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This is the external appearance of anormal heart.The epicardial surface

is smooth and glistening.The

amount of epicardial fat is

usual.The left anterior descending

coronary artery extends down from

the aortic root to the apex.
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The anterior surface of the heart

demonstrates an opened left anteriordescending coronary artery.Within the

lumen of the coronary can be seen a dark

red recent coronary thrombosis. The dull

red color to the myocardium as seen below

the glistening epicardium to the lower right

of the thrombus is consistent with

underlying myocardial infarction.
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RISK FACTORS

The prevalence and severity of the disease

among individuals and groups are related to a

number of factors,

uncontrollable,

potentially capable of control.

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NonModifiable Risk Factors

Age

Sex

Family History

Genetics abnormalities

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Potentially Controllable Major

Risk Factors,

Diabetes

Hypertension

Smoking

Hyperlipidemia

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Other risk factors

Stress

Physical inactivity

Obesity

Postmenopausal estrogen deficiency

High carbohydrate intake

Lipoproteins

Chlamydia pneumoinae

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Reduction ( 75%) in the lumen of coronary artery

Acute plaque changes

Fissuring

Hemorrhages

Rupture

Markedly eccentric

Large soft core of necrotic debries

Macrophages metalloproteases

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Coronary artery thrombosis

Exposure of sub-endothelial collagen

Platelet aggregation

Thrombus formation

Complete occlusion

Partial occlusion

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Coronary artery spasm

Exact mechanism is not clear

Thromboxane A2 vasospastic mediater

Platelet aggregates

Endothelial dysfunction

reduced relaxing factor NO

Increased adrenergic activity

Smoking

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LCA

Anterior descending

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RCA (posterior wall)

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LCA - circumflex (lateral wall)

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Acute occlusion (on minimal stenosis)

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M I at 08 hours

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M I at 824 hours

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M I at 24 hours3 days

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M I at 310 days

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M I after 10 days

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After weeks and months

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Sequence of changes in MI

S f h i MI

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Sequence of changes in MI

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Complications

Cardiac arrhythmias (7590 %)

Left ventriculer failure (60 %)

Cardiogenic shock (10 %)

Rupture of wall , papillary muscle (4

8%)

Thromboembolism (1549 %)

Acute pericarditis ( 15%)

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Lab.diagnosis

Creatine kinase

CK

MB

Troponins

SGOT

Lactate dehydrogenase

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This is the external appearance of anormal heart.The epicardial surface

is smooth and glistening.The

amount of epicardial fat is

usual.The left anterior descendingcoronary artery extends down from

the aortic root to the apex.
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This is the normal appearance of myocardial

fibers in longitudinal section. Note the centralnuclei and the syncytial arrangement of the

fibers, some of which have pale pink

intercalated disks.

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This is the tricuspid valve. The leaflets and thin anddelicate. Just like the mitral valve, the leaflets have

thin chordae tendineae that attach the leaflet margins

to the papillary muscles of the ventricular wall below.

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The coronary artery shown here has narrowingof the lumen due to build up of atherosclerotic

plaque. Severe narrowing can lead to angina,

ischemia, and infarction.

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At high magnification, the dark red thrombus is

apparent in the lumen of the coronary. Theyellow tan plaques of atheroma narrow this

coronary significantly, and the thrombus

occludes it completely.

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A thrombosis of a coronary artery is shown here in

cross section. This acute thrombosis diminishes blood

flow and leads to ischemia and/or infarction, marked

clinically by the sudden onset of chest pain.

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This section of coronary artery demonstrates

remote thrombosis with recanalization to leave

only two small, narrow channels.

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There is a pink to red recent thrombosis in this

narrowed coronary artery. The open, needle-like

spaces in the atheromatous plaque are

cholesterol clefts.
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A coronary artery has been opened longitudinally. The

coronary extends from left to right across the middle of the

picture and is surrounded by epicardial fat. Increased

epicardial fat correlates with increasing total body fat. There is

a lot of fat here, suggesting one risk factor for atherosclerosis.

This coronary shows only mild atherosclerosis, with only an

occasional ellow-tan li id la ue and no narrowin .
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This is the left coronary artery from the aortic root on

the left. Extending across the middle of the picture tothe right is the anterior descending branch. This

coronary shows severe atherosclerosis with extensive

calcification. At the far right, there is an area of

si nificant narrowin .

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This is coronary atherosclerosis with the

complication of hemorrhage into atheromatousplaque, seen here in the center of the

photograph. Such hemorrhage acutely may

narrow the arterial lumen.

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Cross sections of this anterior descending coronary artery

demonstrate marked atherosclerosis with narrowing. This is

most pronounced at the left in the more proximal portion ofthis artery. In general, the worst atherosclerosis is proximal,

where arterial blood flow is more turbulent. More focal lesions

mean that angioplasty or bypass can be more useful

rocedures.

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The anterior surface of the heart

demonstrates an opened left anteriordescending coronary artery.Within the

lumen of the coronary can be seen a dark

red recent coronary thrombosis. The dull

red color to the myocardium as seen below

the glistening epicardium to the lower right

of the thrombus is consistent with

underlying myocardial infarction.

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There is pale white collagen within theinterstitium between myocardial fibers. This

represents an area of remote infarction.

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This is the left ventricular wall which has been

sectioned lengthwise to reveal a large recent

myocardial infarction. The center of the infarct

contains necrotic muscle that appears yellow-tan.

Surrounding this is a zone of red hyperemia.

Remainin viable m ocardium is reddish- brown.

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The myocardium beneath the endocardialsurface at the top demonstrates pale fibrosis with

collagenization following healing of a

subendocardial myocardial infarction.

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The heart is opened to reveal the left ventricular free

wall on the right and the septum in the center. Therehas been a remote myocardial infarction that

extensively involved the anterior left ventricular free

wall and septum. The white appearance of the

endocardial surface indicates the extensive scarrin .

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There has been a previous extensive

transmural myocardial infarction

involving the free wall of the left

ventricle. Note that the thickness ofthe myocardial wall is normal

superiorly, but inferiorly is only a

thin fibrous wall. The infarction was

so extensive that, after healing, theventricular wall was replaced by a

thin band of collagen, forming an

aneurysm. Such an aneurysm

represents non-contractile tissue that

reduces stroke volume and strains

the remaining myocardium. The

stasis of blood in the aneurysm

predisposes to mural thrombosis.

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A cross section through the heart reveals a

ventricular aneurysm with a very thin wall at the

arrow. Note how the aneurysm bulges out. The

stasis in this aneurysm allows mural thrombus,

which is present here, to form within the

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This patient underwent coronary artery bypass grafting with

autogenous vein (saphenous vein) grafts. The largest of these

runs down the center of the heart to anastomose with the leftanterior descending artery distally. Another graft extends in a

"Y" fashion just to the right of this to branches of the

circumflex artery. A white temporary pacing wire extends

from the mid left surface.
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This cross section through the heart demonstrates the

left ventricle on the left. Extending from the anterior

portion and into the septum is a large recent

myocardial infarction. The center is tan with

surrounding hyperemia. The infarction is "transmural"

in that it extends through the full thickness of the wall.

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The earliest change histologically seen with acute

myocardial infarction in the first day is contraction

band necrosis. The myocardial fibers are beginning tolose cross striations and the nuclei are not clearly

visible in most of the cells seen here. Note the many

irregular darker pink wavy contraction bands

extendin across the fibers.
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This high power microscopic view of the myocardium

demonstrates an infarction of about 1 to 2 days in duration.

The myocardial fibers have dark red contraction bands

extending across them. The myocardial cell nuclei have almostall disappeared. There is beginning acute inflammation.

Clinically, such an acute myocardial infarction is marked by

changes in the electrocardiogram and by a rise in the MB

fraction of creatine kinase.
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In this microscopic view of a recent myocardialinfarction, there is extensive hemorrhage along with

myocardial fiber necrosis with contraction bands and

loss of nuclei.

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This myocardial infarction is about 3 to 4 days old.There is an extensive acute inflammatory cell infiltrate

and the myocardial fibers are so necrotic that the

outlines of them are only barely visible.

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This is an intermediate myocardial infarction of 1 to 2

weeks in age. Note that there are remaining normal

myocardial fibers at the top. Below these fibers are

many macrophages along with numerous capillaries

and little collagenization.

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One complication of a transmural

myocardial infarction is rupture of

the myocardium. This is mostlikely to occur in the first week

between 3 to 5 days following the

initial event, when the myocardium

is the softest. The white arrow

marks the point of rupture in this

anterior-inferior myocardial

infarction of the left ventricular free

wall and septum. Note the dark red

blood clot forming thehemopericardium. The

hemopericardium can lead to

tamponade.

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In cross section, the point of rupture of the

myocardium is shown with the arrow. In this case,there was a previous myocardial infarction 3 weeks

before, and another myocardial infarction occurred,

rupturing through the already thin ventricular wall 3

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Thank you

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Documents

1. IHD