Myocardial infarction

According to Lewis

“ Myocardial Infarction occurs as a result of sustained ischemia, causing

irreversible cell death( necrosis), due to which thrombus develops ,
perfusion to the myocardium distal to the occlusion is halted resulting in
necrosis.”
 INCIDENCE
 Cardiovascular diseases (CVDs) have now become the leading cause of
mortality in India. A quarter of all mortality is attributable to CVD.

 Ischemic heart disease and stroke are the predominant causes and are
responsible for >80% of CVD deaths.

 The Global Burden of Disease study estimate of age standardized CVD

death rate of 272 per 100 000 population in India.

 CVD in India increased by 59%, from 23.2 million (1990) to 37 million

(2010).

 In Western populations only 23% of CVD deaths occur before the age of
70 years; in India, this number is 52%.

 According to the Global Burden of Disease study age-standardized

estimates (2010), nearly a quarter (24.8%) of all deaths in India are
 The most common vascular disease.
 Characterized by thickening or hardening of
medium & large sized arteries due to the
accumulation of cholesterol & other lipids,
leads to formation of plaque & results in
endothelial damage.
 Atherosclerosis is a progressive disorder that
narrows & ultimately blocks the arteries.
 Stage I:
 Formation of foam cells: Increased levels of
cholesterol for prolonged periods will favour
deposits in the subintimal region of arteries.
 Aorta, coronary arteries & cerebral vessels
are predominantly affected by this
process.
 LDLC, especially oxidized LDL particles are
 The oxidized LDLC is taken up by
macrophages of immune
system.
 Free radical induced oxidative damage of
LDL will accelerate this process.
 These macrophages are overloaded with
lipid (cholesterol & oxi-LDLC) & these are
called as “foam cells”.
 These form the hallmark of atherosclerotic
plaques.
 Stage II: Progression of atherosclerosis:
 Smooth muscle cells containing lipid droplets
are seen in the lesion.
 Plaques are composed of smooth muscle
cells, connective tissue, lipids & debris that
accumulate in intima of arterial wall.
 Plaque progresses with age as follows.
 Endothelial cell of the artery wall are injured
either by oxidized LDL or mechanically.
 The injured area is exposed to blood &
attracts monocytes which are converted to
macrophages that engulf oxidized LDLC &
converted to foam cells, which accumulate
causing a fatty streak to develop within
blood vessel.
 Stage III:
 Fibrous proliferation:
 Due to liberation of various growth factors
by macrophages & platelets, lipoproteins,
& collagen are accumulated.
 Thus there is a definite component of
inflammation in atherosclerosis.
 Damaged endothelial cells cannot produce
prostaglandins I2 & prostacyclin (which
inhibit platelet aggregation).
 Platelets begin to aggregate & release
thromboxane A2 (TXA2).
 Thromboxane A2 stimulate platelet
aggregation.
 Stage IV: Advancing fibrous plaque:
 Damaged endothelial cells also release
platelet derived growth factor (PDGF).
 The growth factors cause proliferation of
smooth muscle cells, which migrate from
medial to intimal layer arterial wall &
contributes to the formation of
atherosclerosis plaques.
 This leads to narrowing of
blood vessels & leads to heart
attacks.
 2 3
1

1. Normal artery
2. Early plaque formation
3. Advanced plaque formation
RISK FACTORS
 Risk Factors ( Non Modifiable)
Age
The risk of having a heart attack increases with age.
Men are at a higher risk of a heart attack after age 45.
Women are at a higher risk of a heart attack after age 55.

Family history

risk is especially high if you have male family members

who developed heart disease before age 55 or if you have
female family members who developed heart disease before
age 65.
 Risk Factors ( Non modifiable)

Ethenicity

Highest among South Asian as compared to

western group of people.

Heredity

Immediate family members are at greater risk.

Menopause in women
 Risk Factors ( Modifiable)
1. Smoking increases a person's
risk for heart disease to about 4
times greater than non-
smokers.
• 2. Obesity and physical inactivity People who
have excess body fat — especially at the waist
— are more likely to develop
heart disease even if they have
no other risk factors.

3. Acute and prolonged intake of high

quantities of alcoholic drinks (3-4
or more) increase the risk of a heart
attack
 Risk Factors ( Modifiable)
Bad cholesterol
Bad cholesterol, also called low-density lipoprotein (LDL), is
one of the leading causes of a blockage in the arteries.
Saturated fats
Saturated fats may also contribute to
the buildup of plaque in the coronary
arteries. Saturated fats are found
mostly in meat and dairy products,
including beef, butter, and cheese.
High blood pressure
Having high blood pressure damages
your arteries and accelerates the
buildup of plaque.
• Diabetes and high blood sugar levels
• Diabetes is a condition that causes blood sugar, or glucose, levels
to rise. High blood sugar levels can damage blood vessels and
eventually lead to coronary artery disease.

• Obesity
• Obesity is associated with various conditions that increase the
risk of heart attack, including:
diabetes
high blood pressure
high cholesterol levels
high triglyceride levels
• Lack of exercise has been linked to 7–12% of cases
 Classification
1
The two main types of acute myocardial infarction,9
based on pathology, are:
 Transmural infarction- Transmural infarcts extend
through the whole thickness of the heart muscle and
are usually a result of complete occlusion of the
area's blood supply.
 Subendocardial (nontransmural) infarction -
involves a small area in the subendocardial wall of
the left ventricle, ventricular septum, or papillary
muscles.

A transmural infarct is sometimes referred to as an “ST

elevation myocardial infarct” (STEMI) and a
subendocardial
These serial sections of a coronary artery demonstrate
grossly the appearance of lumenal narrowing with
atherosclerosis.
(2) ofthe tip of
the anterior wall
of the heart (an
apical infarct)
after occlusion
(1) of a branch
of the left
coronary
artery(LCA, right
coronar
Stages of Myocardial Infarction
Stage 1. Early coagulative necrosis -->

release of necrotic dead cell contents into the blood.

Edema, hemorrhage, wavy fibers are all common in the

first 24 hours after an MI. Neutrophils begin to appear on the
scene as first responders in the hours after an MI.

Stage 2. Extensive coagulative necrosis continues a day after the

MI. Inflammation begins in the day after the MI upwards of 3 days
after the MI. Neutrophils begin to appear in the inflammation.
Borders of the infarcted tissue become redder due to hyperemia.
Stage 3. Around a week after the MI, macrophages appear on the
scene to clear the dead cells and tissue and granulation begins to
form at the margins. The infarcted heart becomes soft and turns a
yellow-brown color. It is softened by 10 days post MI. There is a
hyperemic border present surrounding the yellow-tan infarcted heart
tissue.

Stage 4. Scar formation and increased collagend deposition and

acellularity occurs approximately 2 weeks to several months after the
MI. Gray -white granulation tissue appears in the infarcted region.
After 2 months a dense collagenous scar finishes forming.
Ohr 2hr
24hr
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.
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
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.
Remote myocardial infarction (weeks to years)
 Gross morphologic changes evolve
over time as follows:
Time from
Onset
•Gross Morphologic Finding
18 - 24 Hours

•Pallor of
24 -myocardium
72 Hours

•Pallor with
3 - 7 some
Days
hyperemia

10 - 21
Days
•Hyperemic border with
central 7yellowing White
weeks fibrosis
This is normal myocardium. There are cross striations and central nuclei. Pale
pink intercalated disks are also present.
Microscopic features:
• Within 1 hour of ischemic injury, there is
intercellular edema and “wavy fibers” may be
present at the periphery of the infarct. These are
noncontrctile dead fibers, stretched by the adjacent
viable contracting myocytes
• Electron microscopy shows reversible changes
(swelling of mitochondria & endoplasmic
reticulum and relaxation of myofibrils).
• Histochemically, there is loss of oxidative
enzyme & fall of glycogen.
• In 12 to 72 hours, there is infiltration of
neutrophils with progressive coagulative necrosis of
myocytes. Dead myocytes become hypereosinophilic
with loss of nuclei.
•
This is an early acute myocardial infarction. (<iday) Note
the prominent pink contraction bands.
1-2 daysThis is an early acute myocardial infarction. There is increasing loss
of cross striations, and some contraction bands are also seen, and the
nuclei are undergoing karyolysis. Some neutrophils are beginning to
infiltrate the myocardium.
 1-2days This is an acute myocardial infarction. There is loss of cross
striations, and the nuclei are not present. There is extensive
hemorrhage here at the border of the infarction, which accounts for
the grossly apparent hyperemic border.
3-4 days This is an acute myocardial infarction of several days'
duration. There is a more extensive neutrophilic infiltrate
along with the prominent necrosis and hemorrhage.
• Between 3 and 7 days after onset, dead myocytes
begin to disintegrate and are removed by macrophages and
enzyme proteolysis. There is proliferation of fibroblasts with
formation of granulation 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 of precipitated myofibrils in dead myocytes is usually
seen at the edge of an infarct or with reperfusion (e.g. with
thrombolytic therapy).

• Reperfusion of an infarct: Reperfusion of an infarct is

also associated with more hemorrhage, less acute
inflammation, less limitation of the acute inflammation to the
periphery in the first few days, reactive stromal cells, more
macrophage infiltration earlier and a more patchy distribution
of necrosis, especially around the periphery.
 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.
 weeks –years After a couple of weeks, healing is well under way, and
there is more extensive collagen deposition.
wks –yrs The remote myocardial infarction is evidenced by
a collagenous scar seen here in a subendocardial location.
 Microscopic morphologic changes evolve over time
as follows:
Time from Microscopic Morphologic
Onset Finding
1-3 Wavy myocardial
Hours fibers
Staining defect with tetrazolium or
2-3
basic fuchsin dye
Hours

Coagulation necrosis with loss of cross

4 - 12 striations, contraction bands, edema,
Hours hemorrhage, and early neutrophilic
infiltrate

Continuing coagulation necrosis, pyknosis

18 - 24
of nuclei, and marginal contraction bands
Hours

Total loss of nuclei and striations along

24 - 72
with heavy neutrophilic infiltrate
Hours
Macrophage and mononuclear
3-7
infiltration begin, fibrovascular response
Days
begins
Fibrovascular response with prominent
10 - 21
granulation tissue
Days
7 Fibrosis
• Clinical Manifestation
Symptoms of a possible heart attack include Severe chest pain and pain
that radiates down 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.
 Blood pressure decreased because of
Signs and Symptoms of an
decreased contractility,
Coronary Artery Disease
impending cardiogenic shock,
Cardiovascular System
Pulse deficit may indicate atrial fibrillation.
Severe Chest pain or discomfort,

palpitations.  ST-segment and T-wave changes, ECG

may show tachycardia, bradycardia, and
Heart sounds may include dysrhythmias.
S3, S4, and new onset of a murmur.

Increased jugular venous distention

may be seen if the MI has caused heart
failure.

Blood pressure may be elevated because

of sympathetic stimulation or
Respiratory
Shortness of breath,
dyspnea,
tachypnea,
and crackles if MI has caused pulmonary congestion.
Pulmonary edema may be present.

Gastrointestinal

Nausea and
 vomiting.

Genitourinary

Decreased urinary output may indicate cardiogenic shock.

Integumentary system

Cool,

clammy,

diaphoretic,

and pale appearance due to sympathetic

stimulation from loss of contractility may indicate

cardiogenic shock.

Dependent edema may also be present due to poor

contractility.
Neurological System

Anxiety,

restlessness,

light-headedness may indicate increased sympathetic stimulation

or a decrease in contractility and cerebral oxygenation.

The same symptoms may also herald cardiogenic shock.

Headache,
visual disturbances,

altered speech,

altered motor function,

and further changes in level of consciousness may indicate

cerebral bleeding if patient is receiving thrombolytic.

Psychological

Fear with feeling of

impending doom, or

patient may deny

that anything is wrong.
 Screening and Diagnosis

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HISTORY
Assessment

• patients with CAD describe a heaviness, choking, or smothering sensation.

• Patients often describe the sensation as “someone sitting on my chest.”

• The substernal pain can radiate to the neck, left arm, back, or jaw.

• Unlike the pain of angina, the pain of an MI is often more prolonged and unrelieved
by rest or sublingual nitroglycerin.

• Associated findings on history include nausea and vomiting, especially for the
patient with an inferior wall MI.

• These gastrointestinal complaints are believed to be related to the severity of the

pain and the resulting vagal stimulation.
PHYSICAL EXAMINATION

Patients usually appear restless and in distress.

The skin is warm and moist.

Breathing may be labored and rapid. Fine crackles, coarse

crackles,
• or rhonchi may be heard when auscultating the lungs.

an increased blood pressure related to anxiety or a decreased

blood pressure caused by heart failure.

The heart rate may vary from bradycardia to tachycardia.

When the patient is placed in the left lateral decubitus position,

On auscultation, the first heart sound may be diminished as
a result of decreased contractility.

A fourth heart sound is heard in almost all patients with

MI, whereas a third heart sound is detected in only about
10% to 20% of patients.

Transient systolic murmurs may be heard

After about 48 to 72 hours, many patients acquire a

pericardial friction rub
The Electrocardiogram

• An ECG can be used to detect patterns of ischemia,

injury, and infarction Ischemia.

• On the ECG, myocardial ischemia results in T-wave

inversion or ST segment depression in the leads facing the
ischemic area.

• The inverted T wave representative of ischemia is

symmetrical, relatively narrow, and somewhat pointed.
• ST segment depressions of 1
to 2 mm or more for a duration of
0.08 second may indicate
myocardial ischemia.

• Ischemia also should be

suspected when a flat or
depressed ST segment makes a
sharp angle when joining an
upright T wave rather than
merging smoothly and
Injury.

• the injury process begins in the subendocardial layer and moves

throughout the thickness of the wall of the heart like a wave.
• If the injury process is not interrupted, it eventually results in a
transmural MI.

• On ECG, the hallmark of acute myocardial injury is the presence of ST

segment elevations.

• In the normal ECG, the ST segment should not be elevated more than 1
mm in the standard leads or more than 2 mm in the precordial leads.

• With an acute injury, the ST segments in the leads facing the injured area
are elevated.

• The elevated ST segments also have a downward concave or coved shape

and merge unnoticed with the T wave
(A)ST segment elevation without
T-wave inversion.

(B) ST segment elevation with T-

wave inversion.
The elevated ST segments have
a downward concave or coved
shape and merge unnoticed with
the T wave.
Infarction. When myocardial injury persists, MI is the result.
• During the earliest stage of MI, known as the hyperacute phase, the T waves
become tall and narrow.

• This configuration is referred to as hyperacute or peaked T waves.

• Within a few hours, these hyperacute T waves invert.

• Next, the ST segments elevate, a pattern that usually lasts from several hours to
several days.

• In addition to the ST segment elevations in the leads of the ECG facing the
injured heart, the leads facing away from the injured area may show ST segment
depression.

• This finding is known as reciprocal ST segment changes.

• Reciprocal changes are most likely to be seen at the onset of infarction, but their
presence on the ECG does not last long.
Q waves indicate tissue necrosis and are permanent. A pathologic Q wave is one that is
greater than 3 mm in depth or greater than one-third the height of the R wave.
Laboratory Tests

• Creatine Kinase

• CK-MB appears in the serum in 6 to 12 hours, peaks between

12 and 28 hours, and returns to normal levels in about 72 to 96
hours.
• Serial samplings are performed every 4 to 6 hours for the first 24 to
48 hours after the onset of symptoms

• Creatine Kinase Isoforms:

•
• CK-MB1 is the isoform found in the plasma, and CK-MB2 is
found in the tissues. In the patient with an MI, the CK-MB2 level
rises, resulting in a CK-MB2 to CK-MB1 ratio greater than one
• Myoglobin:

• Myoglobin is an oxygen-binding protein found in

skeletal and cardiac muscle. Myoglobin’s release from
ischemic muscle occurs earlier than the release of CK.

• The myoglobin level can elevate within 1 to 2 hours

of acute MI and peaks within 3 to 15 hours.
•
• Because myoglobin is also present in skeletal muscle,
an elevated myoglobin level is not specific for the diagnosis
of MI. onsequently, its diagnostic value in detecting an MI
is limited
• Troponin. (troponin T and troponin I):

• Troponin I levels rise in about 3 hours, peak at

14 to 18 hours, and remain elevated for 5 to 7 days.

• Troponin T levels rise in 3 to 5 hours and

remain elevated for 10 to 14 days
Release of cardiac markers after acute
myocardial infarction (AMI).
• Complications: It depends on the size ,
location duration 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.
Rupture of papillary muscle…..mitral incompetence.
 is the bulge seen
Left ventricular aneurysm
containing mural thrombus here in the left
ventricular wall.
Note the very
thin white wall
of the aneurysm
toward the apex.
 Other Tests
•Blood tests: used to evaluate kidney and
thyroid function as well as to check
cholesterol levels and the presence 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 the heart’s movement
•Ejection fraction (EF): determines how well
heart pumps with each beat.
 Management
Medical Management ( Pharmacological )
 Management

EARLY MANAGEMENT
• The patient’s history and 12-lead ECG are the
primary methods used to determine initially the
diagnosis of MI.
• The ECG is examined for the presence of ST
segment elevations of 1 mV or greater in
contiguous leads.
• 1. Administer aspirin, 160 to 325 mg chewed.
• 2. After recording the initial 12-lead ECG, place
the patient on a cardiac monitor and obtain
serial ECGs.
• 3. Give oxygen by nasal cannula.
• 4. Administer sublingual nitroglycerin (unless the
systolic blood pressure is less than 90 mm Hg or
the heart rate is less than 50 or greater than 100
beats/minute).

• 5. Provide adequate analgesia with morphine

sulfate. Provide adequate analgesia with morphine
sulfate.
 Thrombolytic Therapy

• Thrombolytic drugs lyse coronary thrombi by converting

plasminogen to plasmin.

• Thrombolytic therapy provides maximal benefit if given

within the first 3 hours after the onset of symptoms.
• Significant benefit still occurs if therapy is given up to 12
hours after onset of symptoms.

Contraindications
■ Previous hemorrhagic stroke at any time; other stokes
or cerebrovascular events within 1 year
■ Known intracranial neoplasm
■ Active internal bleeding (does not include menses)
■ Suspected aortic dissection
 Thrombolytic Therapy

Cautions/Relative Contraindications

■ Severe uncontrolled hypertension on presentation (blood

pressure >180/110 mm Hg)

■ History of prior cerebrovascular accident or known

intracerebral disease not covered in contraindications

■ Current use of anticoagulants in therapeutic doses

(international normalized ratio [INR] ≥2:3); known bleeding
diathesis

■ Recent trauma (within 2–4 weeks), including head trauma

or traumatic or prolonged (>10 minutes) cardiopulmonary
• ■ Noncompressible vascular punctures
• ■ Recent (within 2–4 weeks) internal bleeding
• ■ For streptokinase/anistreplase: prior exposure
(especially within 5 days to 2 years) or prior allergic
reaction
• ■ Pregnancy
• ■ Active peptic ulcer
• ■ History of chronic severe
Primary Percutaneous Translumin(PTCA) is an effective alternative
to reestablish blood flow to ischemic myocardium.

Primary PTCA is an invasive procedure in which the infarct-related

coronary artery is dilated during the acute phase of an MI without
prior administration of thrombolytic agents.

Primary PTCA may be an excellent reperfusion alternative for

patients ineligible for thrombolytic therapy.
The nurse must carefully monitor the patient after a primary PTCA
for evidence of complications.

These complications can include retroperitoneal or vascular

hemorrhage, other evidence of bleeding, early acute reocclusion,
and late restenosis.
 INTENSIVE AND INTERMEDIATE CARE MANAGEMENT
• Prophylactic antidysrhythmics during the first 24 hours of hospitalization are not
recommended.

• IV nitroglycerin is continued for 24 to 48 hours.

• Daily aspirin is continued on an indefinite basis.

• Clopidogrel may be used for patients who are intolerant of aspirin.

• IV beta blocker therapy should be administered within the initial hours of the evolving
infarction, followed by oral therapy provided there are no contraindications.

• Beta blockers are one of the few pharmacological agents

• that have been shown to reduce morbidity and mortality
• in the patient with an MI.

• They reduce oxygen demand by decreasing the heart rate and contractility.
• They also increase coronary artery filling by prolonging
• diastole.
 Calcium channel blockers may be given to patients in whom
beta blocker therapy is ineffective or contraindicated.
 Angiotensin-converting enzyme (ACE) inhibitors are
administered to patients with anterior wall MI and to
patients who have an MI with heart failure in the absence
of significant hypotension.
 ACE inhibitors help prevent ventricular remodeling
(dilation) and preserve ejection fraction.
 Heparin is given to patients undergoing percutaneous or
surgical revascularization and for those receiving
thrombolytic therapy with alteplase.
 Low–molecular-weight heparin should be used for patients
with non–Q-wave MI
Hemodynamic Monitoring
• Use of a pulmonary artery catheter for hemodynamic
monitoring is indicated in the patient with MI who has
severe or progressive congestive heart failure or
pulmonary edema, cardiogenic shock, progressive
hypotension, or suspected mechanical complications.

Additional Diagnostic Tests:

• Radionuclide Imaging
• Echocardiogram
• Stress Test
• Coronary Angiography
 Complications

Vascular Complications Myocardial Complications

• Recurrent ischemia • Diastolic dysfunction
• Recurrent infarction • Systolic dysfunction
Mechanical Complications • Congestive heart failure
• Hypotension/cardiogenic
• Left ventricular free wall
shock
rupture
• Right ventricular infarction
• Ventricular septal rupture • Ventricular cavity dilation
• Papillary muscle rupture with • Aneurysm formation (true,
acute mitral regurgitation false)
 Complications

Pericardial Complications Electrical Complications

• Pericarditis • Ventricular tachycardia
• Dressler’s syndrome • Ventricular fibrillation
• Supraventricular
• Pericardial effusion
tachydysrhythmias
Thromboembolic Complications • Bradydysrhythmias
• Mural thrombosis • Atrioventricular block (first,
• Systemic thromboembolism second, or third degree)
• Deep venous thrombosis
• Pulmonary embolism
 Nursing Diagnoses

• Anxiety related to chest pain, fear of death, threatening

environment
• Acute Pain related to oxygen supply and demand imbalance
• Decreased Cardiac Output related to impaired contractility
• Activity Intolerance related to insufficient oxygenation to
perform activities of daily living, deconditioning effects of
bed rest
• Risk for Injury (bleeding) related to dissolution of protective
clots
R/ Revascularization procedures
 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.
 2) Angioplasty
•a balloon catheter is passed through the guiding catheter to the area
near 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) Bypass surgery

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

• blood vessel is used to create new blood flow path in
your heart
• the “bypass graft” enables blood to reach your heart
by flowing

around (bypassing) the

blocked portion of the
diseased artery. The
increased blood flow
reduces angina and
the risk of heart attack.
•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.