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• Myocardial infarction (MI) is the irreversible

necrosis of heart muscle secondary to prolonged

ischemia. This usually results from an imbalanceof oxygen supply and demand.

CLASSIFICATION

1. Transmural: :(Q –wave infarction) : mostinfartcts are transmural involve the full

thickness of ventricular wall in the distribution

of single coronary artery.These infracts are caused by ch atherosclerosis,

acute plaque changes b y occlusive thrombi and

less commonly thromboemboli or vasospasm.

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2. Subendocardial: these infarcts involve inner one

third to one half of ventricular wall as subendo

cardial zone is less perfused area of myocardialzone. The infarcts are caused by hypoperfusion

of myocardium and not by coronary occlusion.

These occur in hypotensive shock, and by typical

ECG findings these are so called non Q wave infar

Less common causes of MI:

o vasculitis PAN and kawasaki disease.

o Cocain use

o Embolization of plaque material

o Thrombosis syndrome

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These serial sections of a coronary artery demonstrate grossly the

appearance of lumenal narrowing with atherosclerosis.

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• Grossly :Before 6 to 12 hours: No visible lesion is

seen.

• By 18 to 24 hours: Infarct area becomes pale tocyanotic & swollen.

• In the first week: The infarct area becomes

progressively more sharply defined, yellow andsoftened.

• By the 7 to 10 days, circumference of the infarct

area becomes hyperemic, and progressively

expands.

• By the 6 weeks, fibrous scar is well established.

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Ohr 2hr24hr

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This is an acute myocardial infarction in the septum. After several days,

there is a yellowish center with necrosis and inflammation surrounded

by a hyperemic border.

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This is an acute myocardial infarction of the anterior left ventricular free wall and

septum in cross section. Note that the infarction is nearly transmural. There is a

yellowish center with necrosis and inflammation surrounded by a hyperemic borde

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When the infarction is 3 to 5 days old, the necrosis and inflammation are most

extensive, and the myocardium is the softest, so that transmural infarctions may be

complicated by rupture. A papillary muscle may rupture as well to produce sudden

valvular insufficiency. Rupture through the septum results in a left-to-right shunt

and right heart failure.

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Remote myocardial infarction (weeks to years)

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Time from Onset Gross Morphologic Finding

18 - 24 Hours Pallor of myocardium

24 - 72 Hours Pallor with some hyperemia

3 - 7 DaysHyperemic border with central

yellowing

10 - 21 Days Maximally yellow and softwith vascular margins

7 weeks White fibrosis

Gross morphologic changes evolve over time as follows:

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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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Microscopic features:

• Within 1 hour of ischemic injury, there is intercellularedema and “wavy fibers” may be present at the

periphery of the infarct. These are noncontrctile deadfibers, stretched by the adjacent viable contractingmyocytes

• Electron microscopy shows reversible changes

(swelling of mitochondria & endoplasmic reticulum andrelaxation of myofibrils).

• Histochemically, there is loss of oxidative enzyme & fallof glycogen.

• In 12 to 72 hours, there is infiltration of neutrophils

with progressive coagulative necrosis of myocytes.Dead myocytes become hypereosinophilic with loss ofnuclei.

•

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This is an early acute myocardial infarction. (<iday) Note the

prominent pink contraction bands.

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• Between 3 and 7 days after onset, dead myocytes begin todisintegrate and are removed by macrophages and enzymeproteolysis. There is proliferation of fibroblasts with formation ofgranulation tissue, which progressively replaces necrotic tissue.

• After 6 weeks, healing is complete by fibrosis.Contraction band necrosis: Contraction band necrosis,

characterized by hypereosinophilic transverse bands ofprecipitated myofibrils in dead myocytes is usually seen at theedge of an infarct or with reperfusion (e.g. with thrombolytic

therapy).

• Reperfusion of an infarct: Reperfusion of an infarct is alsoassociated with more hemorrhage, less acute inflammation, lesslimitation of the acute inflammation to the periphery in the first

few days, reactive stromal cells, more macrophage infiltrationearlier and a more patchy distribution of necrosis, especiallyaround the periphery.

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2-3 wks Toward the end of the first week, healing of the infarction becomes

more prominent, with capillaries, fibroblasts, and macrophages filled with

hemosiderin. The granulation tissue seen here is most prominent from 2 to

3 weeks following onset of infarction.

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weeks –years After a couple of weeks, healing is well under way, and there

is more extensive collagen deposition.

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wks –yrs The remote myocardial infarction is evidenced by a

collagenous scar seen here in a subendocardial location.

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Time from Onset Microscopic Morphologic Finding

1 - 3 Hours Wavy myocardial fibers

2 - 3 HoursStaining 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 HoursContinuing coagulation necrosis, pyknosis of

nuclei, and marginal contraction bands

24 - 72 HoursTotal loss of nuclei and striations along with

heavy neutrophilic infiltrate

3 - 7 DaysMacrophage and mononuclear infiltration

begin, fibrovascular response begins

10 - 21 DaysFibrovascular response with prominent

granulation tissue

7 Weeks Fibrosis

Microscopic morphologic changes evolve over time as follows:

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Symptoms of a possible heart attack include chest pain and pain that radiatesdown the shoulder and arm. Some people (the elderly, people with diabetes, and

women) may have little or no chest pain. Or, they may experience unusual

symptoms (shortness of breath, fatigue, weakness).

Women are more likely than men to have symptoms of nausea, vomiting, back or

jaw pain, and shortness of breath with chest pain.

• Clinical features Chest pain 20 30% does not

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• Clinical features: Chest pain- 20-30% does not

cause chest pain, common in patients with

diabetes mellitus, hypertension, & in elderly

patients.

• 2. Nausea, diaphoresis and dyspnea.

• Fate of the patient: hospitalized patients

(where angiography, echocardiography and

perfusion scintigraphy are available) usual fate

are:

• i) About 25 % of patients dye of cardiogenicshock or fatal arrythmia.

• ii) Patients who survive the acute phase may

develop:

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Screening and Diagnosis

Stress

Test Coronary

Angiography

Electro-

cardiogram

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• Diagnosis:It is based on symptoms,

electrocardiographic change and serum

elevation of myocardial enzymes (creatinekinase-MB isoenzyme) or other proteins

(troponin I, troponin T or myoglobin), that

leak out of dead cells. • The classic EKG findings: ST segment

elevation, followed by T wave inversion and Q

waves, are associated with transmuralinfarction. ST segment depression and T wave

inversion are associated with subendocardial

infarction.

• The laboratory diagnosis of myocardial infarction:

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• The laboratory diagnosis of myocardial infarction:

1) This has been based on elevation of creatine

phosphokinase (CPK), with an MB fraction >5% of

the total CPK or a relative index >3 (if the MB Theelevation of CPK begins around 8 hours after the

onset of infarction, peaks around 18 hours and

ends around 48 hours .• 2) The late diagnosis of myocardial infarction can

be based on elevation of lactate dehydrogenase

(LDH), with an LDH-1 fraction >40% of the totalLDH or LDH-1/LDH-2 ratio >1, because this peaks

around 5 days.

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• 3) Recently, the early and late diagnosis of

acute myocardial infarction has been based on

elevated serum levels of cardiac troponin. Thiselevation begins around 4 hours after the onset

of infarction and lasts longer than LDH; this test

has a sensitivity similar to CPK-MB fraction andbetter than LDH.

• For the diagnosis of acute myocardial infarction

even earlier than detectable by troponin levels,myoglobin can be tested.

• Elevated levels of myoglobin can be detected

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• around 2 hours after the onset of infarction, but

this has only about 60% specificity for the heart.

• A new type of test being evaluated for thediagnosis of acute myocardial infarction is CPK

MB isoform assay, which has a 96% sensitivity

and 93% specificity for infarction within 6 hours

of onset of chest pain.

• The combination of CPK MB and troponin testing

can have even higher sensitivity and is used for

the purpose of "ruling out" myocardial

infarction.

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• Complications: It depends on the size , locationduration of the lesion.

With in minutes to 3 days of onset:

1. Arrythmias :75-95% i) ventricular fibrillation ; ii)block of A-V bundles and its branches causing

acute heart failure.2. Cardiogenic shock 10-15%(usually in large

infarct) causing acute heart failure.

3. Thrombotic complication- 15-40% mural

thrombus over infarct area or Atrial thrombus,causing embolism to brain, kidney etc.

4. Rupture of heart.

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Myocardial RuptureMyocardial aneurysm with

thrombosis inside.

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Rupture (at the arrow) into the pericardial sac can produce a life-

threatening cardiac tamponade, as seen here. The septum may also

rupture.

R t f ill l it l i t

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Rupture of papillary muscle…..mitral incompetence.

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The myocytes here are hypertrophied, marked by the large, dark nuclei, and

there is interstitial fibrosis. This is an example of cardiomyopathy. In this case,

long-standing, severe occlusive atherosclerosis led to "ischemic" cardiomyopathy.

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• 6- Dressler’s syndrome

• Is complication of transmural MI• -an autoimmune disorder resulting from

damage of the myocardium

• -antibodies developed against protein releasefrom necrotic myocardial cells

• -autoimmune pericarditis, pericardial friction

rub and pleurisy.

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•Blood tests: used to evaluate kidney and thyroid

function as well as to check cholesterol levels and thepresence of anemia.

•Chest X-ray: shows the size of heart and whether

there is fluid build up around the heart and lungs.•Echocardiogram: shows a graphic outline of theheart’s movement

•Ejection fraction (EF): determines how well heartpumps with each beat.

Other Tests

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R/ Revascularization procedures

1) Stenting

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1) Stenting

• a stent is introduced into a blood vessel on a balloon

catheter and advanced into the blocked area of the

artery

• the balloon is then inflated and causes the stent to

expand until it fits the inner wall of the vessel,

conforming to contours as needed

• the balloon is then deflated and drawn back

•The stent stays in place permanently, holding the

vessel open and improving the flow of blood.

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2) Angioplasty

• a balloon catheter is passed through the guiding catheter to the areanear the narrowing. A guide wire inside the balloon catheter is then

advanced through the artery until the tip is beyond the narrowing.

• the angioplasty catheter is moved over the guide wire until the

balloon is within the narrowed segment.• balloon is inflated, compressing the plaque against the artery wall

• once plaque has been compressed and the artery has been

sufficiently opened, the balloon catheter will be deflated and

removed.

3) B

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3) Bypass surgery

• healthy blood vessel is removed from leg, arm or chest

• blood vessel is used to create new blood flow path inyour heart

• the “bypass graft” enables blood to reach your heart

by flowing

around (bypassing) the

blocked portion of the

diseased artery. The

increased blood flowreduces angina and

the risk of heart attack.

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•Get regular medical checkups.

•Control your blood pressure.

•Check your cholesterol.

•Don’t smoke.

•Exercise regularly.

•Maintain a healthy weight.

•Eat a heart-healthy diet.

•Manage stress.

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