Acute Coronary Syndrome

SIMBIOSIS NEWSPAPER CARDIOLOGY
ACUTE CORONARY SYNDROME
Acute coronary syndrome (ACS) is used

to describe a range of thrombotic
coronary diseases, including unstable
angina (UA), non-ST elevation
myocardial infarction (NSTEMI), and
ST-elevation myocardial infarction
(STEMI).
Collectively, they represent one of the

most common causes of acute medical
admission to U.S. hospitals.
The term ACS is clinically useful because

the initial presentation and early
management of unstable angina,
STEMI, and NSTEMI are frequently
similar. ACS should be distinguished
from stable angina, which develops

during exertion and resolves at rest.
ACS is due to coronary vessel

atherosclerotic obstruction with
superimposed thrombotic occlusion.
The natural course of coronary

atherosclerotic plaque development and
subsequent occlusion does not proceed
in a step-wise, uniform manner,
gradually progressing to luminal
obstruction (and symptoms) over many
years. This process is characterized by
plaque disruption and mural
thrombosis.
Angiographic data support the concept

that noncritical lesions account for the
majority of the ACS. Thus, the
pathogenic rate-limiting mechanism of
the ACS appears to be acute thrombosis
and the resultant obstruction of the
coronary lumen.
An operational classification is clinically

helpful since it allows the simple
distinction of the different types of ACS.
In this classification, the ECG is the most
important clinical tool.
The initial ECG findings, in particular,

the presence or absence of ST-segment
elevation, will further define the
patient’s condition and dictate
treatment options.
Unstable Angina and NSTEMI
UA and NSTEMI are closely related in

terms of clinical presentation and
pathogenesis, but patients with these
conditions have widely varying risks.
Both are usually caused by
atherosclerotic CAD and present an
increased risk for death and MI.
• NSTEMI is more severe than UA, and

is considered to have occurred if
ischemia produces damage detectable by
biochemical markers of myocardial
injury (troponin I or CK-MB).
• If there are no detectable serum

markers of myocardial injury 12–18
hours after symptom onset, the patient
should be diagnosed with UA.
• At the time of presentation, UA and

NSTEMI may be indistinguishable and
can be identically managed.
• Therefore, in establishing the diagnosis

of NSTEMI, cardiac troponins (elevated
enzymes show evidence of infarction)
should be used to distinguish this entity
from UA.
Outcomes in UA/NSTEMI are generally

better than in STEMI, but certain
UA/NSTEMI patients are at high risk for
MI or death, and it is important to
identify these patients at initial
screening because they may require
intensive monitoring and management.
Thrombolytic therapy is beneficial in

patients with STEMI, but is not effective
in UA or NSTEMI and may be harmful.
Unstable angina is sometimes referred
to as “crescendo” or “preinfarction”
angina. Typically, it is defined as angina
of increasing severity, frequency,
duration; angina showing increasing
resistance to nitrates; or angina
occurring at rest. Experts also regard
any new-onset angina as unstable.
Sudden change in the pattern of angina

usually means a physical change within
the coronary arteries, such as
hemorrhage into an atherosclerotic
plaque or rupture of a plaque with
intermittent thrombus formation.
About 35% of patients with the clinical

syndrome of UA will already have
coronary thrombosis on catheterization.
In fact, untreated UA progresses to MI in

50% of cases, thus the patient with new-
onset or unstable angina should be
hospitalized for intensive medical
treatment.
Most patients with NSTEMI have a

normal physical examination. An
abnormal ECG, particularly dynamic
ST-segment deviation (≥0.5 mm), or
new T-wave inversion (≥2 mm), will
confirm the diagnosis, but the ECG may

be normal or show minor changes in up
to 50% of cases.
High-risk features for patients with

presumed UA/NSTEMI include:
• Repetitive or prolonged chest pain
(>10 min)
• Elevated cardiac biomarkers
• Persistent ECG changes of ST
depression >0.5 mm or new T-wave
inversion
• Hemodynamic instability (SBP <90)
• Sustained ventricular tachycardia
• Syncope
• LV ejection fraction <40%
• Prior angioplasty or prior CABG
• Diabetes
• Chronic kidney disease
General management
Aspirin is recommended (unless
contraindicated) in all patients. High-
risk patients should be treated with
aggressive medical management and
arrangements should be made for
coronary angiography and possible
revascularization, except in those with
severe comorbidities.
Age alone should not be a barrier to

aggressive therapy
Medical management
Antiplatelet therapy (beyond aspirin):
Early treatment should be initiated with
aspirin and clopidogrel or prasugrel,
with the following considerations:
• Avoid clopidogrel in patients likely to

require emergency coronary bypass
surgery.
Prasugrel and ticagrelor are alternatives
to clopidogrel.
• If possible, discontinue clopidogrel 5
days before coronary bypass surgery.
• Use ticagrelor in addition to aspirin for
acute coronary syndromes. It is not
clearly better than clopidogrel or
prasugrel.
• Give heparin along with the
recommended antiplatelet therapy for
UA/NSTEMI.
Antithrombin therapy: Give

unfractionated heparin or subcutaneous
enoxaparin until angiography or for 48–
72 hours. The enoxaparin dose must be
reduced in patients with impaired renal
function.
Glycoprotein (GP) IIb/IIIa inhibitors:

This class of antithrombotic agents
inhibits platelet function by blocking a
key receptor involved in platelet
aggregation.
The use of these agents provides a more

comprehensive platelet blockade than
the combination of aspirin and heparin.
• These drugs take advantage of the fact
that platelets play an important role in
the development of ischemic
complications that may occur in patients
with UA/NSTEMI.
• Tirofiban or eptifibatide is particularly

recommended in high-risk patients in
whom an invasive strategy is planned.
• Concomitant tirofiban is particularly

beneficial and recommended in patients
with diabetes.
• Complications include bleeding and
thrombocytopenia (occurs with all GP
IIb/IIa agents; incidence ranges 1–5.5%
in clinical studies; an immune
mechanism is likely responsible; all
patients receiving parenteral GP IIb/IIa
antagonsists should be monitored for 24
hours for development of
thrombocytopenia).
Other: A beta blocker should be given

unless contraindicated. IV nitroglycerin
(NTG) can be given for refractory pain.
In patients with diabetes, good glycemic

control should be targeted in the
hospital and after discharge. This may
require considering an insulin-based
regimen in hospital.
Invasive management
Early coronary angiography (within 48
hours) and revascularization are
recommended in patients with NSTEMI
and high-risk features, except in patients
with severe comorbidities.
Pain or ischemia refractory to medical

therapy and high-risk features on early
exercise testing can also identify
patients suitable for early invasive
therapy.
ST Elevation MI
The pain of typical MI (STEMI; in the
past referred to as Q wave MI) is
substernal, diffuse with a pressure
quality. It may radiate to the neck or jaw,
shoulders, or arms. Often, the pain is
accompanied by additional symptoms,
such as dizziness (lightheadedness),
nausea or vomiting, diaphoresis, or

shortness of breath (dyspnea).
The symptoms of MI last >20 minutes

and do not respond completely to
nitroglycerin. The duration of the pain is
variable. Pain may resolve completely
after a few hours or may persist for over
a day.
Elderly or diabetic patients are prone to

atypical symptoms such as nausea or
dyspnea as the sole symptoms of
infarction. As many as 20% of MI are
“silent”—that is, whatever symptoms
were present did not impress the patient
enough for them to seek medical care or
even to remember the incident.
The exam usually shows the patient to

have anxiety and pain. Diaphoresis is
often present.
Pulse rate may be normal, but often
bradycardia is present in inferior
infarction.
Tachycardia is often seen with large

infarctions. Blood pressure is often
elevated.
Cardiac exam will usually be normal.

Large infarctions may cause signs of
ventricular failure or valve dysfunction.
A fourth heart sound (S4) is common
due to a stiffened ventricle. Mitral
regurgitation may occur if papillary
muscles malfunction. The second heart
sound may be paradoxically split as the
left ventricular contraction time
increases due to LBBB and weakened
left ventricle.
Later in the course of MI, other findings

may be present: mild fever, pericardial
friction rub, ventral septal defect
murmur due to septal rupture, or severe
mitral regurgitation due to papillary
muscle rupture.
STEMI is defined as clinical symptoms

consistent with ACS and ECG features
including any of these:
• Persistent ST-segment elevation of ≥1
mm in two contiguous limb leads
• ST-segment elevation of ≥2 mm in two
contiguous chest leads
• New LBBB pattern
Initially, you don’t need increased

cardiac biomarkers (troponin, CPK-MB,
etc.) to make the diagnosis of STEMI
(although these are usually eventually
positive at some point during the course

of the disease).
Initial nonspecific management for all

patients with possible MI (anyone with a
compatible chest pain history) is to keep
them on a cardiac monitor. Oxygen
therapy and an IV line should be
established as quickly as possible.
Aspirin should be given unless
contraindicated, as early as possible.
Nitroglycerin and pain control
(morphine) should be given as required.
Patients with STEMI usually have a

completely occluded coronary artery
with thrombus at the site of a ruptured
plaque. This eventually leads to
myonecrosis. Restoring coronary
patency (emergency reperfusion) as
promptly as possible is a key
determinant of short-term and longterm

outcomes.
Patients with STEMI who present within

12 hours of the onset of ischemic
symptoms should have a reperfusion
strategy implemented promptly.
Reperfusion may be obtained with
fibrinolytic therapy or percutaneous
coronary intervention (PCI).
Patients presenting with NSTEMI will

not benefit from thrombolytics
Anteroseptal STEMI with Changes in V1 –V3

Inferior STEMI with Changes in II, III, and aVF
NSTEMI Affecting Leads II, III, and aVF

Localization of STEMI
Typical Electrocardiographic Evolution of a STEMI
Emergent reperfusion therapy
The choice of reperfusion therapy is

between PCI and thrombolysis therapy.
PCI is the best available treatment if
provided promptly. PCI improves short-
term and long-term outcomes

(reduction of deaths and MI) in patients
with STEMI presenting within 12 hours
when compared with thrombolytic
therapy. This benefit over thrombolysis
may occur only if the additional time
delay associated with PCI is <1 hour. In
general, a time delay of 90 minutes from
first medical encounter to PCI is the
maximum desirable. For patients
presenting with STEMI at a facility
without PCI access, transfer to another
facility capable of performing PCI
usually takes too long. Where PCI is
delayed or not available, reperfusion
with thrombolytic therapy should occur
unless contraindicated.
Thrombolytics (Fibrinolytics)
Thrombolytics such as streptokinase or

tissue-type plasminogen activator (tPA)
restore perfusion to the ischemic area by
lysing the clot, thereby reducing infarct
size and improving survival.
Thrombolysis benefits patients with all

types of ST elevation infarction, but the
benefit is several times greater in those
with anterior infarction. The earlier the
treatment is given, the greater the
absolute benefit. The greatest benefit is
in patients with ST elevation or new left
bundle branch block who have had
symptoms for <12 hours.
Streptokinase and alteplase are given by

IV infusion. Reteplase and tenecteplase
can be given by rapid bolus injection.

tPA is the most common agent used in
the U.S. Prolonged persistence of
antibodies to streptokinase may reduce
the effectiveness of subsequent
treatment; therefore, streptokinase
should not be used if used within the
previous 12 months in the same patient.
Complexity of administration differs

among the different thrombolytics:
tenecteplase and reteplase are ready in
about one minute; for streptokinase or
tPA, the typical time from physician
order to administration is 12 to 15
minutes.
Bottom line: consider a thrombolytic

agent as an alternative to primary PCI in
suitable candidates with:
• ST-elevation MI (>1 mm ST elevation
in 2 contiguous leads)
• New LBBB
Contraindications to thrombolytic
therapy:
• Absolute contraindications:
• Active bleeding or bleeding diathesis
• Significant closed head or facial trauma
within 3 months
• Suspected aortic dissection
• Prior intracranial hemorrhage
• Ischemic stroke within 3 months
Relative contraindications:
• Recent major surgery (<3 weeks)
• Traumatic or prolonged
cardiopulmonary resuscitation
• Recent (within 4 weeks) internal
bleeding
• Active peptic ulcer
• Severe, poorly controlled HTN

• Ischemic stroke (<3 months)
Late presentation (>12 hours after

symptom onset): Reperfusion therapy
with either PCI or fibrinolysis is not
routinely recommended in patients who
are asymptomatic and hemodynamically
stable, and who present >12 hours after
symptom onset.
Other interventions may include

coronary artery bypass grafting (CABG).
CABG surgery may occasionally be more
appropriate—particularly in patients
who have suitable anatomy and are not
candidates for fibrinolysis or PCI. CABG
surgery may also be considered in
patients with cardiogenic shock or in
association with mechanical repair.
Adjuvant therapy used together

with reperfusion
Antiplatelet Therapy
Aspirin should be given to all patients

with presumed STEMI unless
contraindicated, and, in the absence of
significant side effects, low-dose therapy
should be continued in the long term.
Clopidogrel or prasugrel should be

prescribed in addition to aspirin for
patients undergoing PCI with a stent.
Ticagrelor is an alternative to
clopidogrel or prasugrel.
In patients selected for fibrinolytic

therapy, clopidogrel should be given in
addition to aspirin, unless
contraindicated. Note, however, that if it
is thought that the patient is likely to

require CABG acutely, clopidogrel
should be withheld.
Clopidogrel should be continued for at

least a month after fibrinolytic therapy,
or for up to 9–12 months after stent
implantation, depending on the type of
stent used.
Antithrombin Therapy
With PCI: Antithrombin therapy should
be used in conjunction with PCI. The
dose of unfractionated heparin therapy
will depend on concomitant use of
glycoprotein (GP) IIb/IIIa inhibitors.
It may be advisable to give a bolus of

heparin while the patient is in transit to
the catheterization laboratory.
The role of enoxaparin in acute STEMI

in conjunction with PCI remains to be
fully determined, but it appears to be
safe and effective.
With fibrinolysis: Antithrombin therapy

should be used with fibrin-specific
fibrinolytic agents.
IV unfractionated heparin should be

given as an initial bolus, adjusted to
attain the activated partial
thromboplastin time (APTT) at 1.5 to 2
times control. IV unfractionated heparin
is used when rapid reversal is needed.
The half-life is shorter with
unfractionated heparin.
Glycoprotein IIb/IIIa Inhibitors

It is reasonable to use abciximab with
primary PCI. Epifibatide and tirofiban
are the other GPIIb/IIIa inhibitors. Full-
dose GP IIb/IIIa inhibitors should be
avoided with fibrinolytic therapy as
there is evidence of excessive bleeding
(including intracranial hemorrhage)
with this combination.
The combination of GP IIb/IIIa

inhibitors with reduced doses of
fibrinolytic therapy is not
recommended. There is no significant
advantage over full-dose fibrinolytic
therapy alone, and the risk of bleeding is
increased, particularly in the elderly.
Cardiac surgery
Emergency bypass surgery should be
considered in patients with STEMI and:
(1) failed PCI with persistent pain or
hemodynamic instability and coronary
anatomy suitable for surgery or
(2) persistent or recurrent ischemia
refractory to medical therapy and
suitable anatomy
Cardiac surgery
Emergency bypass surgery should be
considered in patients with STEMI and:
(1) failed PCI with persistent pain or
hemodynamic instability and coronary
anatomy suitable for surgery or
(2) persistent or recurrent ischemia
refractory to medical therapy and
suitable anatomy
Secondary prevention through the
control or elimination of known risk
factors for coronary artery disease (e.g.,

hyperglycemia in patients with diabetes
mellitus, HTN control, tobacco
cessation, physical inactivity) also
should be part of discharge planning.
You are asked by your patient, who has a

history of ischemic heart disease, about
drug treatments that have been shown to
decrease mortality in his case. (It doesn’t
matter if he has stable angina or prior
history of acute coronary syndrome.)
Answer: Lipid lowering agents

(statins), ASA, B-blocking agents and
CABG in patients with triple vessel
disease or left main disease.
Other testing in ACS

Exercise ECG testing: Increasingly,
submaximal testing is performed 4–7
days after infarction.
A maximal test can be performed at 3–6
weeks postinfarction. It is used to assess
prognosis and to identify those patients
with reversible ischemia who should
then have an angiogram (if one has not
been done) to assess the need for
coronary artery bypass graft.
Myocardial perfusion imaging can be

performed before hospital discharge to
assess the extent of residual ischemia if
the patient has not already undergone
cardiac catheterization and
angiography.
Complications of ACS
Electrical disturbances dysrhythmias
• Bradycardia: sinus, atrioventricular
junctional, idioventricular. These are
treated acutely with atropine and
temporary pacing if severe.
• Premature beats: atrial, ventricular.
No treatment is needed for ectopy such
as these.
• Tachyarrhythmias (supraventricular):
atrial tachycardia, atrial fibrillation,
atrial flutter, AV junctional; are seldom
caused by ischemia
• Tachyarrhythmias (ventricular):
ventricular tachycardia, accelerated
idioventricular rhythm, ventricular
fibrillation.
Conduction Abnormalities
• Atrioventricular nodal: first-, second-,
and third-degree block
• Intraventricular: hemiblocks (left
anterior, left posterior), bundle branch
block, thirddegree atrioventricular block
Pump dysfunction
• Contractile dysfunction: left
ventricular, right ventricular, and
biventricular failure; true ventricular
aneurysm; infarct expansion
• Mechanical disruption: acute mitral
regurgitation (papillary muscle
dysfunction or rupture), ventricular
septal rupture, free wall rupture,
pseudoaneurysm; treated with
emergency surgical repair
• Electromechanical dissociation
Ischemia
• Postinfarction ischemia: ischemia in
the infarct and ischemia distant to the
infarct
• Early recurrent infarction or infarct
extension
• Postinfarction angina after
thrombolytics or PCI should be treated
with bypass surgery
Pericarditis—Dressler syndrome
(late)
Treated with aspirin, NSAIDs, and later
steroids if there is no response.
Thromboembolic
• Mural thrombus with systemic
embolism
• Deep vein thrombosis with prolonged
immobilization
Sudden cardiac death

Most often due to arrhythmia.
• Ventricular fibrillation (most
commonly)
• Ventricular tachycardia
Right ventricular infarction

Accompanies 30% of inferior MIs. It is
diagnosed with RV leads and treated
with fluids.
Non-Cardiac Complications of ACS

Depression is 3x more common in those
who have had a heart attack than in the
general population, with 20% of heart
attack victims qualifying for a diagnosis
of major depressive disorder, and a far
greater proportion experiencing
increased levels of depressive
symptoms.
Beyond the accompanying emotional

distress and suffering, depression also
increases one’s risk of having another
heart attack or dying over the ensuing
months and years.
There is reliable evidence that both
antidepressant medications and certain
forms of psychotherapy are effective in
reducing depression in the post-MI
state. Selective serotonin reuptake
inhibitors (SSRIs) such as sertraline and
citalopram have been found to be both
effective in reducing depression and

relatively safe for use in patients with
coronary heart disease.
Cognitive behavior therapy has also

been found to be effective in treating
depression.
Erectile dysfunction (ED) is prevalent

among patients with CAD and post-MI
(in some series ~ 40%).
• ED complicates the recovery of those
post-MI.
• Treatment of post-MI patients includes
management of depression,
reassurance, and modification of
medications that may cause ED.
• Sildenafil should be used cautiously in

men post-MI who are taking nitrates of
up to 55 mm Hg, because it can cause a
drop in BP. Due to this synergistic effect,

it is therefore contraindicated in
patients taking nitrates.
• ED is a complication of the conditions

that are primary risk factors for
developing CAD, in particular, diabetes,
hypertension, dyslipidemias, and
arteriosclerosis.
• Smoking and stress are implicated in

the development of ED.
In evaluating risk of MI associated with

intercourse in patients with cardiac
disease, it has been estimated that <1%
of MIs occur during sexual activity.
Although sexual activity can trigger MI,
the relative risk is low with a slight
increase in risk within 2 hours of sexual

activity.
However, even in high-risk individuals

with previous MI the annual risk is
1.10% vs. 1.0% in the population at large.
This risk appears to apply equally to men
and women.
Patients can therefore be risk-stratified

and counseled about safely returning to
or continuing sexual activity:
• Low risk: asymptomatic patients with
fewer than 3 risk factors for CAD, stable
angina, recent uncomplicated MI, mild
valvular heart disease, mild CHF,
controlled hypertension, or post
successful revascularization; patients
can generally be managed medically and
followed at regular intervals
• Intermediate risk: those with recent MI
(but beyond 2 weeks), moderate CHF
(New York Heart Association class II)

and those with >3 risk factors for CAD;
patients may benefit from functional
testing, i.e., exercise treadmill tests
(ETT), echocardiography, or nuclear
imaging study with re-stratification
based on results of testing
– ETT can assist in gauging cardiac risk
of sexual activity, both for induction of
ischemia or arrhythmia. In general, if a
patient can achieve 5 METs on ETT
without demonstrable ischemia or
significant arrhythmia, he is not at high
risk to resume normal sexual activities
– Similarly, if echocardiography does
not yield evidence of more than
moderate left ventricular dysfunction,
resumption of sexual activity is probably
safe.
High-risk: those with unstable angina,

MI within 2 weeks, poorly controlled
hypertension, severe CHF (New York

Heart Association class III/IV),
significant arrhythmias, severe
cardiomyopathies; patients should be
referred for cardiovascular evaluation
and stabilization prior to recommending
resumption of sexual activity.
Nonatherosclerotic Acute
Coronary Syndromes
Although thrombotic complications of
the atherosclerotic process account for
most cases of acute coronary syndromes,
there are a few rare etiologic factors that
have been proposed as causes of or
contributors to acute coronary
occlusion. These causes include
coronary artery spasm, spontaneous
coronary dissection, coronary artery
embolization, coronary arteritis, and

hypercoagulability states such as factor
V gene mutation, deficiencies of proteins
C and S, antithrombin III deficiency,
antiphospholipid antibody syndrome,
and prothrombin gene mutation.
Cocaine use has been documented to

induce coronary vasoconstriction in
nondiseased coronary segments but is
more pronounced in atherosclerotic
segments.
Prinzmetal angina, or variant angina,

is a very uncommon condition in which
episodes of severe angina are triggered
when one of the major coronary arteries
suddenly goes into spasm. These
episodes are accompanied by ST-
segment elevation on the ECG. Although
the spasm almost always terminates
spontaneously, Prinzmetal angina may
be associated with acute MI, serious

ventricular arrhythmias, and sudden
death.
As opposed to typical angina, Prinzmetal

angina usually occurs during periods of
rest, most often at night and in the early
morning hours. Frequently, episodes
appear in clusters.
In men, Prinzmetal angina is often

associated with atherosclerosis; in
women it is not. Women with Prinzmetal
tend to have few risk factors for CAD,
though many have a history of migraine
headaches (another condition
associated with arterial spasm).
Exercise testing and routine coronary

angiography usually give normal results.
Ergonovine has been used to trigger
coronary artery spasm in susceptible
patients, confirming the diagnosis.
Treatment with calcium channel

blockers or nitrates eliminates spasm in
most of these patients. Once adequately
treated, their prognosis is good.
During an acute episode of pain and ST

segment elevation, you cannot tell who
has Prinzmetal variant angina and who
has an acute ST elevation MI. Therefore,
you must initially treat everyone with
chest pain and ST elevation as if they
were having an acute MI.
Prinzmetal angina can be confirmed

only after coronary angiography.
Causes of MI without Coronary

Atherosclerosis
Vasculitis
– Systemic lupus erythematosus
– Polyarteritis nodosa
– Takayasu arteritis
– Mucocutaneous lymph node
syndrome (Kawasaki)
• Anomalous origin of coronary
artery
• Coronary spasm
– Variant angina
– Cocaine abuse
• Coronary artery embolus
– Atrial myxoma
– Atrial or ventricular thrombus
• Hypercoagulable states
– Polycythemia vera
– Thrombocytosis
– Factor V Leiden
– Protein C deficiency
– Antiphospholipid antibodies

Acute Coronary Syndrome

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Acute Coronary Syndrome

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SIMBIOSIS NEWSPAPER CARDIOLOGY

ACUTE CORONARY SYNDROME

Acute coronary syndrome (ACS) is used

Collectively, they represent one of the

The term ACS is clinically useful because

from stable angina, which develops

ACS is due to coronary vessel

The natural course of coronary

Angiographic data support the concept

An operational classification is clinically

The initial ECG findings, in particular,

Unstable Angina and NSTEMI

UA and NSTEMI are closely related in

• NSTEMI is more severe than UA, and

• If there are no detectable serum

• At the time of presentation, UA and

• Therefore, in establishing the diagnosis

Outcomes in UA/NSTEMI are generally

Thrombolytic therapy is beneficial in

Sudden change in the pattern of angina

About 35% of patients with the clinical

In fact, untreated UA progresses to MI in

Most patients with NSTEMI have a

confirm the diagnosis, but the ECG may

High-risk features for patients with

Age alone should not be a barrier to

• Avoid clopidogrel in patients likely to

Antithrombin therapy: Give

Glycoprotein (GP) IIb/IIIa inhibitors:

The use of these agents provides a more

• Tirofiban or eptifibatide is particularly

• Concomitant tirofiban is particularly

Other: A beta blocker should be given

In patients with diabetes, good glycemic

Pain or ischemia refractory to medical

nausea or vomiting, diaphoresis, or

The symptoms of MI last >20 minutes

Elderly or diabetic patients are prone to

The exam usually shows the patient to

Tachycardia is often seen with large

Cardiac exam will usually be normal.

Later in the course of MI, other findings

STEMI is defined as clinical symptoms

Initially, you don’t need increased

positive at some point during the course

Initial nonspecific management for all

Patients with STEMI usually have a

determinant of short-term and longterm

Patients with STEMI who present within

Patients presenting with NSTEMI will

Anteroseptal STEMI with Changes in V1 –V3

Inferior STEMI with Changes in II, III, and aVF

NSTEMI Affecting Leads II, III, and aVF

Typical Electrocardiographic Evolution of a STEMI

Emergent reperfusion therapy

The choice of reperfusion therapy is

term and long-term outcomes

Thrombolytics such as streptokinase or

Thrombolysis benefits patients with all

Streptokinase and alteplase are given by

can be given by rapid bolus injection.

Complexity of administration differs

Bottom line: consider a thrombolytic

• Severe, poorly controlled HTN