerosis.

• Eyes:

–Retinopathy – Ischemia, infarction.

• Brain:

– Ischemia, infarction, Haemorrhages.

Thickening of blood vessel:

Onion Skin Thickening

Of arterioles.

Narrow Lumen

Hypertrophy of heart:

Left Ventricular Hypertrophy

Cardiomyopathy

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

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

Dilated heart in myocarditis

Myocarditis : T lymphocyte infiltrate and myocyte necrosis.

This is usually either viral or of unknown cause.

Toxic myocarditis: There is some inflammation, myocyte

changes (big nucleolus). Myocyte necrosis also happens.

Giant Cell Myocarditis

• Myocyte necrosis

• Multinucleated giant cells

• Lymphocytes, plasma cells, macrophages,

eosinophils, and neutrophils

• Rapid progression to death

Giant Cell Myocarditis

Cardiomyopathies

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

Dilated cardiomyopathy

Cardiomyopathy – loss of myofibrils

• Cardiomyopathy – trichrome stain showing extensive fibrosis

(blue) between the myocytes. The myocytes also vary in size, and

some have partial loss of myofibrils.

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%)

• 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.

Hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy – myofiber dysarray – not all

fibers are pulling the same direction. Thus the contraction is

ineffective.

Restrictive Cardiomyopathy

• Endomyocardial fibrosis; subendocardial fibrosis

• Loeffler’s endocarditis – eosinophilic infiltrate

• Endocardial fibroelastosis

Amyloidosis – notice the

pink material between the

myocytes.

Amyloidosis – Congo Red is

very, very positive.

Amyloidosis: this heart is thickened, pale, and has a rubbery

consistency that interferes with cardiac expansion during

diastole.

Specific Heart Muscle Diseases

• Toxic: alcohol, cocaine, Adriamycin

• Metabolic: hemochromatosis, hyperthyroidism

• Neuromuscular: muscular dystrophy

• Storage disease: glycogen

• Infiltrative: sarcoidosis

Note the fibrosis and loss of myofibrils in some cells.

Hemochromatosis: note the brown perinuclear deposits of

hemosiderin. It is the soluble iron.

Hemochromatosis – iron stain (iron is blue).

Cardiac tumors

• Primary tumors are rare (most common benign)

• Metastases far more common.

Metastatic neoplasms

• Most common cardiac neoplasms.

– Lung

– Breast

– Melanomas

– Lymphomas

– Leukemias