Angina Pectoris:
Typical and Atypical Angina Pectoris:
Angina pectoris is, until proven otherwise, the result of myocardial
ischemia, secondary to coronary artery disease. Angina
pectoris can be divided into typical and atypical angina
pectoris. In typical angina pectoris, the discomfort or
pain is located substernally and often radiates. It is precipitated
by exertion or emotion and promptly relieved
by rest.
Atypical chest pain is located in the left chest, sometimes
confined to a small area, does not radiate, and is described
as sharp, stabbing, or tearing. In atypical angina
pectoris the pain can occur repetitively for short periods
of time (seconds) or last for hours. It is unrelated to exercise
and not relieved by rest or nitroglycerin. Atypical
chest pain is often noncardiac in origin
DIFFERENTIAL DIAGNOSIS OF ISCHEMIC PAIN:
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Stable and Unstable Angina Pectoris:
The distinction between stable and unstable angina pectoris is of great
clinical importance. In chronic stable angina pectoris
the discomfort is predictably provoked by exertion and
relieved by rest. A chronic stable coronary stenosis is, in
most cases, the pathophysiological explanation of
chronic stable angina pectoris.
Unstable angina pectoris occurs with minimal exertion
or at rest. The pain is new in onset or increasing in
intensity. Character and location are typical, however
the intensity is often more severe and the duration
longer than in chronic stable angina pectoris.
Pathophysiologically, unstable angina pectoris is
associated with ruptured plaques and thrombi, which
obstruct the coronary lumina. Occasionally, coronary
vasoconstriction or spasms contribute to the typical
dynamic clinical manifestation of unstable angina
pectoris.
It is important to note that myocardial ischemia may
present itself in forms other than angina pectoris. Particularly
in elderly patients, myocardial ischemia may
cause nausea and stomach ache without chest pain.
In those patients the first manifestation of coronary
artery disease may be an acute myocardial infarction,
heart failure, or cardiac arrest.
About one-third of patients, predominantly diabetic
patients, do not experience any discomfort with
myocardial ischemia
Clinical Characteristics of Angina
Pectoris:
The discomfort or pain of angina pectoris is typically dull and tightening. It is often described as “pressing,” “tearing,” “constricting,” “squeezing,”
“burning,” or as chest heaviness, a “band across the
chest,” or “weight in the center of the chest”
Angina pectoris is often accompanied by dyspnea. Dyspnea
is caused by pulmonary congestion, secondary to
increased left ventricular filling pressures. In fact, occasionally
dyspnea may be the only symptom of myocardial
ischemia and may represent an “angina equivalent.”
Radiation of angina pain is common. Angina pain
radiates most typically to the left shoulder and arm, although
many other locations are possible
Occasionally, the pain is only felt at the radiation point,
e. g., in the jaw or the arm. Angina pectoris pain occurs
with physical exertion and abates promptly (less than
five minutes) at rest. Angina can also be provoked by exertion,
emotions, heavy meals, and cold, windy weather.
Not infrequently, patients wake up from sleep having
angina pain and quite often the pain occurs with the
first physical activity in the morning. Stable, and most
often also unstable angina pectoris is promptly relieved
by nitrates. The response to nitroglycerin may be used to
differentiate angina pain from other causes of chest
pain. However, keep in mind that pain originating from
a hiatal hernia, esophageal spasm, or mild biliary colic
may abate after nitroglycerin, too. The severe pain in
acute myocardial infarction is often preceded by episodes
of typical and atypical chest pain. This is an expression
of the intermittent flow obstruction, secondary
to the varying thrombus size at the site of the ruptured
plaque.
Differential Diagnosis of Angina Pectoris: Emotional distress
is a very common cause of atypical chest pain
(Tab. 6.2). Functional chest pain should be considered, if
the pain lacks a reasonable relationship to precipitating
factors or features of anxiety and neurosis are present.
Functional pain occurs at rest, lasts from seconds to
hours, and is often localized to one point in the left
chest. However, be aware that ischemic chest pain
causes anxiety and therefore it may be at times difficult
to differentiate between ischemic and functional pain.
Pericarditis can result in severe chest pain originating
from the heart. Pericardial pain is sharper and more
tearing than ischemic pain. Pericardial pain lasts for
hours and the intensity can be aggravated by changing
body position or by breathing.
Aortic dissection is suggested by sudden onset, sharp,
tearing chest pain, felt in or radiating to the back.
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Musculoskeletal pain of the chest is a very common problem. Chest wall pain is usually located to one site of the chest and can be provoked by posture, motion, or pressure. Sometimes a local tenderness is present. The most common causes of chest wall pain are arthritis, chondritis, intercostal muscle injury, and coxsackie
virus infection (e. g., Bornholm disease).
Special Forms of Angina Pain
Prinzmetal Angina:
Prinzmetal angina occurs at rest and is (sometimes) associated with grotesque ST segment elevations . Prinzmetal angina is caused by a
focal vasospasm of one of the coronary arteries and is
therefore also called vasospastic angina. In the vast majority
of patients with Prinzmetal angina, minimal
atherosclerotic changes are present. However, in about
10% of patients the coronary arteries are normal. Prinzmetal
angina is sometimes associated with migraine or
Raynaud disease. Apart from this extreme form of
vasospastic angina, vasospasm may contribute to many
angina pectoris attacks.➤ In nocturnal angina pectoris the increased vagal tone
may induce vasospasm.
➤ Angina pectoris provoked by cold or emotion is most
certainly secondary to a general vasoconstriction and
possibly a vasospasm at the site of an eccentric coronary
lesion.
➤ Hyperventilation can result in vasospasm and angina
pectoris.
“Walking-through” Phenomenon:
Walking-through describes the phenomenon that exercise-induced angina
can abate despite, or because of, continued exercise. The
pathophysiological explanation of this phenomenon is
the recruitment of collaterals during exercise. Increasing
blood flow via collaterals provides enough oxygen,
such that ischemia decreases and the pain subsides.
Angina Pectoris, Secondary to Left Ventricular Hypertrophy:
Patients with aortic stenosis, aortic insufficiency,
hypertension, or hypertrophic obstructive cardiomyopathy
often experience typical exercise-induced
angina pectoris. The cause of angina pectoris in these
cases is a transient myocardial ischemia of the hypertrophied
left ventricle. Ischemia is the result of a decreased coronary flow reserve and an impaired vasomotion of the resistance vessels (arterioles). In a normal
(nonhypertrophied) ventricle, the coronary blood flow
can be increased four- to fivefold with physical activity.
In left ventricular hypertrophy, coronary flow at rest is
already increased (to meet the needs of the increased
demand) and cannot be further increased during exercise.
This results in a relative underperfusion of the
hypertrophied ventricle and causes ischemia in the subendocardium
Angina Pectoris after Percutaneous Coronary Interventions
(PCI).
PCIs are performed to alleviate angina pectoris. The technique involves the dilation of coronary stenosis with a balloon catheter. Over 90% of the dilations
are completed with the implantation of a stent to
prevent early reocclusions and decrease restenosis rate
. Despite this, chest pain may reoccur after a
PCI. Early (i. e., usually within the first 30 days after an
intervention) crushing chest pain associated with ST
segment elevations may occur. The cause is an acute
thrombotic occlusion of the coronary artery at the dilated
lesion. The clinical presentation of this so-called
subacute stent thrombosis is that of amyocardial infarction.
Late after an intervention (i. e., within three to nine
months) typical and atypical angina pectoris may reoccur.
The discomfort usually resembles the discomfort
before the intervention. It is caused by a renewed narrowing
of the dilated stenosis, the so-called restenosis.
Restenosis is the result of an extensive intimal hyperplasia
at the site of the intervention. Angina pectoris necessitating reinterventions (i. e., clinically driven reintevention
after PCI) had to be performed in 10−12% of
patients treated with bare metal stents. The new drug−
eluting stents have decreased this rate to 2−3%
Cardiac Syndrome X:
In cardiac syndrome X, patients
with normal epicardial coronary arteries suffer from
angina pectoris. The cause is a decreased coronary flow
reserve, which in this case is the result of a dysfunction
of the resistance vessels.
Angina Coerulea.
Dyspnea is the leading symptom of
severe pulmonary hypertension. However, patients with
pulmonary hypertension sometimes report an exertional
chest pain, which can persist for some time at
rest. The cause of this angina pectoris is most likely a
relative underperfusion of the hypertrophied right ventricle
resulting in myocardial ischemia during exercise.
Decubitus Angina.
In severe coronary artery disease,
angina pectoris may be provoked in recumbency. It is
thought that the increased return of blood to the heart,
and the resulting increase in filling pressures, precipitates
angina pectoris. Similarly, the symptoms of an
acute myocardial infarction can be aggravated in the recumbent
position.
Silent Myocardial Ischemia.
Myocardial ischemia that
does not cause angina pectoris is called “silent”
ischemia. The prognosis of silent ischemia is similar to
that of symptomatic myocardial ischemia
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