|
Angina Pectoris
|
 |
Objectives
- Define angina.
- Learn the classification of angina.
- Learn the clinical signs and symptoms of angina.
- Understand the clinical work-up of angina, including appropriate history,
physical examination, and laboratory and other testing.
- Learn appropriate indications for cardiac exercise testing and nuclear
stress testing.
- Learn appropriate management of chronic stable angina and unstable angina,
including the role of pharmacotherapy, PTCA, and CABG.
Definitions
Angina pectoris is a syndrome characterized by chest pain resulting from an
imbalance between oxygen supply and demand, and is most commonly caused by the
inability of atherosclerotic coronary arteries to perfuse the heart under conditions
of increased myocardial oxygen consumption. It may also occur in patients with
seemingly normal coronary arteries subjected to acute or chronic increase in
myocardial work, such as aortic stenosis, hypertension, or hypertrophic cardiomyopathy.
Coronary artery spasm, superimposed upon normal or diseased arteries, can provoke
pain in the absence of increased myocardial demands such as variant (Prinzmetal's)
angina and some cases of stable or unstable angina. There is also a group of
patients who have angina without demonstrable evidence of coronary artery disease.
Classification
of Angina Pectoris
Once the history has indicated that chest pain is most likely angina,
it has to be decided which of the several clinical syndromes of angina
the patient manifests.
-
Chronic Stable Angina: The most common anginal syndrome.
Character: More often described as a discomfort, pressure, or squeezing
sensation. Less commonly as burning, sticking, or sharp.
Location: Most often in the substernal area, precardium, or epigastrium
with radiation to the left arm, jaw, or neck. Less commonly felt only in
radiation areas and not in the chest.
Precipitation: Often provoked by exertion, emotion, exposure
to cold, eating (4 "E"s), or smoking, and relieved by rest, removal of
provoking factors, or sublingual nitrates.
Duration: Usually lasts a few minutes, rarely over 20-30 minutes.
The frequency and severity of the symptoms change little with daily
activities, and pain does not usually occur at rest.
Unstable angina pectoris is probably not a single entity, but a combination
of syndromes which have been referred to by various names, such as preinfarction
angina, impending myocardial infarction, progressive or crescendo angina,
coronary insufficiency, new onset angina, etc.
Unstable angina pectoris usually presents in one of three patterns:
-
angina pectoris of recent onset (less than 1 month) that is provoked by
minimal exertion.
-
chronic stable angina showing a crescendo pattern, with chest pain occurring
more frequently, with greater severity and duration, with less provocation,
and requiring larger doses of nitroglycerine to abort attacks.
-
prolonged chest pain at rest, clinically indistinguishable from acute MI
at the time of presentation.
Variant Angina Pectoris (Prinzmetal's
Angina)
This type of angina results from transmural myocardial ischemia caused
by coronary artery spasm and may occur in patients with or without coronary
atherosclerosis. Pain occurs principally at rest, usually unprovoked, but
since coronary artery disease may coexist, pain may also be provoked by
exercise. The pain may occur in a circadian manner, often in the early
morning hours. The pain is associated with ST-segment elevation, in contrast
to typical angina pectoris. Often subclinical (painless) episodes occur
with ST- segment elevations, often associated with arrhythmias, or bundle
branch block.
Evaluation
The diagnosis of angina pectoris is established by obtaining a reliable
description of the chest discomfort and its relationship to activity. The
likelihood of coronary artery disease is enhanced by age, history of hyper-tension,
hyperlipidemia, smoking, diabetes mellitus, or a family history of ischemic
heart disease in first degree relatives.
Though often normal, the physical examination may supply important information
that will affect evalua-tion: the appearance of the patient, especially
in an episode of pain; xanthelasmia; hypertension; evi-dence of peripheral
arterial disease; tenderness of the chest wall suggest-ing pain of musculoskeletal
origin; abnormal pulsations on palpation over precardium; basilar rales;
an S4, especially during pain; murmurs of aortic stenosis, IHSS, mitral
valve prolapse; or arrhythmias.
Basic screening for anemia, polycythemia, hyperglycemia, hyperlipidemia,
etc.
A resting ECG is often normal in stable angina pectoris in the absence
of a previous MI or a cause for LVH. During pain the ECG may show transient
ST- segment depression, T wave inversion, and/or ventricular arrhythmia.
Abnormal ECG changes are more common with unstable angina pectoris. ST-segment
eleva-tion rather than depression occurs during attack in variant angina.
Especially with 2D echocardiogra-phy, the assessment of left ventricu-lar
wall motion, volume, and ejection fraction is feasible, as is detection
of IHSS, AS, and LVH.
Most, but not all, physically able patients with stable angina pectoris
should have an exercise stress test as it is very helpful in reproducing
symptoms, documenting ischemic ECG changes, and assessing the level of
severity. Patients with high grade coronary artery disease may manifest
inability to elevate the heart rate or blood pressure during exer-cise,
or develop marked ST-changes at low level exercise. Exercise-induced arrhythmias
or left ventricu-lar dysfunction provide diagnostic information with important
therapeu-tic potential. The exercise stress test may be combined with echocardio-graphy
(Echo Stress Test) for more specificity. This is particularly useful in
females, as they tend to have a higher rate of false positive tests.
-
Ambulatory Holter Monitoring
Ambulatory monitoring with equip-ment designed to show ST-T changes is
useful in some cases and is especially good for detecting silent ischemia.
Radionuclide scintigraphy enhances the sensitivity and specificity of the
exercise stress test. The patient with a normal ECG at rest may require
only a standard exercise test. If ab-normal at rest, such as ST-T abnor-malities
or LBBB, etc., the patient is best evaluated with Thalium scinti-graphy
performed during the exer-cise stress test. Nuclear ventriculo-gram using
tecnetium Tc 99 m tagged to the patient's RBCs permits evaluation of left
ventricular wall motion and measurement of ejection fraction.
Although not necessary for the diagnosis of coronary artery disease in
most instances, cardiac catheteri-zation and coronary angiography is the
"court of last resort" for evalua-ting patients with chest pain. It is
the only currently available diagnostic test that depicts coronary anatomy
and defines the extent of the coro-nary artery disease. It is a necessary
procedure for all patients who are potential surgical candidates. How-ever,
not all patients with angina pectoris require surgical therapy, and thus
not all are in need of arterio-graphy. A logical approach to the work-up
should be undertaken, reserving angiography for those patients who are
potential surgical candidates or for the unusual patient in whom the cause
of chest pain is unknown after non-invasive study.
Some of the usual indications for coronary arteriography in angina pectoris
include:
-
angina refractory to medical management.
-
unstable angina (after medical stabilization).
-
marked ST-T changes at low level or persisting after cessation of exercise
stress testing.
-
angina or myocardial infarction in patients under 35 years of age.
-
patients with persistent angina and/or low level EST abnormalities after
myocardial infarction.
-
suspected variant (Prinzmetal's) angina.
-
when needed for clarification of an obscure case.
Management
-
Stable Angina Pectoris
-
General Therapeutic Considerations (Table 1)
-
Drug Therapy
Table 1.
General Therapeutic Considerations |
Risk factor reduction: Discontinue smoking, control hypertension
and diabetes, lower hyperlipidemia, and maintain an ideal body weight. |
Work adjustment, stress reduction, and behavioral modification. |
Exercise: The prescription for exercise must be made carefully with
the
knowledge of each individual patient taken into consideration. |
The drugs most frequently used in the treatment of stable angina pectoris
are the nitrates, the beta blockers, and the calcium channel blockers.
Some patients with very mild, stable angina pectoris get along very
well by adhering to the general therapeutic measures stated above, and
using an occasional sublingual nitroglycerine tablet PRN. Some patients
also do well on a regular dose of a long-acting nitrate, and sublingual
TNT PRN. Some authorities feel that no one agent can adequately control
significant angina, and initiate treatment using two or more different
agents. Selecting which drug to employ and in what dosage depends on the
severity of the angina and associated conditions.
For routine patients with no other problems, a good regimen would be
a nitrate and a beta blocker. For patients with asthma, CHF, or insulin-dependent
diabetes mellitus, the beta-blockers are relatively con-traindicated and
a calcium channel blocker should be employed. Some patients do not respond
to the nitrates and beta blockers, and some do not tolerate nitrates or
beta blockers because of side effects, so calcium channel blockers are
added or sub-stituted respectively. Some physicians prefer to start the
patient on calcium channel blockers as initial therapy. Some patients may
require all three medications, and occasionally combinations of calcium
channel blockers are used.
-
Percutaneous Transluminal Coronary Angioplasty (PTCA)
Transluminal coronary angioplasty has become an accepted method of treating
selected patients with angina due to atheromatous coronary artery disease.
This procedure is particular-ly useful in patients with single or double
vessel disease, especially for lesions of the left anterior descending
coronary artery.
-
Coronary Artery Bypass Grafting (CABG)
Coronary artery bypass grafting can provide significant relief from angina
in over 80% of patients with disab-ling angina and has a low operative
mortality. Since it neither reverses the disease process nor assures per-manent
revascularization, its use is limited to those patients who cannot be managed
medically, those with markedly abnormal ECG response to exercise, and those
found to have significant left main coronary steno-sis or significant proximal
lesions in all three coronary arteries.
Hospitalization with bed rest, nasal O2, and sedation in an ECG-moni-tored
environment is indicated for almost all patients with unstable an-gina.
Most patients with unstable angina will respond to medical man-agement
and can then be evaluated for extent of severity with the diag-nostic tests
used for stable angina. A small percentage will fail to respond to medical
management and will pro-ceed to myocardial infarction. Ano-ther small percentage
will remain unstable with unremitting pain, and will require more aggressive
management. More than 30% to 40% of medically treated patients will have
PTCA or CABG surgery.
Once the diagnosis is suspected, obtaining an ECG during pain is paramount.
Variant angina is not a benign syndrome. Myocardial infarction can occur
in the region affected by the coronary artery spasm in about 25% of patients,
and either heart block or ventricular fibrillation can occur during an
episode of spasm.
Table 2. Drugs |
Nitrate |
Sublingual nitrates usually reverse spasm within 30-60 seconds. Oral or
tropical
nitrates can reduce the frequency of attacks. However, nitrates are not
always
successful, and abrupt withdrawal can provoke spasm. so it is important
to taper
off regardless of their seeming ineffectiveness. |
Calcuim Channel Blockers |
Effective in 60%-75% of patients, with or without nitrates. |
Beta Blockers |
Beta Blockers are ususally ineffective and may actually be deleterious
in variant angina. |
-
PTCA/Coronary Bypass Surgery
Variant angina is usually not amenable to PTCA or CABG surgery except in
select cases with fixed subtotal obstructions which are the site of reproducible
superimposed spasm.
B. Pope, MD
updated 8/30/05