Archive for the ‘ L3-Patho Arthero/IHD/AP/MI ’ Category

L3- Patho of Atherosclerosis,Ischemic HD,Angina Pectoris,n Myocardial Infarction

CLINICAL PRESENTATION

  1. Artherosclerosis

  2. Ischemic Heart Disease

  3. Angina Pectoris

  4. Myocardial Infarction

Atherosclerosis

– The commonest arterial disease characterized by formation of fibro fatty plaques, formed of a deeper soft part and a hard sclerotic fibrous cap

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Epidemiology….

a. Most common cause of morbidity caused by vascular disease.

b. Highest incidence in Finland, Western Europe, USA and Canada.

c. Increased incidence with advanced age.

d. More in males than females up to the age of menopause.

Risk factors

– Constitutional risk factors.

– Hard risk factors

– Soft risk factors

Constitutional risk factors

Age

The number and severity of atheromatous lesions increase with age.

Sex

more common in males than females up to the age of 55 years. Estrogen has a protective effect ??

Familial predisposition

Hard risk factors

– Hyperlipidemia

-Increased level of cholesterol and LDL is associated with increased risk of atherosclerosis.
– Familial hyperlipidemia (especially types II and III) is associated with increased risk of atherosclerosis.
– On the contrary, HDL has a protective effect against atherosclerosis.

– Hypertension

– Diabetes mellitus

due to associated hyperlipidemia

– Cigarette smoking

Soft risk factors

– Exercise

Reduces the incidence of atherosclerosis and death from ischemic heart diseases

– Overweight

atherogenic diet high in animal saturated  fatty acids and cholesterol.
– High complex sugars in diet.
– Low vegetables and fish.

– Stress and personality

Personality A

Pathogenesis of Atherosclerosis

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•Current concept (Reaction to injury formulation)

Injury (or dysfunction) of arterial endothelium
leads to…
a. Entry of monocytes and lipids to subendothelim.
b. Platelet adhesion and aggregation.
c. Release of mitogenic factors from platelets and macrophages…..proliferation and migration of smooth muscle fibers.
d. Monocytes and smooth muscle cells engulf lipid and cause lipid deposition into the lesion.

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Pathology of atherosclerosis

Sites

* Aorta, especially descending
* Coronaries  and cerebrals
* Femoral , renal, superior mesenteric and internal carotids.

Grossly

– Multiple irregular patches more around ostea of branches.
– Color ranges from yellow to white according to relative amount of fat and fibrous tissue.
– Covered by glistening intima (if not complicated)

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•The plaques are formed of

1- Central core of cholesterol and cholesterol esters, lipid laden macrophages (foam cells), necrotic debris and calcification.

2- Subendothelial fibrous cap formed of proliferated smooth muscle cells, foam cells and extra cellular matrix

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Atheroma of coronary artery

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Complications of atherosclerosis

1- Narrowing of vascular lumen…chronic ischemia.

2- Superimposed thrombosis…acute ischemia.

3- Ulceration with liberation of fatty core … acute ischemia, fat emboli, DIC.

4- Pressure atrophy of the media with fibrosis….weakening of the wall …. Aneurysmal dilatation.

5- Dystrophic calcification.

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Ischemic Heart Diseases


– A group of diseases due to insufficient arterial blood flow to the myocardium.

– Chronic ischemia results in angina pectoris which may be stable or unstable.

– Acute ischemia results in myocardial infarction.

Angina pectoris

An episode of pain in the substernal area of the chest precipitated by exercise or excitement and relieved by rest.

– It is due to temporary acute ischemia on top of chronic ischemia.

Causes:-

1- Coronary atherosclerosis
2- Coronary vasospasm.
3- Aortic valve disease (stenosis or incompetence)

– Types:-

1- Stable angina-evoked by exercise and relieved by rest.

2- Unstable angina-severe pain precipitated by less and less effort (pre-infarction angina)

3- Prinzmetal (vasospastic) angina-occurs at rest, due to coronary spasm, relieved by vasodilator (nitroglycerine)  therapy. 

Myocardial infarction

It is anoxic necrosis of myocardial cells caused by ischemia.

It may be

* Transmural

involving the whole thickness of the heart in certain anatomical areas

* Circumferential subendocardial

involving the subendocardium of left and less commonly right ventricles.
– Caused by hypo-perfusion not actual coronary artery occlusion.

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CAUSES

1-Complicated coronary atheroma (thrombosis, ulceration or hemorrhage of a plaque).

(RARELY)

2- Embolism

3- Poly Arteritis Nodosa

4- Occlusion of coronary ostea by dissecting aortic aneurysm or syphilis.

5- Coronary spasm.

Thrombosis of the coronary artery

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Thrombosis on top of atheroma of the coronary artery

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Pathology Of Myocardial Infarction

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1-6 hours

– Before 6 hours of the occurrence of the infarction, no gross or microscopic changes are detected on the myocardium.

12-24 hours

Infarct area is pale
opaque and dry.
It is slightly swollen

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-Cytoplasm becomes more acidophilic
– striations lost.
– Nuclei disappear

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24-72 hours

– Neutrophils infiltrate the area of infarction

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3-10 days

-Infarct area is yellow, surrounded by a zone of hyperemia.

-Red granulation tissue invades the infarct area from outside inwards.

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-Macrophages replace  neurophils. They engulf necrotic debris.

-Starting invasion of the infarct by young granulation tissue from the periphery to the center

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Weeks -months

-Increasing pallor of the infarct due to progressive fibrosis till a well developed grey-white scar is formed.

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– Progressive maturation of granulation tissue with collagenization.

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Healed Myocardial infarction

– Necrotic tissue is removed.

– Scar tissue is formed.

-Myocardial thinning predisposes to myocardial aneurysm.

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Diagnosis of myocardial infarction

1-ECG and echocardiography

2-Laboratory diagnosis

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Complications of myocardial infarction

1- Arrhythmia

most common cause of death in the first few hours following infarction.

2- Myocardial (pump) failure

can lead to congestive heart failure and/or cardiogenic shock.

3- Myocardial Rupture

– Occurs within 4-7 days after Infarction (due to neutrophilic liquifactive enzymes).

– Can lead to cardiac temponade and compression of the heart by hemorrhage into the pericardial space.

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4- Myocardial aneurysm with thrombosis inside.

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5- Rupture of papillary muscle…..mitral incompetence.

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6- Dressler’s syndrome

-an autoimmune disorder resulting from damage of the myocardium

-release of auto-antigens

-autoimmune pericarditis and pleurisy.

7- Chronic heart failure.

8- Acute pericarditis.

9- Prolonged confinement to bed +wk cardiac action

-leg thrombosis & pulmonary embolism.