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A 50 – year – old male teacher

notices the sudden onset of “chest

CASE 2 tightness” when he walks across the
parking lot to and from the school.
The pain, which is localized over the
sternum, goes away when he sits
down. He does not experience any
pain or discomfort at other times. He
has mild hypertension, for which he is
on dietary therapy. His cholesterol
level is elevated. He does not smoke.

Clinical Scenario: History

Male, 50 yrs. Old

 Chest tightness when walking for a Short distance
 Pain over the Sternum
Pain is relieved by Sitting down
On Diet Therapy
Differential Diagnosis

Acute Myocardial Infarction
Stable Angina Pectoris
What Is Pericarditis?
Is a condition in which the membrane, or sac, around your heart is
inflamed. This sac is called the pericardium.
The pericardium holds the heart in place and helps it work properly.
The sac is made of two thin layers of tissue that enclose your heart.
Between the two layers is a small amount of fluid. This fluid keeps the
layers from rubbing against each other and causing friction.
Figure A shows the pericardium—the sac surrounding the heart. Figure B is
an enlarged cross-section of the pericardium that shows its two layers of
tissue and the fluid between the layers.
What Causes Pericarditis?

e cause of about half of all pericarditis cases (both acute
and chronic) is unknown.
ral infections are likely the most common cause of acute
pericarditis, but the virus may never be found.
Pericarditis often occurs after a respiratory infection.
Bacterial, fungal, and other infections also can cause
Less often, pericarditis is
caused by:
Autoimmune disorders, such as

lupus, scleroderma, and rheumatoid arthritis

Heart attack and heart surgery

Kidney failure, HIV/AIDS,

cancer, tuberculosis, and other health problems

Injury from accidents or

radiation therapy
Certain medicines, like
phenytoin (an antiseizure medicine), warfarin and heparin (blood-thinning medicines), and
procainamide (a medicine to treat abnormal heartbeats)
The causes of acute and chronic

pericarditis are the same.

Who Is At Risk for Pericarditis?

ericarditis occurs in people of all ages. However, men

between the ages of 20 and 50 are more likely to get

eople who are treated for acute pericarditis may get it

again. This may happen in 15 to 30 percent of people
who have the condition. A small number of these
people go on to develop chronic pericarditis.
What Are the Signs and Symptoms of
Sharp, stabbing chest pain is a common symptom of acute
pericarditis. The pain usually comes on quickly. It often is felt
in the middle or the left side of the chest.
The pain tends to ease when you sit up and lean forward.
Lying down and deep breathing worsens it. For some people,
the pain feels like a dull ache or pressure in their chests.
Fever is another common symptom of acute pericarditis. Other
symptoms are weakness, trouble breathing, and coughing.
Chronic pericarditis often causes tiredness,
coughing, and shortness of breath. Chest
pain is often absent in this type of
pericarditis. Severe cases of chronic
pericarditis can lead to swelling in the
stomach and legs and low blood pressure
What symptoms are associated with
most common symptom caused by pericarditis is chest pain. The pain
can severe, and is often made worse by changing position or with deep
breathing. Patients can also have shortness of breath, or fever.
carditis can produce complications, namely tamponade, chronic
pericarditis, and constriction. These complications - which are discussed
below – can produce reduced cardiac pumping, lung congestion, and
organ failure.
Complications of Pericarditis

Two serious complications of

pericarditis are:

 cardiac tamponade

chronic constrictive pericarditis.

Cardiac tamponade
occurs when too much fluid collects in the
pericardium (the sac around the heart). The
extra fluid puts pressure on the heart. This
prevents the heart from properly filling with
blood. As a result, less blood leaves the heart.
This causes a sharp drop in blood pressure. If
left untreated, cardiac tamponade can cause
Chronic constrictive pericarditis

is a rare disease that develops over time. It

leads to scar-like tissue throughout the
pericardium. The sac becomes stiff and
can’t move properly. In time, the scarred
tissue compresses the heart and prevents it
from working correctly.
Myocardial Infarction (MI)
What is MI?
"Myocardial Infarction" (abbreviated as "MI")
means there is death of some of the muscle cells of
the heart as a result of a lack of supply of oxygen
and other nutrients.
is the rapid development of myocardial necrosis
caused by a critical imbalance between oxygen
supply and demand of the myocardium
Cause of MI:
The most frequent cause of
myocardial infarction (MI) is
rupture of an atherosclerotic plaque
within a coronary artery with
subsequent arterial spasm and
thrombus formation.
Other causes:
Coronary artery vasospasm
Ventricular hypertrophy (eg, left ventricular hypertrophy [LVH], idiopathic
hypertrophic subaortic stenosis [IHSS], underlying valve disease)
Hypoxia due to carbon monoxide poisoning or acute pulmonary disorders
(Infarcts due to pulmonary disease usually occur when demand on the
myocardium dramatically increases relative to the available blood supply.)
Coronary artery emboli, secondary to cholesterol, air, or the products of
Cocaine, amphetamines, and ephedrine
Other causes:

Coronary anomalies, including aneurysms of
the coronary arteries
Increased afterload or inotropic effects, which
increase the demand on the myocardium
Aortic dissection, with retrograde involvement
of the coronary arteries
Risk factors:
Age-older than 45 years old
Male gender
Hypercholesterolemia and hypertriglyceridemia,
including inherited lipoprotein disorders
Diabetes mellitus
Poorly controlled hypertension
Family history
Sedentary lifestyle
Signs & Symptoms:

Chest pain
Nausea& abdominal pain
Lightheadedness with or without syncope
Nausea with or without vomiting
Complication type: Manifestations:

•Ischemic •Angina, reinfarction, infarct

•Heart failure, cardiogenic shock,
•Mechanical mitral valve dysfunction, aneurysms,
cardiac rupture
•Arrhythmic •Atrial or ventricular arrhythmias,
sinus or atrioventricular node
•Embolic dysfunction
•Central nervous system or peripheral
Angina pectoris

most common clinical manifestation of CAD

results from an imbalance between myocardial O2

supply and demand, most commonly resulting from
atherosclerotic coronary artery obstruction.

Other major conditions that upset this balance and

result in angina include
 aortic valve disease,
 hypertrophic cardiomyopathy,
 coronary artery spasm.
• Usually develops gradually with exertion,
emotional excitement, or after heavy
• •Rest or treatment with nitroglycerin leads
to relief.
• In contrast, pain that is fleeting is rarely
ischemic in origin.
• Pain that last for several hours is unlikely
to represent angina.
• Most myocardial perfusion occurs during
diastole, when there is minimal pressure
opposing coronary artery flow.
• Tachycardia decreases the percentage of
time in which the heart is in diastole. It
decreases myocardial perfusion.
• Similar in quality to angina pectoris.
• More prolonged ang severe.
• Occur with the patient at rest, or
awakened from sleep.
• Sublingual nitroglycerin may lead to
transient or no relief.
• Accompanying Sx: Diaphoresis, dyspnea,
nausea and light-headedness.
• Auscultation: During ischemic episodes
there will be presence of third or fourth
heart sounds.
• This reflects myocardial systolic or
diastolic dysfunction.
• Presence of transient murmur of mitral
regurgitation suggests ischemic papillary
muscular dysfunction.
• CAUSES: The spasm often occurs in
coronary arteries that have not become
hardened due to plaque buildup
(atherosclerosis ). However, it also can
occur in arteries with plaque buildup.
• The coronary artery may appear normal
during angiography , but it does not
function normally.
• Coronary artery spasm occurs most
commonly in people who s moke or who
have high c holesterolo r high blood
• It may be triggere d by:Alcohol
withdrawal,emotionalstress ,exposure to
cold,medications, and stimulant drugs
such as ampheta mines and cocaine.
• Symptoms: Spasm may be "silent" --
without symptoms -- or it may result in
chest pain or angina.
• If the spasm lasts long enough, it may
even cause a heart attack.
• The main symptom is a type of chest pain
called angina, felt under the chest bone
and is described as:
• Constricting, crushing, pressure, squeezing,
• It is usually severe. The pain may spread
to the neck, jaw, shoulder, or arm.
•The pain often occurs at rest and may
occur at the same time each day,usually
between midnight and 8:00 AM
• Lasts from 5 to 30 minutes
• The person may lose consciousness.
• Chest pain and shortness of breath are
often not present during walking and
Angina Pectoris
 P( provoking) – eating too much
• exercise
• emotion
• cold
 P ( Palliating/ relieving) – Rest and Nitroglycerin ( sublingual)
 Q ( quality) – steady; precordial pressure (“hollow-block”)
 - dull, aching, squeezing
 R ( region) – precordial
 R ( radiation) - radiate to Left axilla, left under surface of
arms and forearms—little finger then it goes up— left shoulder
and jaw.
 S (severity) – mild-severe
Etiology of the Signs &
Chest Tightness (relieved by rest)

– Ischemia manifests most frequently as chest


Myocardial ischemia occurs when the oxygen
supply to the heart is not sufficient to meet
metabolic needs. This mismatch can result from a
decrease in oxygen supply, a rise in demand, or

The most common underlying cause of myocardial
ischemia is obstruction of coronary arteries by
– Vascular radius and compliance of resistance arteries
are important determinants of arterial pressure
– With atherosclerosis, results to narrowing of the blood
vessel lumen; damage of the arteries
– Consequently small decreases in lumen size significantly
increase resistance causing increased arterial pressure
Elevated Cholesterol Level
– Major risk factor in the development of atherosclerosis
– The incidence of CHD is correlated with elevated
levels of LDL cholesterol and triacylglycerols and with
low levels of HDL cholesterol.
– Cholesterol levels may be elevated as a result of an
individual's lifestyle (for example, by lack of exercise
and consumption of a diet containing excess saturated
fatty acids)
Clinico- Pathologic
Heart sounds

Normal heart sound Pericardial Friction rub


Myocardial Ischemia
Myocardial Ischemia

(also known as angina) is a heart condition

caused by a temporary lack of oxygen-rich
blood to the heart. There are three types, each
of which is signified by pain. The stable type
occurs when the heart is working harder than
usual and generally goes away with rest;
unstable myocardial ischemia is dangerous and
requires emergency treatment; variant (also
called Prinzmetal's angina) occurs at rest and
can be relieved by medicine.
Myocardial Ischemia

There is an imbalance between the supply and

demand of the heart for oxygenated blood.
In more than 90% of cases, the cause of
myocardial ischemia is reduction in coronary
blood flow due to atherosclerotic coronary
arterial obstruction. In most cases, there is a
long period (decades) of silent, slowly
progressive, coronary atherosclerosis before
these disorders become manifest.
Atheroma of coronary

A fixed obstructive lesion

of 75% or greater (i.e.,
only 25% or less lumen
remaining) generally
causes symptomatic
ischemia induced by
Stable angina results from increases in myocardial
oxygen demand that outstrip the ability of markedly
stenosed coronary arteries to increase oxygen delivery
but is not usually associated with plaque disruption.
A 90% stenosis can lead to inadequate coronary blood flow
even at rest. Slowly developing occlusions may stimulate
collateral vessels over time, which protect against distal
myocardial ischemia and infarction even with an eventual
high-grade stenosis.

Smoking tobacco

• Smoking and long-term exposure to

secondhand smoke damage the interior
walls of arteries — including arteries to your
heart — allowing deposits of cholesterol to
collect and block blood flow.

Diabetes is the inability of your body to produce or

respond to insulin properly.
Insulin, a hormone secreted by your pancreas,
allows your body to use glucose, which is a form of
sugar from foods.
Diabetes greatly increases the risk of coronary
artery disease, which leads to angina and heart
attacks by speeding up atherosclerosis and
increasing your cholesterol levels
High blood pressure

Blood pressure is determined by the amount of blood your

heart pumps and the amount of resistance to blood flow in
your arteries.
Over time, high blood pressure damages arteries by
accelerating atherosclerosis.
High blood pressure can be an inherited problem.
The risk of high blood pressure increases as you age, but
the main causes are eating a diet too high in salt, stress,
inadequate exercise and being overweight.
High blood cholesterol or triglyceride
 Cholesterol is a major part of the deposits that can narrow arteries
throughout your body, including those that supply your heart. A high level
of the wrong kind of cholesterol in your blood increases your risk of
angina and heart attacks.
 Low-density lipoprotein (LDL) cholesterol (the "bad" cholesterol) is most
likely to narrow arteries.
 A high LDL level is undesirable and is often a byproduct of a diet high in
saturated fats and cholesterol.
 A high level of triglycerides, a type of blood fat related to your diet, also is
 However, a high level of high-density lipoprotein (HDL) cholesterol (the
"good" cholesterol) is desirable and lowers your risk of angina and heart
Personal or family history of heart
If you have coronary artery disease or if you've had a heart
attack, you're at a greater risk of developing angina.
Older age. Men older than 45 and women older than 55 have
a greater risk than younger adults.
Lack of exercise. An inactive lifestyle contributes to high
blood cholesterol levels and obesity. Exercise is beneficial in
lowering high blood pressure. However, it is important to
consult with your doctor before starting an exercise program.

Obesity raises the risk of angina and heart

disease because it's associated with high
blood cholesterol levels, high blood pressure
and diabetes.
Also, your heart has to work harder to
supply blood to the excess tissue.

*You may respond to stress in ways that can

increase your risk of angina and heart attacks.
• If you're under stress, you may overeat or
smoke from nervous tension.
• Too much stress, as well as anger, can also raise
your blood pressure.
• Surges of hormones produced during stress can
narrow your arteries and worsen angina.
of Angina

The typical patient with angina is a man

>50 years or a woman > 60 years who
complains of chest discomfort, usually
described as heaviness, pressure,
squeezing, smothering, or choking and
only rarely as frank pain.

When the patient is asked to localize the sensation,

he/she will typically press on the sternum,
sometimes with a clenched fist, to indicate a
squeezing, central, substernal discomfort ( Levine’s
The angina is usually crescendo – decrescendo in
nature and usually lasts 2 – 5 mins and can radiate
to the left shoulder and to both arms, especially to
the ulnar surface of the forearm and hand.

It can also radiate to the back,

interscapular region, root of the
neck, jaw, teeth, and epigastrium.
Angina rarely localize below the
umbilicus or above the mandible.

Although episodes of angina are typically

caused by exertion or emotion and are
relieved by rest, they may also occur at rest
and at night while the patient is recumbent.
The patient may be awakened at night
distressed by typical chest discomfort and

The threshold for the development of

angina pectoris may vary by time of day and
emotional state.
Many patients report fixed threshold for
angina, which occurs predictably at a certain
level of activity, such as climbing two flights
of stairs at a normal pace.

Angina may also be precipitated by unfamiliar tasks, a

heavy meal, exposure to cold, or a combination.
It is also important to uncover family history of Ischemic
Heart Disease and presence of diabetes mellitus,
hyperlipidemia, hypertension, and cigarette smoking.
The history of typical angina pectoris establishes the
diagnosis of Ischemic Heart Disease until proven
Physical Examination
This is often normal in patients with stable
angina, but it may reveal evidence of
atherosclerotic disease at other sites, such as an
abdominal aortic aneurysm, carotid arterial
bruits, and diminished arterial pulse in the lower
There may also be signs of anemia, thyroid
disease, and nicotine stains on the fingertips
from cigarette smoking.
Physical Examination

Palpation may reveal cardiac enlargement

and abnormal contraction of the cardiac
Auscultation can uncover arterial bruits, a
third or fourth heart sound, and if acute
ischemia or previous infarction has impaired
papillary muscle function, an atypical
systolic murmur due to mitral regurgitation
Physical Diagnosis

Examination during and anginal attack is useful,

since ischemia can cause transient left ventricular
failure with the appearance of a third or fourth
heart sound, a dyskinetic cardiac apex, mitral
regurgitation and even pulmonary edema.
Tenderness of the chest wall or reproduction of
pain with palpation of the chest discomfort makes
it unlikely that it is caused by angina.
Laboratory Examination
The urine should be examined for evidence of
diabetes mellitus and renal disease (including
microalbuminuria) since these conditions
accelerate atheroschlerosis.
Similarly examination of the blood should
include measurements of lipids (total
cholesterol, LDL, HDL, and triglycerides),
glucose, creatinine, hematocrit and thyroid
Laboratory Examination

A chest x-ray is important, since it may

show the consequences of IHD like
cardiac enlargement, ventricular
aneurysm, or signs of heart failure.
These signs support the diagnosis of
IHD and are important in assessing the
degree of cardiac damage.
Chest X-ray findings:
A 12 – lead ECG recorded at rest is normal in about half
of the patients with typical angina pectoris, but there
may be signs of an old myocardial infarction.
Repolarization abnormalities like ST – segments and T-
wave changes as well as intraventricular hypertrophy
and intraventricular conduction disturbances, are
suggestive of IHD, but they are nonspecific, since they
can also occur at pericardial, myocardial and valvular
heart disease.

Typical ST – segment and T – wave

changes that accompany episodes of
angina pectoris and disappear
thereafter are more specific.
Stress Testing

The most widely used test for both the diagnosis of

IHD and estimating the prognosis involves
recording the 12 – lead ECG before, during, and
after exercise, usually on a treadmill.
The test consists of a standardized incremental
increase in external workload while the symptoms,
ECG, and arm blood pressure are monitored.
Stress Testing

Performance is usually symptom – limited,

and the test is discontinued upon evidence
of chest discomfort, severe shortness of
breath, dizziness, severe fatigue, ST –
segment depression, a fall in systolic blood
pressure or the development of ventricular
Stress Testing

This test seeks to discover any limitation in

exercise performance, to detect typical ECG signs
of myocardial ischemia, and to establish their
relationship to chest discomfort.
When interpreting ECG stress tests, the
probability that coronary artery disease (CAD)
exists in the patient should be considered.
Stress Testing

Overall, false – positive or false – negative

results occur in one third of cases.
However a positive result on exercise
indicates that the likelihood of CAD is 98%
in males >50 years with a history of typical
angina pectoris and who develop chest
discomfort during the test.
Stress Testing

It is increased in patients taking cardioactive drugs

such as digitalis and quinidine, or in those with
intraventricular conduction disturbances, resting ST –
segment and T – wave abnormalities, ventricular
hypertrophyor abnormal serum potassium levels.
Since the overall sensitivity of exercise stress
electrocardiography is only 75%, a negative result does
not exclude CAD, although it makes the likelihood of
three – vessel or left main CAD extremely unlikely.
Cardiac Imaging

The imaging is carried out both

immediately after cessation of exercise
to detect regional ischemia and 4 h
later to confirm reversible ischemia and
regions of persistent absent uptake that
signify infarction
Cardiac Catheterization Laboratory

Contrast Media
via Moving
Cardiac Imaging

Two dimensional echocardiography can

asses both global and regional wall motion
abnormalities of the left ventricle due to
myocardial infarction or persistent ischemia.
Stress echocardiography may cause the
emergence of regions of akinesis or
dyskinesis not present at rest.
Cardiac Imaging

Echocardiography or radionuclide
angiography should be carried out to asses
left ventricular function in patients with
chronic stable angina and in patients with a
history of a prior myocardial infarction,
pathologic Q waves or clinical evidence of
heart failure.
2- D Echo
Coronary Arteriography

This diagnostic method outlines the lumina

of the coronary arteries and can be used to
detect or exclude serious coronary
obstruction. However, coronary
arteriography provides no information
regarding the arterial wall, and severe
atherosclerosis that does not encroach on
the lumen may go undetected
Coronary Arteriography

Coronary arteriography is indicated in

 patients with chronic stable angina pectoris who
are symptomatic despite medical therapy and who
are being considered for revascularization
 patients with troublesome symptoms that present

diagnostic difficulties in whom there is need to

confirm or rule out the diagnosis of IHD.
 Patients with known or possible angina pectoris

who have survived cardiac arrest

Coronary Arteriography

Coronary arteriography is indicated in

 Patients with angina or evidence of ischemia on
noninvasive testing with clinical or laboratory
evidence of ventricular dysfunction
 Patients judged to be at high risk of sustaining
coronary events based on signs of severe
ischemia on noninvasive testing, regardless of the
presence or severity of symptoms.
of Angina

 Cardiac arrhythmias
 Ventricular tachycardia
 Heart block
 Atrial fibrillation

Congestive heart failure

Myocardial infarction
Dressler’s syndrome
Mitral regurgitation
Pulmonary embolism
Sudden death
Ventricular aneurysm
Cardiac arrhythmia

 Abnormal heart rate/ rhythm

 Any abnormality or disturbance in the impulse can
result in arrhythmia
Congestive Heart Failure

 Heart’s function as a pump is inadequate to meet the

body’s need
 May affect the left ventricle, right ventricle or both
Myocardial Infarction

 Occurs when a blood clot completely obstructs an

artery supplying blood to the heart
Dressler’s Syndrome-complication that can occur after
a heart attack
-inflammation of the pericardium that is thought to
be an autoimmune disease
-chest pain worsens with leaning forward or taking a
deep breath
 Mitral Regurgitation-backflow of blood from the left
ventricle to the left atrium due to mitral insufficiency
from incomplete closure of the mitral valve
 Pericarditis-inflammation of the sac surrounding the
-mostly caused by viral infection
-chest pain worsens with movement and taking a
deep breath
Pulmonary embolism

Pulmonary embolism
-obstruction of the pulmonary artery or branch of it
leading to the lung by a blood clot that breaks off
-prevents blood from reaching the lung
Shock- life threatening condition that prevents the
heart and bloodstream from delivering enough
oxygen to keep up with the demand of the body
 Stroke- sudden onset focal neurologic deficit
 Sudden death
 Ventricular aneurysm- bulging in the ventricle of the

 Principal prognostic indicators in Patients with IHD

 functional state of the left ventricle
 Location and severity of coronary artery narrowing
 Severity of myocardial ischemia
Increased risk for adverse coronary events

 Angina pectoris of recent onset

 Unstable angina
 Angina unresponsive / poorly responsive to therapy accompanied by
symptoms of CHF
 Most importantly,
Signs during noninvasive testing
 Strongly positive exercise test showing onset of myocardial
ischemia at low workloads before completion of stage II (Bruce
Protocol) exercise test
 Decline in systolic pressure >10mmHg during exercise
 Development of large /multiple perfusion defects or increased lung
uptake during stress radioisotope perfusion imaging
 -decrease in left ventricular ejection fraction during
exercise on radionuclide ventriculography or during
stress echocardiography
 Cardiac catheterization
-elevation in left ventricular end diastolic pressure
and ventricular volume
-reduced ejection fraction
 Excellent prognosis- patient with chest discomfort but
normal left ventricular function
 Obstructive lesion of the left anterior descending coronary
artery proximal to the origin of 1st septal artery- associated
with greater risk than lesion of the R/L circumflex
 Stenosis of left main coronary is associated with mortality
rate of 15%/ year
 Stable angina- marker of underlying CHD
Angina Pectoris

Stop doing whatever it is that causes the

Call for help
Lie down in comfortable position with head up
Bring to Hospital Emergency department
At the Hospital

IV line
Aspirin (unless taken one)
Oxygen (face mask or canula)
 sublingual, transdermal
 relieves angina symptoms by expanding blood
vessels and decreasing the muscle's need for
 taken only when the patient actually has
symptoms or expect to have them.
 Slow - or long-acting nitroglycerin can be used as
a preventative treatment for angina but not until
beta blockers are tried first.
Calcium channel blockers
 are used primarily when beta blockers cannot be used
and/or the patient is still having angina with beta blocker
 also lower blood pressure and certain ones slow heart
 taken every day

ACE inhibitors
 also vasodilators with both symptomatic and
prognostic benefit
 Statins
 lower cholesterol and stabilize the fatty plaque on the inner lining of
the coronary artery, even when the blood cholesterol is normal or
minimally increased.
 Low density lipoprotein (LDL) levels should be less than 70 mg/dL
for those at high risk of heart disease.

 Beta blockers:
 lessen the heart's workload
 slow the heart rate, decrease blood pressure, and lessen the force of
contraction of the heart muscle, this decreases the heart's need for
oxygen and thus decreases angina symptoms
 Beta blockers are taken every day, regardless of whether the patient
is having symptoms, because they are proven to prevent heart attacks
and sudden death.
Heparin medications
enoxaparin (Lovenox®), dalteparin (Fragmin®), and
nadroparin (Fraxiparin®)
Frequent blood tests are needed to monitor the
concentration of heparin in the blood.
IIb/IIIa inhibitors
eptifibatide (Integrelin®), tirofiban (Aggrastat®), and
abciximab (ReoPro®).
almost completely prevent the formation of blood clots and
may help dissolve existing blood clots.
Adding these agents to standard treatment regimens for
unstable angina may reduce the risk for unstable angina
progressing to heart attack.
Warfarin (Coumadin®)
anticoagulant that is prescribed for patients who have a
history of or are at risk for formation of blood clots
Daily aspirin therapy is mandatory to decrease the
possibility of sticky platelets in the blood starting a blood clot
Clopedigrol (Plavix®)
slightly more potent than aspirin, is considered a long-term
alternative to aspirin therapy. Clopedigrol is usually taken in
a dose of one 75 mg tablet daily
Heparin medications
enoxaparin (Lovenox®), dalteparin (Fragmin®), and
nadroparin (Fraxiparin®)
Frequent blood tests are needed to monitor the
concentration of heparin in the blood.
IIb/IIIa inhibitors
eptifibatide (Integrelin®), tirofiban (Aggrastat®), and
abciximab (ReoPro®).
almost completely prevent the formation of blood clots and
may help dissolve existing blood clots.
Adding these agents to standard treatment regimens for
unstable angina may reduce the risk for unstable angina
progressing to heart attack.
 Warfarin (Coumadin®)
 anticoagulant that is prescribed for patients who have a history
of or are at risk for formation of blood clots (thrombosis)
Miscellaneous anti-anginal drugs
 In 2006, the FDA approved ranolazine (Ranexa). Because of its side
effects (potential to cause abnormal heart rhythm), is indicated only
after other conventional drug treatments are found to be ineffective
If inhibitor
 ivabradine
 provides pure heart rate reduction leading to major anti-ischemic and
antianginal efficacy.
Zinc supplementation
 Percutaneous Transluminal Coronary Angioplasty
 PTCA, angioplasty, balloon dilation or balloon angioplasty
 coronary arteriography
 a thin, flexible plastic tube (catheter) with a balloon is inserted into an artery in the
arm or groin with local sedation and advanced to the blockage. Then the balloon is
inflated, squeezing open the fatty plaque deposit. Then the balloon is deflated and
the catheter is withdrawn. Often a stent, which is a small metal sleeve, is also
placed to hold the artery open.
 Coronary Artery Bypass Surgery
 chest and rib cage are opened up
 The narrowed part of the artery is bypassed by a piece of vein removed from the
leg, or with a piece of artery behind the sternum (internal mammary artery), or a
portion of the radial artery taken from the lower arm or forearm.
 Several arteries can be bypassed in one operation.
by Stenting
Transmyocardial Revascularization
 for people who cannot undergo angioplasty or surgery.
 simple incision is made in the chest, and a laser is used to "drill" small
holes through the outside wall of the heart into the left ventricle.
 About 20-40 holes are made.
 Bleeding from these holes is minimal and usually stops after a few
minutes of pressure.
 not clear why this helps relieve angina. One theory is that it stimulates
growth of new blood vessels that improve blood flow to the heart.
Other investigators believe it is a placebo effect.
 Current research is focusing on trying to find growth factors that could
be injected into coronary arteries or directly into the left ventricle to
encourage growth of new blood vessels
Laser angioplasty
a catheter with a laser on its tip is used to
open the blockage
may be accompanied by stent placement
a catheter has a rotating shaver on its tip to
cut away the plaque
may be accompanied by stent placement
Enhanced External Counterpulsation (EECP® therapy)
with chronic stable angina that is unresponsive to medical
noninvasive outpatient procedure, it usually is
administered during 35 treatment hours, divided into one
or two 60-minute treatment sessions per day, 5 days per
patient lies on a padded table and adjustable cuffs are
wrapped firmly around the calves, lower thighs, and upper
thighs. These cuffs are connected to inflation and deflation
valves that are controlled by an electrocardiogram. When
the heart rests, the cuffs are inflated sequentially and
rapidly from the lower leg to the upper leg and then are
deflated just before the heart beats. This results in an
increased blood supply to the heart while reducing its
 Stop smoking and using nicotine in any form.
 Control high blood pressure.
 Lower blood fats
 Maintain a healthy weight.
 Control diabetes and blood sugar
 If a person already has atherosclerosis and angina, they can learn to
take precautions to avoid having symptoms. Avoiding the "triggers"
 Do not use caffeine, cocaine, amphetamines, or other stimulants
 Drink alcohol moderately (no more than 1-2 drinks daily)
 Avoid large and heavy meals that leave you feeling "stuffed"
 Decrease stress
 regular exercise routine If the patient has been exercising
strenuously, they may need to cut back to avoid symptoms.
 aspirin daily
-The end-