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Acute Myocardial

Infarction

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Acute Myocardial Infarction
Definition

The term myocardial infarction is derived from


myocardium (the heart muscle) and infarction (tissue
death due to oxygen starvation)

Ischemic myocardial necrosis usually resulting from


abrupt reduction of coronary blood flow to a segment
of myocardium.

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Acute Myocardial Infarction

Epidemiology
It is a medical emergency, and the leading cause of death for
both men and women all over the world

Important Risk factors:


• Older age
• Male gender
• Family history
• Cigarette smoking
• Hypercholesterlemia (especially high LDL and low HDL)
• Diabetes
• High blood pressure
• Obesity (defined by a BMI of more than 30 kg/m2)
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Acute Myocardial Infarction

Most common cause of AMI is an


occlusive coronary thrombus at the
site of a pre-exixting atherosclerotic
plaque

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Other causes:
• Coronary artery spasm
Variant angina
Cocaine abuse

• Coronary artery embolus


Atrial myxoma
Atrial or ventricular thrombus
• Vasculitis

• Hypercoagulable states
Polycythemia vera
Thrombocytosis

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Acute Myocardial Infarction
Mechanism of AMI

Over decades atherosclerosis causes gradual buildup


of cholesterol and fibrous tissue in plaques
in the wall of coronary arteries

Coronary artery lumen narrows as a result of


decades of advancing atherosclerosis

Plaques can become unstable due to inflammation,


rupture, and promote a thrombus that occludes the
artery; this can occur in minutes

Plaque rupture leads to myocardial infarction


A collagen scar forms in its place
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Acute Myocardial Infarction

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Acute Myocardial Infarction

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Clinical Findings
Symptoms
• Chest pain:
• prolonged (>20 min)
sensation of tightness, pressure, squeezing
Radiation to left arm, lower jaw, neck, right arm, back, epigastrium

• Dyspnea: shortness of breath


• Diaphoresis: an excessive form of sweating
• Weakness or Fatigue
• Light-headedness
• Nausea and vomiting
• Palpitations
• Loss of consciousness
• Sudden death
• Silent, without chest pain or other symptoms
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Acute Myocardial Infarction

Diagram of pain zones in myocardial infarction


dark red = most typical area,
light red = other possible areas

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Signs
General:

Appearance: Anxious and sweating


Tachycardia or Bradycardia
Blood pressure high or low
Fever: low grade
Jugular venous distention (JVD)±
Edema ±
Cyanosis ±
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Chest:
Clear lungs, or basilar rales

Heart:
May be normal
Abnormally located ventricular Impulse
Soft heart sounds
Atrial gallop S4 or ventricular gallop S3
Systolic murmur due to papillary muscle or
ventricular septal rupture
Pericardial friction rub

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Acute Myocardial Infarction
ECG Change Onset Disappearance

Electrocardiogram (ECG)
Hyper acute T Immediately 6-24 hours
waves (Tall Peaked
T waves in leads
facing infarction)

ST Segment Immediately 1-6 weeks


elevation

Q waves longer One to Years to never


than 0.04 sec several days

T wave inversion 6-24 hours Months to years

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Acute Myocardial Infarction
Main Coronary blood supply

Right Coronary Artery Left Coronary Artery

Arises from Aorta behind the Arises from the Aorta behind
right aortic sinus of valsalva the left aortic Sinus of valsalva
Supplies: Left anterior descending (LAD)
•Posterior Inferior wall of LV Supplies:
•Right Ventricle and atrium via Anterior wall of left ventricle
marginal branch Anterior two thirds of
•SA and AV node interventricular septum
Left Circumflex (LCX)
Supplies:
Lateral wall of left ventricle

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Acute Myocardial Infarction

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Acute Myocardial Infarction
Location of Myocardial Infarction
Area of Infarction ECG Changes in leads Artery involved

Inferior wall II, III, aVf Right Coronary


Anteroseptal V1-V3 Left anterior descending

Anterior wall V2-V4 Left anterior descending

Lateral wall I, aVL, V4, V5 and V6 Left anterior descending


or circumflex

Posterior wall V1-V2: Tall broad Posterior descending


initial R wave, ST
depression, Tall
Upright T wave, in
association with
Inferior or lateral MI

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Cardiac Enzymes

• Cardiac markers or cardiac enzymes are


proteins from cardiac tissue found in the blood

• These proteins are released into the


bloodstream when damage to the heart occurs,
as in the case of a myocardial infarction

• Serial measurement of cardiac enzymes is the


most valuable diagnostic test

• Creatinine Kinase (CK-MB) and Troponin I or T


(TNI) are the most specific and widely used
assays
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CK-MB begins to elevate at 4-6 hours
after onsetof chest pain and peaks
at 12-24 hours

Troponin I begins to elevate 4-6


hours after onset of pain and
Remains elevated for 1-2 weeks

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Chest X-Ray:
May be normal or may show signs of Congestive heart failure

Echocardiography:
Provides assessment of ventricular function and wall motion.
Doppler echo is used to diagnose post infarction mitral
regurgitation or ventricle septal defect

Other Laboratory tests:


Leukocytosis
Scintigraphic studies:

Angiography:

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Acute Myocardial Infarction

A chest X-ray
showed large
Cardiac silhouette
and
bilateral interstitial
markings
consistent with
pulmonary edema.

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Acute Myocardial Infarction
Diagnostic criteria

1. Clinical history of ischaemic type chest


pain lasting for more than 20 minutes
2. Changes in serial ECG tracings
3. Rise and fall of serum cardiac biomarkers
such as CK-MB and Troponin I specific for
the heart

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Acute Myocardial Infarction
Types of AMI

STEMI : ST-elevation myocardial infarction


NSTEMI : Non-ST-elevation myocardial infarction

Q-wave infarction
Non-Q wave infarction

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Acute Myocardial Infarction
Treatment

A heart attack is a medical emergency


which demands immediate attention

The ultimate goal of the management in the


acute phase of the disease is to salvage
as much myocardium as possible and
prevent further complications.

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Acute Myocardial Infarction
General Measures

• CCU(coronnary care unit) Monitoring


• Oxygen(2-4 L/min)
• Aspirin
• Glyceryl trinitrate (nitroglycerin)
• Analgesia (usually morphine)

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Acute Myocardial Infarction
Reperfusion therapy

The concept of reperfusion has become


so central to the modern treatment of
acute myocardial infarction, that we are
said to be in the reperfusion era

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Acute Myocardial Infarction
Reperfusion therapy

• Thrombolytic therapy
• Percutaneous coronary intervention
(PCI)
• Bypass surgery

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Acute Myocardial Infarction

Fibrinolysis is the process


where a fibrin clot, the product
of coagulation, is broken down
by an enzyme plasmin
Fibrin-specific thrombolytic
agents have have the property
of fibrin-enhanced conversion
of plasminogen to plasmin.

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Thrombolytic Agents
Recombinant tissue plasminogen
activator (rtPA)
Patients <70 years, Anterior MI, within 4 hours of onset and with
pump failure.

Streptokinase
Older patients with concomitant hypertension (>160mmHg), no
previous exposure to streptokinase or recent streptococcal
infection.

Urokinase
Alteplase
Reteplase
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Thrombolytic therapy

Indications
1. Within 12 hours of the onset of typical chest pain of AMI
2. ST elevation of > 1mm in two contiguous leads or Q waves
3. New Left bundle branch block

Contraindications
1. Dissecting aortic aneurysm
2. Uncontrolled hypertension > 180/110
3. Active peptic ulcer
4. Bleeding Diathesis
5. History of cerebrovascular disease
6. Recent trauma or surgery especially of head or spine
7. Traumatic CPR
8. Pregnancy
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Percutaneous coronary intervention (PCI)
• PCI done to abort a myocardial infarction is
known as primary PCI

• Goal of primary PCI: open the artery preferably


within 90 minutes of the patient presenting to the
emergency room

• Primary PCI involves performing a coronary


angiogram to determine the anatomical location
of the infarcting vessel, followed by balloon
angioplasty (and frequently deployment of an
intracoronary stent) of the thrombosed arterial
segment

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Other pharmacologic agents given in AMI

• Beta blockers
• Angiotensen-converting enzyme inhibitors
• Anticoagulation (typically with heparin)
• Antiplatelet agents such as Clopidogrel

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Complications

1. Infarct extension and post infarction Ischemia

• Inadequate blood flow though a recanalized vessel or


reocclusion
• Medical therapy with nitrates, beta blockers, calcium
channel blockers as well as heparin and aspirin is given
• If medical therapy fails then early catheterization and
revascularization by Percutaneous transluminal
coronary angioplasty (PTCA) or Coronary artery bypass
graft (CABG) is performed

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2. Life threatening arrhythmias
Electrical characteristics of the infarcted
tissue is changed so arrhythmias are a
frequent complication
The re-entry phenomenon may cause too fast
heart rates like ventricular tachycardia and
even ventricular fibrillation and ischemia in the
electrical conduction system of the heart may
cause a complete heart block

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3. Myocardial Dysfunction
Cardiac dysfunction is proportionate to the extent of myocardial
necrosis

■Congestive heart failure:


signs/symptoms: Dyspnoea, Diffuse rales in the lung, Arterial
hypoxemia
Treatment: Oxygen, Diuretics, morphine sulphate, vasodilators nitrates,
ionotropic agents dopamine or dobutamine

■Hypotension and shock:


Systolic BP<100 mmHg, low urine output, cold extremities and
confusion
Treatment: Dopamine, Norepinephrin, Intra-aortic baloon
counterpulsation IABC

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4. Mechanical defects

• Paplillary muscle rupture and Interventricular


septum rupture can occur in AMI

• Detected by appearance of new systolic murmer with


clinical deterioration and pulmonary edema

• Treatment is by surgical repair

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5. Myocardial rupture
 Myocardial rupture is most common three to five days after
AMI
• Shear stress between the infarcted segment and the
surrounding normal myocardium makes it a nidus for
rupture
• Occur in the free walls of the ventricles
• The weakness may also lead to ventricular aneurysm
• Rupture is usually a catastrophic event that may result a
life-threatening process known as cardiac tamponade

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6. Pericarditis

• As a reaction to the damage of the heart muscle, inflammatory cells


are attracted and may reach out and affect the heart sac causing
pericarditis
• In Dressler's syndrome this occurs several weeks after the initial event.
• Treated with aspirin, NSAIDs and later steroids

7. Mural Thrombus

• Common in large anterior infarctions


• Systemic embolization is a potential threat
• Detected by echocardiography
• Treatment is anticoagulation with heparin followed by warfarin therapy

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Acute Myocardial Infarction
Post Infarction Management
Stress testing

Coronary angiography

Medical Therapy

Antiplatelet drug therapy: Aspirin or clopidogeral


Beta Blocker
ACE- Inhibitors
Lipid lowering Therapy
Smoking cessation
Regular exercise
Sensible diet for patients with heart disease,
Limitation of alcohol intake

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