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 Definition

The term u
  


 is
derived from u
u (the heart
muscle) and  

 (tissue death
due to oxygen starvation)

Ischemic myocardial necrosis usually

resulting from abrupt reduction of
coronary blood flow to a segment of
myocardium.
 ïcute 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:

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

Most common cause of ïMI is an

occlusive coronary thrombus at the
site of a pre-existing atherosclerotic
plaque
Other causes:
h Coronary artery spasm
Variant angina
Cocaine abuse

h Coronary artery embolus

ïtrial myxoma
ïtrial or ventricular thrombus
h Vasculitis

h Hypercoagulable states
Polycythemia vera
Thrombocytosis
 pathogenesis
Mechanism of ïMI

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

ï collagen scar forms in its place
ïcute Myocardial
Infarction
 Clinical Findings
Symptoms
h Chest pain:
h prolonged (>20 min)
sensation of tightness, pressure, squeezing
Radiation to left arm, lower jaw, neck, right arm, back, epigastrium

h Dyspnea: shortness of breath

h Diaphoresis: an excessive form of sweating
h Weakness or Fatigue
h Light-headedness
h Nausea and vomiting
h Palpitations
h Loss of consciousness
h Sudden death
h Silent, without chest pain or other symptoms (elderly
and diabetic neuropathy)
 ïcute Myocardial Infarction

Diagram of pain zones in myocardial infarction

dark red = most typical area,
light red = other possible areas
 Signs
General:
ïppearance: ïnxious and sweating
Tachycardia or Bradycardia
Blood pressure high or low
Fever: low grade
Jugular venous distention (JVD)m
Edema m
Cyanosis m
Chest:
Clear lungs, or basilar rales

Heart:
May be normal
ïbnormally located ventricular Impulse
Soft heart sounds
ïtrial gallop S4 or ventricular gallop S3
Systolic murmur due to papillary muscle or
ventricular septal rupture
Pericardial friction rub
ïcute 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 6-24 hours Months to

inversion years
ïcute Myocardial Infarction
Main Coronary blood supply
Right Coronary ïrtery
ïrises from ïorta behind the
right aortic sinus of valsalva
Supplies:
hPosterior Inferior wall of LV
hRight Ventricle and atrium via
marginal branch
hSï and ïV node
Left Coronary ïrtery
ïrises from the ïorta behind
the left aortic Sinus of valsalva
Left anterior descending (LïD)
Supplies:
ïnterior wall of left ventricle
ïnterior two thirds of
interventricular septum
Left Circumflex (LCX)
Supplies:
Lateral wall of left ventricle
ïcute Myocardial
Infarction
ïcute Myocardial Infarction
Location of Myocardial Infarction
ïrea of Infarction ECG Changes in leads ïrtery involved

Inferior wall II, III, aVf Right Coronary

ïnteroseptal V1-V3 Left anterior
descending
ïnterior 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
initial R wave, ST descending
depression, Tall
Upright T wave, in
association with
Inferior or lateral MI
 Cardiac Enzymes

h Cardiac markers or cardiac enzymes are

proteins from cardiac tissue found in the blood

h These proteins are released into the

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

h Serial measurement of cardiac enzymes is the

most valuable diagnostic test

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

(TNI) are the most specific and widely used
assays
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
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
ïngiography:
ï chest X-ray showed large cardiac silhouette and
bilateral interstitial markings consistent with pulmonary
edema°
ïcute Myocardial
Infarction
Diagnostic criteria (WHO)

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
ïcute Myocardial
Infarction
Types of ïMI

STEMI : ST-elevation myocardial

infarction
NSTEMI : Non-ST-elevation myocardial
infarction

Q-wave infarction (transmural)

Non-Q wave infarction (subendocardial)
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 Treatment

ï 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.
ïcute Myocardial
Infarction
General Measures

h CCU(coronnary care unit) Monitoring

h Oxygen(2-4 L/min)
h ïspirin
h Glyceryl trinitrate (nitroglycerin)
h ïnalgesia (usually morphine)
ïcute 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
ïcute Myocardial
Infarction
Reperfusion therapy

h Thrombolytic therapy
h Percutaneous coronary intervention
(PCI)
h Bypass surgery
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 Thrombolytic ïgents
Recombinant tissue plasminogen activator (rtPï)
Patients <70 years, ïnterior 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
ïlteplase
Reteplase
Tenecteplase
 Thrombolytic therapy

Indications
1. Within 12 hours of the onset of typical chest pain of ïMI
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. ïctive 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
 Percutaneous coronary intervention (PCI)

h PCI done to abort a myocardial infarction is

known as primary PCI

h Goal of primary PCI: open the artery

preferably within 90 minutes of the patient
presenting to the emergency room

h 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
 Other pharmacologic agents given in ïMI

h Beta blockers
h ïngiotensin-converting enzyme inhibitors
h ïnticoagulation (typically with heparin)
h ïntiplatelet agents such as Clopidogrel
 Complications
1. Infarct extension and post infarction
Ischemia

h Inadequate blood flow though a recanalized vessel

or reocclusion
h Medical therapy with nitrates, beta blockers,
calcium channel blockers as well as heparin and
aspirin is given
h If medical therapy fails then early catheterization
and revascularization by Percutaneous
transluminal coronary angioplasty (PTCï) or
Coronary artery bypass graft (CïBG) is performed
 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
 3. Myocardial Dysfunction
 
 
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h Papillary muscle rupture  Interventricular

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 6. Pericarditis

h ïs a reaction to the damage of the heart muscle, inflammatory

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

7. Mural Thrombus

h Common in large anterior infarctions

h Systemic embolization is a potential threat
h Detected by echocardiography
h Treatment is anticoagulation with heparin followed by warfarin
therapy
ïcute Myocardial
Infarction
Post Infarction Management
Stress testing

Coronary angiography

Medical Therapy

ïntiplatelet drug therapy: ïspirin or clopidogeral

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