ACTUAL PRACTICE ON THE

MANAGEMENT OF CARE OF ANGINA

PATIENTS PROFILE - 1

Name: M.I.
Age: 69
Sex: Female
Diagnosis: Unstable Angina Secondary
to Ischemic Heart Disease, HACVD
Attending Physician: Dr. Sajonas
CC: Chest discomfort

MANAGEMENT

Laboratory/Diagnostic Examinations

CBC
Urinalysis
FBS
Lipid Profile
Troponin I
CKMB
BUA
Creatinine

MANAGEMENT

Laboratory/Diagnostic Examinations

SGOT
SGPT
EKG
Chest X-ray PA
Serum Na, K
For 2D-Echo with Doppler
Coronary Angiogram with possible
angioplasty

MANAGEMENT

PNSS I liter X KVO

Full low salt low fat diet
02 inhalation at 2-3 LPM via NC
For referral to Cardiologist Dra. E. Mallillin
Medications:

ISMN 10 mg. 1 tab TID

Celecoxib 200 mg.I cap BID pc
Omeprazole 20 mg. 1 tab BID ac
Aspirin 80 mg OD pc dinner
Trimetazidine 35 mg 1 tab OD at HS

MANAGEMENT

Medications
Isordil 5 mg SL PRN for chest pain
Vessel due 1 cap po BID
Felodipine 5 mg. 1 tab po OD
Avoid straining and lifting heavy objects

PATIENTS PROFILE - 2

Name: M.P.
Age: 53
Sex: Male
Diagnosis: Stable Angina, Acute
Gastritis
Attending Physician: Dr. Sajonas
CC: Chest pain

MANAGEMENT

Laboratory/Diagnostic Examinations

CBC
Urinalysis
FBS
Lipid Profile
BUA
Creatinine
Troponin I

MANAGEMENT

Laboratory/Diagnostic Examinations
12-lead EKG
Chest X-ray PA

MANAGEMENT

PNSS I liter X KVO

Low salt low fat diet
02 inhalation at 1-2 LPM via NC
Medications:

ISDN 5 mg. SL now

Omeprazole 40 mg. IV q12
Isoket 10 mg. 1 tab TID
Maalox 30 cc TID pc
HNBB 1 amp IV for abdominal colic

MANAGEMENT

Medications
Isordil 5 mg 1 tab SL PRN for chest pain

Moderate high back rest

PATIENTS PROFILE - 3

Name: E.L.
Age: 51
Sex: Female
Final Diagnosis: Unstable Angina,
Menopausal Syndrome
Attending Physician: Dr. Socan
CC: Chest pain

MANAGEMENT

Laboratory/Diagnostic Examinations

CBC
Urinalysis
FBS
Lipid Profile
Troponin I
BUA
Creatinine

MANAGEMENT

Laboratory/Diagnostic Examinations
EKG
Chest X-ray PA

MANAGEMENT

PNSS I liter X 10 gtts

Full low salt low fat diet
02 inhalation at 2-3 LPM via NC
Medications:

Isoptin 240mg. tab po BID

Aspilet EC 80 mg. 1 tab OD after lunch
Celecoxib 200 mg. 1 cap po BID pc
Fenofibrate 100 mg 1 cap OD

MANAGEMENT
Avoid straining and lifting heavy objects

PATIENTS PROFILE - 4

Name: P.P
Age: 63
Sex: Male
Diagnosis: Acute Coronary Syndrome
Unstable Angina, Ischemic
Cardiomyopathy
Attending Physician: Dr. Sajonas
CC: Chest pain for few hours

MANAGEMENT

Laboratory/Diagnostic Examinations

CBC
Troponin I
CK-MB
12 lead EKG
X-ray
Serum potassium, sodium
Creatinine
Lipid Profile

MANAGEMENT

Laboratory/Diagnostic Examinations

Urinalysis
SGPT
BUA, BUN
FBS
2D-Echo

MANAGEMENT

PNSS I liter X 15 gtts

Low salt low fat diet
02 at 2-3 LPM via NC
For referral to Cardiologist Dra. E. Mallillin
Medications:

Aspirin 80 mg. 2 tabs now

Lanoxin 0.25 mg 1 tab now
Isordil SL 5 mg 1 tab SL now
Ketorolac 1 amp IV now then q6 for pain

MANAGEMENT

Medications

Clopidogrel 75 mg 1 tab OD pc lunch

Isoket 10 mg 1 tab po TID
Lanoxin 0.25 mg tab OD
Micardis 40 mg 1 tab OD
Trimetazidine 35 mg 1 tab BID po
Atorvastatin 40 mg 1 tab OD at HS
Isordil 5 mg SL PRN for chest pain

STANDARD OF CARE
ANGINA

AHA GUIDELINES
2000

GUIDELINES

Class I:Conditions for which there

is evidence and/or general
agreement that a given procedure
or treatment is useful and effective.
Class II:Conditions for which there
is conflicting evidence and/or a
divergence of opinion about the
usefulness/efficacy of a procedure
or treatment.

GUIDELINES
Class IIa:Weight of evidence/opinion is
in favor of usefulness/efficacy.
Class IIb:Usefulness/efficacy is less
well established by evidence/opinion.
Class III:Conditions for which there is
evidence and/or general agreement
that the procedure/treatment is not
useful/effective and in some cases may
be harmful.

Initial Triage
1. Patients with symptoms that
suggest possible ACS should not
be evaluated solely over the
telephone but should be referred
to a facility that allows evaluation
by a physician and the recording
of a 12-lead electrocardiogram
(ECG). (Level of Evidence: C)

Initial Triage
2. Patients with a suspected ACS with
chest discomfort at rest for >20
minutes, hemodynamic instability, or
recent syncope or presyncope should
be strongly considered for immediate
referral to an emergency department
(ED) or a specialized chest pain unit.
Other patients with a suspected ACS
may be seen initially in an ED, a chest
pain unit, or an outpatient facility.
(Level of Evidence: C)

Early Risk Stratification

Class I
1. A determination of the likelihood (high,
intermediate, or low) of acute ischemia
caused by CAD should be made in all
patients with chest discomfort. (Level of
Evidence: C)
2. Patients who present with chest discomfort
should undergo early risk stratification that
focuses on anginal symptoms, physical
findings, ECG findings, and biomarkers of
cardiac injury. (Level of Evidence: B)

Early Risk Stratification

3. A 12-lead ECG should be obtained
immediately (within 10 minutes) in
patients with ongoing chest
discomfort and as rapidly as
possible in patients who have a
history of chest discomfort
consistent with ACS but whose
discomfort has resolved by the time
of evaluation. (Level of Evidence: C)

Early Risk Stratification

4. Biomarkers of cardiac injury should be
measured in all patients who present with
chest discomfort consistent with ACS. A
cardiac-specific troponin is the preferred
marker, and if available, it should be
measured in all patients. CK-MB by mass
assay is also acceptable. In patients with
negative cardiac markers within 6 hours of
the onset of pain, another sample should be
drawn in the 6- to 12-hour time frame (eg,
at 9 hours after the onset of symptoms).
(Level of Evidence: C)

Early Risk Stratification

Class IIa
1. For patients who present within 6 hours
of the onset of symptoms, an early
marker of cardiac injury (eg, myoglobin or
CK-MB subforms) should be considered in
addition to a cardiac troponin. (Level of
Evidence: C)
Class IIb
1. C-reactive protein(CRP) and other
markers of inflammation should be
measured. (Level of Evidence: B)

Early Risk Stratification

Class III
1. Total CK (without MB), aspartate
aminotransferase (AST, SGOT),hydroxybutyric dehydrogenase,
and/or lactate dehydrogenase
should be the marker for the
detection of myocardial injury in
patients with chest discomfort
suggestive of ACS. (Level of
Evidence: C)

Diagnosis of Noncardiac
Causes of Symptoms
Class I
1. The initial evaluation of the
patient with suspected ACS should
include a search for noncoronary
causes that could explain the
development of symptoms. (Level
of Evidence: C)

Immediate Management
Class I
1. The history, physical examination, 12-lead ECG,
and initial cardiac marker tests should be
integrated to assign patients with chest pain to 1 of
4 categories: a noncardiac diagnosis, chronic stable
angina, possible ACS, and definite ACS. (Level of
Evidence: C)
2. Patients with definite or possible ACS but whose
initial 12-lead ECG and cardiac marker levels are
normal should be observed in a facility with cardiac
monitoring (eg, chest pain unit), and a repeat ECG
and cardiac marker measurement should be
obtained 6 to 12 hours after the onset of symptoms.
(Level of Evidence: B)

Immediate Management
3. If the follow-up 12-lead ECG and cardiac marker
measurements are normal, a stress test (exercise
or pharmacological) to provoke ischemia may be
performed in the ED, in a chest pain unit, or on an
outpatient basis shortly after discharge. Low-risk
patients with a negative stress test can be
managed as outpatients. (Level of Evidence: C)
4. Patients with definite ACS and ongoing pain,
positive cardiac markers, new ST-segment
deviations, new deep T-wave inversions,
hemodynamic abnormalities, or a positive stress
test should be admitted to the hospital for further
management. (Level of Evidence: C)

Immediate Management
5. Patients with possible ACS and
negative cardiac markers who are
unable to exercise or who have an
abnormal resting ECG should have a
pharmacological stress test. (Level
of Evidence: B)
6. Patients with definite ACS and STsegment elevation should be
evaluated for immediate reperfusion
therapy. (Level of Evidence: A)

Anti-Ischemic Therapy
Class I
1. Bed rest with continuous ECG
monitoring for ischemia and arrhythmia
detection in patients with ongoing rest
pain. (Level of Evidence: C)
2. Nitroglycerin (NTG), sublingual tablet
or spray, followed by intravenous
administration, for immediate relief of
ischemia and associated symptoms.
(Level of Evidence: C)

Anti-Ischemic Therapy
3. Supplemental oxygen for patients with
cyanosis or respiratory distress; finger pulse
oximetry or arterial blood gas determination
to confirm adequate arterial oxygen
saturation (SaO2>90%) and continued need
for supplemental oxygen in the presence of
hypoxemia. (Level of Evidence: C)
4. Morphine sulfate intravenously when
symptoms are not immediately relieved with
NTG or when acute pulmonary congestion
and/or severe agitation is present. (Level of
Evidence: C)

Anti-Ischemic Therapy
5. A -blocker, with the first dose administered
intravenously if there is ongoing chest pain, followed
by oral administration, in the absence of
contraindications. (Level of Evidence: B)
6. In patients with continuing or frequently recurring
ischemia when -blockers are contraindicated, a
nondihydropyridine calcium antagonist (eg, verapamil
or diltiazem), followed by oral therapy, as initial
therapy in the absence of severe LV dysfunction or
other contraindications. (Level of Evidence: B)
7. An ACEI when hypertension persists despite treatment
with NTG and a -blocker in patients with LV systolic
dysfunction or CHF and in ACS patients with diabetes.
(Level of Evidence: B)

Anti-Ischemic Therapy
Class IIa
1. Oral long-acting calcium antagonists for
recurrent ischemia in the absence of
contraindications and when -blockers and
nitrates are fully used. (Level of Evidence: C)
2. An ACEI for all post-ACS patients. (Level of
Evidence: B)
3. Intra-aortic balloon pump counterpulsation for
severe ischemia that is continuing or recurs
frequently despite intensive medical therapy or
for hemodynamic instability in patients before or
after coronary angiography. (Level of Evidence:
C)

Anti-Ischemic Therapy
Class IIb
1. Extended-release form of
nondihydropyridine calcium
antagonists instead of a -blocker.
(Level of Evidence: B)
2. Immediate-release
dihydropyridine calcium
antagonists in the presence of a blocker. (Level of Evidence: B)

Anti-Ischemic Therapy
Class III
1. NTG or other nitrate within 24
hours of sildenafil (Viagra) use.
(Level of Evidence: C)
2. Immediate-release
dihydropyridine calcium
antagonists in the absence of a blocker. (Level of Evidence: A)

Anti-platelet and
Anticoagulation Therapy
Class I
1. Antiplatelet therapy should be initiated
promptly. Aspirin (ASA) is the first choice
and is administered as soon as possible
after presentation and continued
indefinitely. (Level of Evidence: A)
2. A thienopyridine (clopidogrel or ticlopidine)
should be administered to patients who are
unable to take ASA because of
hypersensitivity or major gastrointestinal
intolerance. (Level of Evidence: B)

Anti-platelet and
Anticoagulation Therapy
3. Parenteral anticoagulation with
intravenous unfractionated
heparin (UFH) or with
subcutaneous LMWH should be
added to antiplatelet therapy with
ASA, or a thienopyridine. (Level of
Evidence: B)

Anti-platelet and
Anticoagulation Therapy
4. A platelet GP IIb/IIIa receptor antagonist
should be administered, in addition to ASA
and UFH, to patients with continuing
ischemia or with other high-risk features
(see Table 2) and to patients in whom a
percutaneous coronary intervention (PCI) is
planned. Eptifibatide and tirofiban are
approved for this use. (Level of Evidence:
A) Abciximab can also be used for 12 to 24
hours in patients with UA/NSTEMI in whom
a PCI is planned within the next 24 hours.
(Level of Evidence: A)

Anti-platelet and
Anticoagulation Therapy
Class III
1. Intravenous thrombolytic therapy
in patients without acute STsegment elevation, a true
posterior MI, or a presumed new
left bundle-branch block. (Level of
Evidence: A)

Post-discharge Therapy
Class I
1. Before hospital discharge, patients and/or designated
responsible caregivers should be provided with wellunderstood instructions with respect to medication
type, purpose, dose, frequency, and pertinent side
effects. (Level of Evidence: C)
2. Drugs required in the hospital to control ischemia
should be continued after hospital discharge in
patients who do not undergo coronary
revascularization, patients with unsuccessful
revascularization, or patients with recurrent
symptoms after revascularization. Upward or
downward titration of the doses may be required.
(Level of Evidence: C)

Post-discharge Therapy
3. Before hospital discharge, patients
should be informed about
symptoms of acute myocardial
infarction and should be instructed
in how to seek help if they occur.
(Level of Evidence: C)
4. All patients should be given
sublingual or spray NTG and
instructed in its use. (Level of
Evidence: C)

Post-discharge Therapy
5. Anginal discomfort that lasts >2 or 3 minutes
should prompt the patient to discontinue the
activity or remove himself or herself from the
stressful event. If pain does not subside
immediately, the patient should be instructed to
take NTG. If the first tablet or spray does not
provide relief within 5 minutes, then a second and
third dose, at 5-minute intervals, should be taken.
Pain that lasts >15 to 20 minutes or persistent pain
despite 3 NTG doses should prompt the patient to
seek immediate medical attention by calling 9-1-1
andgoing to the nearest hospital ED, preferably by
ambulance or the quickest available alternative.
(Level of Evidence: C)

Post-discharge Therapy
6. If the pattern of anginal symptoms changes
(eg, pain that is more frequent or severe, is
precipitated by less effort, or now occurs at
rest), the patient should contact his or her
physician to determine the need for
additional treatment or testing. (Level of
Evidence: C)
7. ASA 75 to 325 mg/d in the absence of
contraindications. (Level of Evidence: A)
8. Clopidogrel 75 mg/d in patients with a
contraindication to ASA. (Level of Evidence:
B)

Post-discharge Therapy
9. -Blockers in the absence of
contraindications. (Level of Evidence: B)
10. Lipid-lowering agents and diet in post ACS
patients including patients who are post
revascularization with low-density lipoprotein
(LDL) cholesterol of >125 mg/dL, including
after revascularization. (Level of Evidence: A)
11. Lipid-lowering agents if LDL cholesterol level
after diet is >100 mg/dL. (Level of Evidence: C)
12. ACEIs for patients with CHF, LV dysfunction
(EF <0.40), hypertension, or diabetes. (Level of
Evidence: A)

OTHER GUIDELINES

TREATMENT

Prehospital Care
Often, patients with angina pectoris rest or lie

down to alleviate the pain. If the patient is not

naive to cardiac disease, he or she may have
access to nitroglycerin. Often, the patient uses
nitroglycerin at home to palliate his or her
symptoms. A patient who has known stable
angina often is able to report what exacerbates
the condition and what (as well as how often) is
a "normal" number of tablets for him or her to
use prior to alleviation of anginal symptoms.

TREATMENT

Prehospital Care
Patients are often instructed by their physicians

that the use of more than 3 tablets of nitroglycerin

necessitates a higher level of care (eg, calling for
an ambulance). Some patients are instructed to
take aspirin as well. A knowledgeable patient who
reports a change in the pattern or presentation of
his or her symptoms should be suspected as
having worsening or unstable angina. However,
any patient who presents to the ED with symptoms
of angina should be assessed promptly for signs of
acute myocardial infarction (AMI).

TREATMENT

Prehospital Care
Most prehospital care for angina pectoris

consists of administering nitroglycerin,

oxygen, and aspirin. The ability to obtain a
prehospital ECG is becoming more
prevalent.

Emergency Department
Care

In the ED, the patient who complains of

chest discomfort needs to be:
immediately assessed for AMI as well as

other high-risk diagnoses (eg, aortic

dissection, pulmonary embolism)
an early ECG and a rapid history and physical
examination
Serial ECGs, especially in the setting of
changing symptoms, is vital. Continuous
telemetry monitoring is recommended for
higher-risk patients.

Emergency Department
Care

The patient who presents with chest

pain is presumed to have underlying
clinically significant cardiac pathology
(ie, unstable angina or NSTEMI).

Emergency Department
Care

The initial treatment consists of

administration of:

oxygen
aspirin
Nitroglycerin
Morphine
beta-blocker.

Emergency Department
Care

Given an altered, yet nondiagnostic ECG

and no contraindications, further
treatment with heparin (low-molecular
weight or unfractionated), clopidogrel,
or other antiplatelet agents may be
initiated. Most often, an additional
abnormal marker (eg, an elevated
serum troponin, myoglobin, or CPK
level) will be verified prior to antiplatelet
therapy.

Emergency Department
Care

For persistent symptoms unresponsive

to initial therapy, glycoprotein
inhibitors can be considered.
Persistent pain, in spite of this
treatment, suggests either AMI or an
alternative diagnosis. In the case of
AMI, angioplasty or thrombolytics
should be administered if available and
not contraindicated.

Emergency Department
Care

Syndrome X and Prinzmetal angina are

not diagnosed in the ED, but the
patient's medical records or primary
care physician may be helpful in
recognizing these disorders.

TREATMENT

Consultation
In the setting of unstable angina or AMI, consultation with a

cardiologist is warranted.

Hospitalization
Admission is indicated for patients with unstable angina.

Patients with angina pectoris who are admitted for alternative

reasons do not routinely require telemetry monitoring.
Low-risk, pain-free patients who are admitted with
nondiagnostic ECGs and negative cardiac marker results,
often do not require telemetry monitoring as inpatients.
Patients admitted with UA/NSTEMI will likely undergo
percutaneous transluminal coronary angioplasty (PTCA) if
clinically indicated. If catheterization is not available, hospital
transfer is suggested.

TREATMENT

Transfer
Transfer of the high-risk patient to an

active catheterization center is

recommended. This may be done from the
inpatient setting after the patient has been
stabilized in the ED.

Follow-up
Any discharged patient with suspected

angina should have close primary or

cardiology follow-up care.

WORK-UPS

Laboratory Studies

The laboratory workup of patients with

angina includes the following tests:
Cardiac enzyme levels, if positive may

suggest nonST-segment elevation

myocardial infarction (NSTEMI); negative
results do not rule out ischemia
Coagulation studies, if anticoagulation or
antiplatelets are anticipated
Type and screen, if surgery or transfusions
are considered

Laboratory Studies

The laboratory workup of patients with

angina includes the following tests:
CBC (anemia, leukocytosis may suggest an

alternative diagnosis)
BUN and creatinine level, if intravenous
contrast is anticipated
Electrolyte levels are of virtually no value
unless the patient is on a diuretic and
concern for an abnormality exists.

Imaging Studies

Chest radiography is used to rule out an

alternative diagnosis or contributing factors (eg,
pneumothorax [PTX], pneumonia [PNA],
congestive heart failure); it is also used to evaluate
the aorta prior to anticoagulant administration.
CT of the chest may be considered for evaluation
of aortic or pulmonary disease; if evaluating the
aorta, include the abdominal aorta. Of note, the
forthcoming "triple rule out CT scan" exposes the
patient to an exorbitantly high dose of radiation
and should only be used in certain circumstances.

Imaging Studies

Limited CT coronary scans may help to

reduce the posttest probability of coronary
artery disease while utilizing potentially less
radiation exposure than the "triple rule out
scan." Coronary artery calcification suggests
the presence of an atherosclerotic plaque.
Calcium scores are determined by the
density of calcium and the total area. Higher
calcium scores may suggest a higher risk of
current or future adverse cardiac events.

Imaging Studies

Nuclear imaging should include V/Q (PE

evaluation) and resting Sestamibi (In the
appropriate clinical setting, a normal
study in a patient with ongoing chest pain
may rule out myocardial ischemia).
ECG results may be normal or show signs
of ischemia. Main use is to establish a
baseline and R/O acute ST-segment
elevation myocardial infarction (STEMI).

Imaging Studies

Intraluminal coronary artery

sonography (ICAS) is a highly invasive
modality that may provide additional
information to a patient's coronary
artery anatomy and disease. If
clincially suspected, ICAS may be
utilized to detect the presence or
absence of atherosclerosis.

Imaging Studies

The use of stress cardiac MRI in an

observation unit may be a cost-saving
alternative to inpatient management for
emergency department patients with chest
pain. In a randomized study in 110
patients, Miller et al reported that an
observation unit strategy with stress
cardiac MRI reduced median hospitalization
cost by approximately $588, with no cases
of missed acute coronary syndrome.[19]

Imaging Studies

While the recent ROMICAT trial showed

the introduction of coronary CT
imaging improved efficiency of the
emergency clinical workup in
comparison to the traditional ED care,
patients who underwent cardiac CT
imaging had increased subsequent
workups and incurred a higher
radiation burden without any reduction
in overall cost.[20]

MEDICATIONS

ANTI-PLATELET AGENTS

Class Summary
These agents inhibit platelet aggregation.

Aspirin (Anacin, Bayer Aspirin,

Ascriptin)
Aspirin inhibits platelet cyclooxygenase-1,

which blocks the formation of thromboxane

A2, thus inhibiting platelet aggregation.
Aspirin is arguably the most cost-effective
medication in medicine.

ANTI-PLATELET AGENTS
Clopidogrel (Plavix)
Selectively inhibits adenosine diphosphate (ADP)

binding to platelet receptor and subsequent ADPmediated activation of glycoprotein GPIIb/IIIa

complex, thereby inhibiting platelet aggregation.
May have a positive influence on several
hemorrhagic parameters and may exert protection
against atherosclerosis not only through inhibition of
platelet function but also through changes in the
hemorrhagic profile.
May have additive effect when used in combination
with aspirin. Useful alternative therapy in patients
with a salicylate allergy

ANTI-PLATELET AGENTS

Ticlopidine (Ticlid)
A thienopyridine that irreversibly alters the

platelet membrane and inhibits platelet

aggregation. Second-line antiplatelet
therapy for patients who cannot tolerate or
fail aspirin therapy. Toxicity includes
neutropenia and diarrhea.

Vasodilators

Class Summary
These agents relieve chest discomfort by

improving myocardial oxygen supply,

which, in turn, dilate epicardial and
collateral vessels, improving blood supply
to the ischemic myocardium.

Vasodilators

Nitroglycerin topical (Nitro-Bid,

Deponit)
Reduces preload and ventricular pressures,

thus reducing myocardial oxygen demand.

NTG also promotes coronary
vasodilatation, which promotes improved
myocardial blood flow. Reflex tachycardia
may be harmful, concomitant beta-blocker
usage may offset this reaction.

Analgesics

Class Summary
These agents reduce pain, which

decreases sympathetic stress, in addition

to providing some preload reduction.

Morphine sulfate (Astramorph, MS

Contin, MSIR)
Reduces pain and possibly anxiety

associated with angina pectoris. Use

judiciously in setting of hypotension.

Beta-adrenergic blockers

Class Summary
This category of drugs has the potential to

suppress ventricular ectopy due to

ischemia or excess catecholamines. In the
setting of myocardial ischemia, betablockers have antiarrhythmic properties
and reduce myocardial oxygen demand,
secondary to elevations in heart rate and
inotropy.

Beta-adrenergic blockers

Metoprolol (Lopressor, Toprol XL)

These agents decrease myocardial oxygen

demand by reducing heart rate,

contractility, and arterial pressure. Shown
to improve survival in patients with MI.

Calcium channel blockers

Class Summary
When beta-blockade is contraindicated in the

setting of continuing angina, a

nondihydropyridine calcium antagonist (eg,
verapamil, diltiazem) may be used as initial
therapy in the absence of severe LV dysfunction
or other contraindications (see ACC/AHA 2007
Guidelines for the Management of Patients With
Unstable Angina/NonST-Elevation Myocardial
Infarction).
Though controversial, long-acting nifedipine may
have some benefit in stable angina.

Calcium channel blockers

Diltiazem (Cardizem CD, Dilacor,

Tiazac)
During depolarization, inhibits the influx of

extracellular calcium across both the myocardial

and vascular smooth muscle cell membranes.
Serum calcium levels remain unchanged. The
resultant decrease in intracellular calcium
inhibits the contractile processes of myocardial
smooth muscle cells, resulting in dilation of the
coronary and systemic arteries and improved
oxygen delivery to the myocardial tissue.

Calcium channel blockers

Diltiazem (Cardizem CD, Dilacor,

Tiazac)
Decreases conduction velocity in AV node.

Also increases refractory period via blockade

of calcium influx. This, in turn, stops
reentrant phenomenon.
Decreases myocardial oxygen demand by
reducing peripheral vascular resistance,
reducing heart rate by slowing conduction
through SA and AV nodes, and reducing LV
inotropy.

Calcium channel blockers

Verapamil (Calan SR, Covera-HS,

Verelan)
During depolarization, inhibits calcium
ion from entering slow channels or
voltage-sensitive areas of vascular
smooth muscle and myocardium.

Anticoagulants

Class Summary
Anticoagulants interfere with platelet

aggregation and clot formation thus reducing

arterial clot burden and promoting continued
myocardial oxygen and glucose delivery.
These agents do not digest present clots,
they help prevent secondary formation
during and after spontaneous fibrinolysis.
Often, the decision of when and which
anticoagulant to use is decided jointly by the
emergency physician and cardiologist.

Anticoagulants

Heparin
Unfractionated heparin potentiates the

effect of antithrombin, an enzyme that

inactivates factors IIa, IXa, and Xa. This
leads to an anticoagulant effect. Because
of a relatively narrow therapeutic window,
laboratory monitoring is required.

Anticoagulants

Enoxaparin (Lovenox)
Low molecular weight heparin produced by partial chemical

or enzymatic depolymerization of unfractionated heparin

(UFH). Binds to antithrombin III, enhancing its therapeutic
effect. The heparin-antithrombin III complex binds to and
inactivates activated factor X (Xa) and factor II (thrombin).
Does not actively lyse but is able to inhibit further
thrombogenesis. Prevents reaccumulation of clot after
spontaneous fibrinolysis.
Advantages include intermittent dosing and decreased
requirement for monitoring. Heparin antifactor Xa levels
may be obtained if needed to establish adequate dosing.
LMWH differs from UFH by having a higher ratio of
antifactor Xa to antifactor IIa compared with UFH.

Platelet aggregation
inhibitors

Class Summary
These agents block the GP IIb/IIIa receptor

on platelets. Once the platelet is activated,

these receptors change configuration,
facilitating fibrinogen and ligand binding.
GP IIb/IIIa receptor binding of fibrinogen is
the final step leading to platelet
aggregation. Thus, these agents stymie
platelet aggregation.

Platelet aggregation
inhibitors

Abciximab (ReoPro)
Chimeric human-murine monoclonal antibody approved

for use in elective/urgent/emergent percutaneous

coronary intervention. Binds to receptor with high affinity
and reduces platelet aggregation by 80% for up to 48 h
following infusion.

Eptifibatide (Integrilin)
Antagonist of the platelet glycoprotein (GP) IIb/IIIa

receptor, which reversibly prevents von Willebrand factor,

fibrinogen, and other adhesion ligands from binding to the
GP IIb/IIIa receptor. Inhibits platelet aggregation. Effects
persist over duration of maintenance infusion and are
reversed when infusion ends.

Platelet aggregation
inhibitors

Tirofiban (Aggrastat)
Nonpeptide antagonist of GP IIb/IIIa

receptor. Reversible antagonist of

fibrinogen binding. When administered IV,
more than 90% of platelet aggregation
inhibited. Approved for use in combination
with heparin for patients with unstable
angina who are being treated medically
and for those undergoing PCI.

Oxygen
Promotes a higher PaO2, thus improving

myocardial oxygen delivery

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