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Diseases of the heart

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Diseases of the heart

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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.”

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

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Classification of HD

• -acute• - chronic

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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.

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Acute heart diseases

• Causes-• Trombosis• Embolizm• Prolong spasmus• Discoordination between blood flow and

cardiac work

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Thrombosis in coronary arteryopened longitudinally.

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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).

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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

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Classifications1) 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.

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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%).

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• 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

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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

Visual Inspection

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• 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.

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

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

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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

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

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

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Aneurysm Formation- Complication of myocardial infarction.

- Can be seen in the bulge of left ventricular wall.- Very thin wall of aneurysm toward apex.

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Complicationsa) 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..

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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.

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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.

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Chronic Ischemic Heart Disease

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DEFINITION

• Chronic disease characterized by lipid-protein metabolism disturbance and accumulation of cholesterol and its

ester into blood vessel walls with their destruction

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• 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

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NORMAL ANATOMY

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Cause - atherosclerosis

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BASIC FACTORS

1) Age• More severe in elderly person

• The risk increase with the increase of age• Dominant influence

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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

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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

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NON-BASIC FACTORS1)Hyperlipidermia

2)Alcoholism3)Arterial hypertension

4)Obesity5)High content of cholesterol in food

6) Stress7)Hypodynamia

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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).

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Lumen becomessmaller, bloodsupply decreases