Tuesday, July 29, 2008

Unstable Angina (Acute Coronary Syndrome)

A. Pathophysiology and Symptoms
The pathophysiology of unstable angina has been
identified. In the majority of cases, disease-causing plaques
are asymmetric with irregular borders and a narrow neck.
Platelets then aggregate on the surface of plaques forming
small thrombi. Lipid-rich plaques have a predilection for
rupture, and rupture of the plaque with an overlying thrombus
is a common finding on angioscopy. Silent ischemia
is fatal and observed in patients with unstable angina.
Prognosis appears to be worse in this subset of patients.
Unstable angina patients represent a heterogeneous
group. Patients usually present with chest pain at rest
lasting from about 10 to 40 minutes; pain usually lasts
more than 20 minutes but less than hour. Patients with
stable angina with chest pain only on exertion who develop
pain with much lower levels of activities or pain at rest
are a subset of unstable angina. Patients with new onset
angina occurring within the past 30 days have high-risk
unstable angina.
B. Management
All patients with unstable angina should proceed to
an emergency room and be administered 160 mg of
chewable aspirin immediately if they have not already
taken the drug.
1. Risk Stratification and New Classification
During the past 50 years the three major complications
of CAD associated with chest pain were classified as
myocardial infarction, severe chest pain without elevated
cardiac enzymes classified as unstable angina, and chest
pain mainly on exertion labeled as chronic, stable angina.
For more information, see the chapter Heart Attacks.
Since 1998 national cardiac societies have altered this
classification as follows:
1. Patients with chest pain who have the characteristics of
a heart attack associated with typical ECG change
demonstrating ST-segment elevation are labeled as an
ST-segment elevation myocardial infarction (see the
chapter Heart Attacks).
2. Patients with chest pain and the characteristics of a
heart attack associated with ECG changes demonstrating
ST-segment depression accompanied by elevated
troponin or CK-MB enzyme elevations are labeled as
non-STelevation myocardial infarction (formerly called
non-Q-wave myocardial infarction).
Cardiac societies in the United States, Canada, and the
UK have introduced a new terminology: acute coronary
syndrome in an attempt to identify high risk patients with
acute chest pain. Classification of ischemic pain, acute
coronary syndrome includes:
1. Subset of patients with ST-segment elevation myocardial
infarction
2. Patients with non-ST elevation infarction (old term:
non-Q-wave MI)
3. Patients with typical features of unstable angina with
elevated troponin levels are reclassified as non-ST
elevation infarction
4. Patients with unstable angina: abnormal ECG changes
with normal troponin levels
5. Patients with unstable angina, normal ECG changes,
and normal troponins are classified as low risk
Patients are stratified into low- or high-risk categories
based on:
1. ECG changes done during pain showing ST-segment
depression indicating ischemic changes; ST-segment
depression greater than 0.05 mm (0.05 mV) indicates
high risk.
2. Patients with abnormal ECG and elevated troponins
are at high risk for serious events; elevated troponin
levels indicate necrosis of myocardial cells or a small
myocardial infarct.
3. Patients with evidence of recent onset of rest pain that is
recurrent, accompanied by ECG changes, are high risk.
4. Patients without rest pain and absence of ECG changes
with normal troponin levels are at low risk.
5. Diabetics with any of the above features are considered
high risk as are those patients who have had a previous
infarction.
6. An elevated C-reactive protein is considered to be
evidence of increased risk (see the chapter C-Reactive
Protein and the Heart).
2. Drug Management
Drug management is an important aspect of treating
unstable angina/acute coronary syndrome.
1. All patients are admitted to a coronary care unit or to
an area where telemetry and blood pressure monitoring
are available.
2. Intravenous nitroglycerin is given to virtually all
patients to relieve chest pain.
3. Morphine in small doses is given to stop pain that
can stimulate autonomic responses that may increase
cardiac arrhythmias and myocardial necrosis.
4. A beta-blocking drug is begun provided there is no
contraindication such as asthma or bradycardia less
than 50 beats per minute present.
5. Chewable aspirin is usually administered in the
emergency room followed by enteric-coated aspirin
325 mg once daily.
6. If A beta-blocking drug is contraindicated, a calcium
antagonist such as diltiazem is administered.
7. Heparin is given subcutaneously; low molecular
weight heparin has been shown to be equally as
effective as intravenous heparin and easier to monitor.
8. A statin is commenced to maintain LDL-cholesterol
levels less than 2.0 mmol/L (80 mg/dl).
9. Powerful antiplatelet agents are commenced, especially
in high-risk patients. Clopidogrel followed by catheterization
and coronary angiography are used to define
the lesion.
10. Glycoprotein IIb/IIIa receptor blockers such as:
abciximab (ReoPro), Integrilin, or tirofiban are
administered to high-risk patients undergoing coronary
angiography and/or angioplasty with or without
stent placement; several studies suggest that mainly
diabetics with acute coronary syndrome benefit
from such therapy. Abciximab has been shown to
have beneficial effects in randomized clinical trials
in acute coronary syndrome patients undergoing
angioplasty or stenting (see the chapter Antiplatelet
Agents).
3. Interventional Therapy
Interventional therapy such as coronary angioplasty with
or without stenting or bypass surgery should be strongly
considered in patients with high-risk unstable angina/acute
coronary syndrome. These patients usually undergo
coronary angiography within 24 h on admission to an
emergency room.
Coronary angiograms define the obstructive lesions, and
balloon angioplasty and stent placement are done in the
majority of patients. Balloon angioplasty with stenting has
transformed the management of unstable angina/acute
coronary syndrome (see the chapters Angioplasty and
Stents).
In most categories of patients and in virtually all
diabetics, interventional therapy has advantages over
medical therapy for amelioration of angina, a return to
normal lifestyle, and probable prolongation of life.
Coronary artery bypass surgery is indicated if angioplasty
or stenting are not possible, particularly in
patients with an ejection fraction of less than 45%,
and in diabetics.
When coronary artery bypass surgery is selected,
patients who can receive an internal mammary artery
graft are most fortunate. The arterial graft has a prolonged
patency of 15–20 years versus approximately 10–12 years
for saphenous vein grafts. Khot et al. have recently shown
that radial artery bypass grafts have an increased occurrence
of angiographically severe stenosis and occlusion
compared with left internal mammary artery grafts and
saphenous vein grafts (see the chapter Coronary Artery
Bypass Surgery).

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