The document discusses diseases of the heart, specifically chronic ischemic heart disease and myocardial infarction. It describes the blood supply to the heart from the coronary arteries and the risks factors, causes, classifications, signs and symptoms, progression, complications and treatment of myocardial infarction. Key points include that myocardial infarction is mainly caused by blockages in the coronary arteries from atherosclerosis, and can lead to complications like arrhythmias, heart failure, cardiogenic shock or cardiac rupture if not properly treated.

1. Diseases of the heart

2. BLOOD SUPPLY OF THE HEART
• 2 coronary arteries
branch from the main
aorta just above the
aortic valve. “No larger
than drinking straws,
they divide and encircle
the heart to cover its
surface with a lacy
network that reminded
physicians of a slightly
crooked crown
(coronary comes from
the Latin coronarius,
belonging to a crown or
wreath). They carry out
about 130 gallons of
blood through the heart
muscle daily.”

3. • This is normal myocardium. There are cross
striations and central nuclei. Pale pink
intercalated disks are also present.

4. Classification of HD
• -acute
• - chronic

5. Epidemiology
- Myocardial infarction is a common presentation of
ischemic
heart disease.
- Ischemic heart disease is the leading cause of death in
developed countries, but 3rd to AIDS and lower
respiratory infections in developing countries.
- In industrialized countries, myocardial infarction accounts
for 10 – 25% of incidences , all deaths.
- About 5% of heart attacks occur in young people under the
age of 40 years old, especially with hypertension, diabetes
mellitus, cigarette smoking and etc.

6. Acute heart diseases
• Causes-
• Trombosis
• Embolizm
• Prolong spasmus
• Discoordination between blood flow and
cardiac work

8. Thrombosis in
coronary artery
opened
longitudinally.

9. Risk factors
• Risk factors for atherosclerosis are generally risk factors for
myocardial infarction:
• Diabetes (with or without insulin resistance) - the single most
important risk factor for ischaemic heart disease (IHD)
• Tobacco smoking
• Hypercholesterolemia (more accurately hyperlipoproteinemia,
especially high low density lipoprotein and low
high density lipoprotein)
• High blood pressure
• Family history of ischaemic heart disease (IHD)
• Obesity[29] (defined by a body mass index of more than 30 kg/m², or
alternatively by waist circumference or waist-hip ratio).

10. Risk factors
• Age: Men acquire an independent risk factor at age 45, Women acquire an
independent risk factor at age 55; in addition individuals acquire another
independent risk factor if they have a first-degree male relative (brother, father)
who suffered a coronary vascular event at or before age 55. Another independent
risk factor is acquired if one has a first-degree female relative (mother, sister) who
suffered a coronary vascular event at age 65 or younger.
• Hyperhomocysteinemia (high homocysteine, a toxic blood amino acid that is
elevated when intakes of vitamins B2, B6, B12 and folic acid are insufficient)
• Stress (occupations with high stress index are known to have susceptibility
for atherosclerosis)
• Alcohol Studies show that prolonged exposure to high quantities of alcohol can
increase the risk of heart attack
• Males are more at risk than females.[20]
• Many of these risk factors are modifiable, so many heart attacks can be prevented
by maintaining a healthier lifestyle. Physical activity, for example, is associated
with a lower risk p

11. Classifications
1) According To The Anatomic Region Of The Left Ventricle
Involved :
- They are called anterior, posterior, lateral, septal and circumferential.
2)According To the Degree Of Thickness Of The Ventricle
Wall Involved :
a) Full-thickness or transmural, when they involve the entire thickness of the
ventricular wall.
b) Subendocardial or lamina, when they occupy the inner subendocardial
half of the myocardium.
3) According To The Age Of Infarcts :
a) Newly-formed infarcts are called acute, recent or fresh.
b) Advanced infarcts are called old, healed or organized.

12. Localizations
- Infarction are most frequently located in the left ventricles :
. Apex
. Anterior or Posterior wall
. Interventricular Septa
- The region of infarction depends upon the area of obstructed blood
supply by one or more of the 3 coronary arterial trunks :
1) Stenosis Of The Left Anterior Descending Coronary Artery
- The most common (40 – 50%).
2) Stenosis Of The Right Coronary Artery
- The next most frequent (30 – 40%).
3) Stenosis Of The Left Circumflex Coronary Artery
- The least frequently (15 – 20%).

13. • Gross morphologic changes evolve over time
as follows:
from Onset Gross Morphologic Finding
8 - 24 Hours Ischemic stage/Pallor of myocardium
24 - 72 Hours Pallor with some hyperemia
3 - 7 Days Hyperemic border with central yellowing
10 - 21 Days
Maximally yellow and soft with vascular
margins
7 weeks White fibrosis

14. Visual Inspection
Development Of
Stages
Visual Inspection
1) Ischemic Stage
- This stage takes 24
hours.
- No sharp changes in visual inspection.
- Not clear foci of myocardium, only in left ventricle pale,
multicoloured zone, flabby consistency.
2) Necrotic Stage
- Begin 24 hours after
pain attack.
- White (ischemic) infarction with red ring (focus of nonregular
form whitish-yellowish colour with dark red border line is
observed).
3) Organization/
Scarring
- Begin at the 3-d, 4-th
days after pain attack,
The end – in 4-6 weeks.
- Postinfarction cardiosclerosis appear :
Big focal scar formation

16. • Microscopic picture of infarction:
• The dominant histologic characteristic is ischaemic coagulative
necrosis in all organs except the brain where the infarct is a
liquefactive necrosis. Coagulative necrosis is characterized by
preservation of the structural outline of the coagulated cells or
tissues, with loss of details and nuclei. This may persist for weeks
after which the necrotic tissue is removed by white blood cells.
• An inflammatory response begins to develop along the margins of
the infarct within few hours. In all infarcts there is gradual
degradation of the dead tissue by the inflammatory cells.
Eventually the inflammatory response is followed by a reparative
response beginning in the margins.

18. Early Acute Myocardial Infarction
- Prominent pink contraction bands can be seen.

19. Acute Myocardial Infarction
- Loss of cross striations and nuclei.
- Extensive hemorrhage at border of infarction, which accounts for the
grossly apparent hyperemic border.

21. Microscopic morphologic changes
evolve over time as follows:
ime from Onset Microscopic Morphologic Finding
1 - 3 Hours Wavy myocardial fibers
2 - 3 Hours Staining defect with tetrazolium or basic fuchsin dye
4 - 12 Hours
Coagulation necrosis with loss of cross striations, contraction bands,
edema, hemorrhage, and early neutrophilic infiltrate
18 - 24 Hours
Continuing coagulation necrosis, pyknosis of nuclei, and marginal
contraction bands
24 - 72 Hours
Total loss of nuclei and striations along with heavy neutrophilic
infiltrate
3 - 7 Days
Macrophage and mononuclear infiltration begin, fibrovascular
response begins
10 - 21 Days Fibrovascular response with prominent granulation tissue
7 Weeks Fibrosis

22. Myocardium Rupture (Arrow)
- Rupture into the pericardial sac can produce a life-threating cardiac
tamponade.
- As seen here, septum may also rupture.

23. Aneurysm
- Wall of aneurysm is
thin.
- But form of
collagenous tissue is
dense.
- So, rupture does not
happen.

24. Aneurysm Formation
- Complication of myocardial infarction.
- Can be seen in the bulge of left ventricular wall.
- Very thin wall of aneurysm toward apex.

25. Complications
a) Arrhythmias
- Most common form of complication of acute myocardial infarction.
b) Congestive Heart Failure
- May be in the form of right ventricular, left ventricular failure or both.
- It is responsible for about 40% of deaths from acute myocardial infarction.
c) Cardiogenic Shock
- Characterized by hypotension with systolic blood pressure of 80 mmHg or less
for
many days.
- Shock may be accompanied by peripheral circulatory failure, oliguria and mental
confusion.
d) Mural Thrombosis and Thromboembolism
- From intracardiac thrombi and thrombosis in the leg veins is observed in
15 – 45% cases of acute myocardial infarction.

26. e) Myocardial Rupture
- It occurs in the free walls of the ventricles, the septum between them, the
papillary muscles, or less commonly the atria.
- Rupture occurs because of increased pressure against the weakened walls of the
heart chambers due to heart muscle that cannot pump blood out effectively.
f) Cardiac Aneurysm
- Often occur in left ventricle, it impairs the function of the heart and is the site for
mural thrombi.
g) Fibrinous Pericarditis
- This complication develops in the patients with transmural myocardial
infarction.
- About 3 – 4% of patients who suffered from acute myocardial infarction develop
post-myocardial infarction syndrome which is characterized by pneumonitis.

27. Main Causes Of Death
1) Angina Pectoris
- Clinical syndrome of ischemic heart disease, resulting from transient
myocardial ischemia.
- Characterized by pain in the pericardial region of the chest, as a result of
dystrophy in the myocardial cells.
2) Chronic Ischemic Heart Disease (Myocardial Fibrosis)
- It may be focal or diffuse. The mechanism of development can be different.
3) Sudden Cardiac Death
- Defined as sudden death within 24 hours of the onset of cardiac symptoms.
- The most causes are ischemic heart disease, myocarditis, hypertrophic
cardiomyopathy, hereditary and acquired defects of the conduction system.
- Autopsy in such cases reveals most commonly critical atherosclerosis coronary
narrowing.

28. Chronic Ischemic Heart Disease

29. DEFINITION
• Chronic disease characterized by lipid-protein
metabolism disturbance and
accumulation of cholesterol and its
ester into blood vessel walls with their
destruction

30. • In other words, artheriosclerosis is characterized
by intimal lesion called atheroma, or
atheromatous or fibrofatty plagues, which
protrude into and obstruct vascular lumens and
weaken the underlying media

31. NORMAL ANATOMY

32. Cause - atherosclerosis

33. BASIC FACTORS
1) Age
• More severe in elderly person
• The risk increase with the increase of age
• Dominant influence

34. 2) Sex
• Male have more severe and more
rapidly
• For woman, the risk increase after
menopause
• Estrogen =>stimulate HDL =>
resulting in decrease in cholesterol
level
• But after menopause => decrease
estrogen level => increase risk of
arteriosclerosis

35. 3)Smoking
• Nicotine stimulate symphathetic nervous
system=> displace oxygen in Hb=> increase
level of carboxyHb => increase blood
adhereness
4) Diabetic Mellitus
• Includes hypercholesterolemia and markedly
increase predisposition of artheriosclerosis
5)Hereditary predisposition/ genetic

36. NON-BASIC FACTORS
1)Hyperlipidermia
2)Alcoholism
3)Arterial hypertension
4)Obesity
5)High content of cholesterol in food
6) Stress
7)Hypodynamia

38. Angina is a specific type of pain in the chest caused by
inadequate blood flow through the blood vessels (coronary
vessels) of the heart muscle (myocardium).

39. Lumen
becomes
smaller, blood
supply
decreases