Angina

PAIN OR DISCOMFORT IN THE CHEST, THROAT,
jaw, or arms caused by severe, but temporary, lack of blood
and oxygen to a part of the heart muscle defines angina
pectoris (see Fig. 1 in the chapter Heart Attacks). Angina is
caused by coronary artery disease (CAD) but often referred
to as coronary heart disease (CHD). Because obstructive
coronary artery disease causes a lack of blood to reach the
heart muscle (ischemia), the condition is also called
ischemic heart disease (IHD). Angina affects men more
commonly than women, and the underlying disease condition
is not surprisingly referred to as ‘‘the widow-maker.’’
II. PATHOPHYSIOLOGY
A. Overview
A high blood cholesterol and other factors including a
genetic background, cause damage to arteries leading to
blockage by atheroma. Obstruction by atheroma occurs
most often in the coronary arteries that feed the heart
muscle with blood (see Fig. 1 in the chapter Heart Attacks
and Fig. 1 in the chapter Atherosclerosis/Atherothrombosis).
The heart muscle is one of the strongest in the body and
as powerful as the muscles of the thigh and legs. The act of
walking or running requires contraction of the leg muscles.
Such muscle work or activity requires efficient delivery of
oxygen, glucose, and other nutrients. These are brought
from the heart to the muscles by blood vessels called
arteries. The heart, our lifeline, functions as a simple pump
that pumps more than 250 million liters of blood in an
individual’s average lifetime. It is surprising, therefore, that
the muscle of this important pump receives a supply of
blood via only three small arteries that have a diameter of
a soda straw, ranging from 3 to 7 mm. The coronary arteries
run along the surface of the heart and are branches of the
largest artery in the body, the aorta; the aorta commences
at the left ventricle, the main pumping chamber of the
heart. In the chapter Anatomy of the Heart and Circulation,
Fig. 8 shows the course of the coronary arteries and
Figs. 5 and 9 show their origin close to the aortic valve.
If the coronary arteries that feed the heart muscle with
blood containing oxygen and nutrients become partially
blocked, the muscle becomes painful when used. The
lack of blood to the heart muscle is called myocardial
ischemia, and it is typified by characteristic ECG
findings of ST-segment depression.

As far back as the time of the Caesars, pain in the legs
due to obstruction of blood flow in arteries to the legs
was labeled as intermittent claudication. The Emperor
Claudius limped because of a painful leg, and the word
claudication is derived from his name. Similarly, angina
occurs because of a reduced blood supply.

C. Mechanism of Pain
When a coronary artery is severely obstructed with plaque,
the heart muscle still receives an adequate amount of
oxygen when the heart is at rest and beating slowly at about
72 beats per minute. During exertion or undue stress,
however, the heart rate may increase from 72 to 90 or more
beats per minute. A faster heart rate entails more work
for the heart, which in turn requires more oxygen to
accomplish the work. The obstruction to the artery does
not allow sufficient oxygenated blood to reach the heart
muscle. During those few moments, the lack of oxygen
causes the heart muscle to become painful, and this
sensation is perceived by the individual as pain or merely
a mild but bothersome discomfort in the chest.
Myocardial ischemia is a dynamic process. Three determinants
play a major role in its pathogenesis:
1. Obstruction of a coronary artery by atheroma occludes
the artery in a concentric process and is commonly
observed in patients with stable angina, but in those
with unstable angina the plaques are eccentric
2. Increased myocardial oxygen demand by the vigorously
pumping heart muscle
3. A release of catecholamine occurs at the onset of angina
and during the episode in most patients with stable
angina; release of catecholamine may actually initiate
ischemia, which stimulates further catecholamine
release, and the vicious circle perpetuates the lack of
oxygen by the myocardium, see Fig. 2
This pathogenesis may manifest as the chest pain of
angina. Occasionally myocardial ischemia may occur
without causing a sensation of chest pain; this condition
is called silent ischemia.
When angina is present in an individual, it is certain
that at least one coronary artery will show a greater than
70% obstruction or stenosis if a balloon angiogram is done
to visualize the coronary arteries. The obstructive plaque of
atheroma is often focal and usually occurs in the proximal
portion of the coronary artery and not too distant from
the origin of the aorta. Because the lesions are focal and
proximal, they are easily reached with the balloon, which
dictates the success of angioplasty and bypass surgery.
In some individuals and in many diabetics, lesions are
multifocal and longer with irregularities that produce a
diffuse disease that is more difficult to treat with angioplasty,
stents, or bypass surgery. A 25% decrease in the
outer radius of a normal coronary artery results in about
a 60% decrease in a cross-sectional area. In an artery with
75% stenosis, a 10% decrease in the outer radius would
produce a complete occlusion.
During periods of exercise or exertion, catecholamine
release causes an increase in heart rate, and an increase in
the velocity and force of myocardial contraction produces
an elevation in blood pressure and an increase in myocardial
oxygen demand. In the presence of significant coronary
artery stenosis, an oxygen deficit occurs. Myocardial
ischemia increases catecholamine release, resulting in
an additional increase in heart rate and blood pressure
with further oxygen lack, and the vicious circle ensues
(Fig. 2). In addition the coronary arteries fill during the
diastolic period, which is shortened during an increase in
heart rate.
Fortunately, no damage happens to the heart muscle
during an attack of angina. Full recovery occurs within
minutes of the attack. Many patients have several episodes
of this fleeting pain or discomfort a few times monthly for
over 15 years and learn to cope with the minor restrictions
to their lifestyle. In some individuals, angina that is well
controlled or stable worsens causing unstable angina that
requires special therapy; some patients go on to have heart
attacks.
III. DIAGNOSIS
A. Pain Pattern
1. Location
The pain of angina is usually felt in the center of the chest
over the breastbone, and only rarely over the breasts (see
Fig. 3 in the chapter Heart Attacks). Pain in the lower jaw
accompanied by pain in the chest or arms during a walk or
strenuous activity is nearly always due to angina, especially
if these symptoms recur during similar activities.
Sometimes the discomfort is only in the upper arm with a
tingling feeling in the fingers; this pain comes mainly
on exertion as opposed to pain produced, for example,
by a pinched nerve. A pinched nerve will cause similar
discomfort in the arms and fingers when the individual
is at rest, but an activity, such as walking, makes little
difference.
2. Severity and Character
The pain of angina may be mild to moderate and only
occasionally severe. Often it is just discomfort. The
individual may even refuse to use the word pain to describe
the peculiar sensation that feels like a tightness or a
heavy weight on the breastbone. To some it is a burning
sensation; to others it is a feeling of strangulation or
suffocation that fortunately disappears within one to five
minutes of rest, either with the individual standing or
sitting. The pain of angina rarely lasts more than 10
minutes. If an individual has pain similar to that described
and lasts more than 15 minutes, the patient should take
two or three soft, chewable aspirins (80 mg each) and go
immediately to a hospital emergency room.

IV. DISEASE PROCESSES CAUSING
ANGINA
Atherosclerosis Atheroma is the main cause of obstruction
of coronary arteries and accounts for more than 90% of
cases of angina and coronary artery disease.
Coronary artery spasm (variant angina) — This is
a rare cause of angina in which spasm of the coronary
artery occurs often without identifiable stimuli. This
condition, also called Prinzmetal’s variant angina, is
more common in the Mediterranean and Italian population.
In some patients, exposure to cold, smoking,
emotional stress, aspirin ingestion, or cocaine use may
trigger coronary spasm. The coronary spasm is usually
relieved by nitroglycerin, nitrates, and calcium antagonists,
and discontinuation of these medications may cause
worsening of spasm. Beta-blocking drugs may increase
coronary artery spasm. The clinical hallmarks of coronary
artery spasm include pain usually occurring at rest, often
during sleep and described as chronic angina at rest, an
ECG during pain showing elevation of the ST segment
which is normalized by the use of nitroglycerin. The ST
segment returns to normal on cessation of pain caused by
coronary spasm.
Anomalous coronary artery — This rare occurrence
may go undetected, see the chapter Congenital Heart
Disease.
Aortic stenosis — Obstruction of blood flow from the
left ventricle through the aortic valve into the aorta may be
impeded by a tight stenotic valve. This severe obstruction
to blood flow imposes a severe workload on the left
ventricular myocardium that requires a greater demand
for oxygen. If the coronary arteries are mildly affected
by atheromatous obstruction, then angina occurs much
earlier than expected. Angina occurring in patients with
severe aortic stenosis carries a poor prognosis and requires
surgical intervention.
Hypertrophic cardiomyopathy — The thickened
and severely hypertrophied left ventricular myocardium
requires more oxygen and the supply may be outstripped
by the demand (see the chapter Cardiomyopathy).
Severe anemia — In patients with moderate atheromatous
obstructive disease severe anemia or loss of blood
can further deprive the myocardium of blood and oxygen;
this can precipitate angina or myocardial infarction.
Kawasaki disease — In this rare disease of childhood
coronary artery aneurysms occur and chest pain caused by
angina may be bothersome (see the chapter Kawasaki
Heart Disease).
Giant cell arteritis — This rare diseases of the walls of
the artery, in particular the temporal artery, may affect the
coronary arteries. This process is called a vasculitis.
Chemotherapeutic agents — The chemotherapeutic
agent 5-fluorouracil is known to cause coronary artery
spasm in some patients that may lead to symptoms of
angina and occasionally myocardial infarction (see the
chapter Chemotherapy-Induced Heart Disease).
Syndrome X — This rare syndrome appears to affect
mainly women, and in these patients angina-like symptoms
may occur in the presence of normal coronary
arteries. There is no evidence of obstruction or spasm in
these patients, and the exact cause for pain remains
obscure.
V. STABLE AND UNSTABLE ANGINA
There are two types of angina: stable and unstable. Angina
is described as stable if the condition has been present for
more than two months, or if there has been no change in
the pattern of pain, particularly no change in the frequency
of attacks, severity, or duration of pain. Patients with stable
angina only get pain at rest with sudden emotional stress.
Angina is described as unstable when angina is present for
less than 60 days, or when there is an increase in the
frequency, severity, and duration of pain and a change in
the known precipitating factors. If pain that normally
occurs only on exertion or moderate activities starts to
occur on minimal activity or at rest but without emotional
stress, a patient should seek urgent attention in the
emergency room.
VII. DRUG TREATMENT
In patients with stable angina treatment with drugs usually
produces about a 75% improvement in symptoms and
quality of life. Three groups of drugs are usually employed:
nitrates, beta-blockers, and calcium blockers (calcium
antagonists). Aspirin is added to prevent coronary thrombosis
which causes heart attacks.
A. Nitrates
Angina sufferers are advised by their doctor to always carry
nitroglycerin, even if the requirement is only two pills
a year. Nitroglycerin is a nitrate that is used under the
tongue or in tablet or spray form. The tablets should be
kept in a dark bottle and not in a pill box, because opening
the box lets in light, which will destroy the effectiveness
of the drug within a few weeks. Remove the cotton wool
from the bottle so the pills can be easily reached when in
a hurry. Leave the cotton wool in a stock bottle kept in the
refrigerator; these tablets will maintain their strength for
more than one year. Tablets in a bottle that is opened often
should be good for three months.
B. Beta-Blockers
1. Actions
Beta-blockers are a group of drugs that reduce the action of
adrenaline (epinephrine) on the heart and arteries. Betablockers
decrease the heart rate so the pulse falls from
a resting level of about 72 beats per minute to a range of
50–60 beats per minute. Second, they reduce blood
pressure and third, they cause the heart muscle to contract
less forcefully. All three effects cause the heart muscle to
require less oxygen, thus preventing angina.
Beta-blockers block the effects of the stimulant stress
hormones adrenaline and noradrenaline at the so-called
beta-receptor sites present on the surface of cells in the
heart and in arterial blood vessels. They therefore prevent
the increase in heart rate, the force of heart muscle
contraction, and the rise in blood pressure normally
produced by these stimulants.
Beta-blockers are recommended as a first-line oral drug
treatment in the management of angina pectoris. Table 4
emphasizes the rationale for the use of beta-blocking drugs
as first-line agents versus that of calcium antagonists and
oral nitrates.
In patients with angina, at least one coronary artery has
a block greater than 75%. At rest, sufficient blood reaches
the heart muscle; however, during moderate activities, the
heart rate and blood pressure increase and the heart muscle
contracts more forcefully to do the work because more
blood containing oxygen is required. The blockage
prevents an adequate supply of oxygen from reaching the
muscle. This oxygen lack causes the heart muscle to
become painful, and the heart rate and blood pressure
may further increase during the stress of pain. Basically,
beta-blockers cause the heart muscle to require less oxygen
to do the same amount of work. The heart rate multiplied
by the systolic blood pressure gives an estimation of the
amount of work and oxygen required by the heart muscle.
Beta-blockers decrease both heart rate and blood pressure,
therefore, less oxygen is required. They also cause the heart
muscle to contract less forcefully so that less oxygen is
used. These drugs divert blood from the areas of the heart
that have an abundant supply to the deprived area.
5. Side Effects
a. The Heart and Vessels

There can be precipitation of heart failure in
patients with a very weak heart muscle, as discussed
above.

Severe slowing of the heart rate to less than 42 beats per
minute in rare cases if the dose is not carefully adjusted;
this is usually quickly spotted by the symptoms of
dizziness and ill feeling, and can be quickly rectified;
hence, in practice this is not a problem.

Extremely cold hands and feet can occur in about 10%
of patients; the condition improves immediately on
discontinuation of the beta-blocker.
b. The Lungs

There can be precipitation of wheezing and difficult
breathing in individuals who are known to have allergic
asthma or severe bronchitis.
c. The Nervous or Muscular System

Dizziness due to excessive slowing of the pulse and
reduction in blood pressure

Vivid dreams in about 10% of patients taking
propranolol; these usually clear up when given an
alternative medication such as atenolol, timolol, or
nadolol

Mild depression occurring in less than 10% of patients,
it is not a major problem in practice; because atenolol
and nadolol do not get into the brain like propranolol,
they cause fewer problems

Weakness and muscle fatigue of varying degree,
occurring in about 10% of patients; a change from
propranolol to metoprolol, atenolol, or nadolol is
advisable; if symptoms persist and no other cause can be
found, beta-blockers should be discontinued

Reduction of libido and impotence that occurs in less
than 5% of patients, it must be monitored by patient
and physician; however, beta-blockers, by decreasing
the heart rate, blood pressure, and heart work can be
useful if pain is precipitated by intercourse
d. Other Side Effects

In some patients insomnia, altered sleep patterns,
nervousness, muscle cramps, and muscle joint pains
can be caused by pindolol
6. Individual Beta-Blockers
Beta-blockers are the most beneficial drugs used in the
treatment of angina. They have been in use in the UK
since 1964 and in the United States since 1969. The first
and most well-known drug in this group is propranolol
(Inderal). Several other beta-blockers have also been
approved by the FDA. Commonly used beta-blockers
include acebutolol, atenolol, bisoprolol, carvedilol,
nadolol, metoprolol, propranolol, and timolol.


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