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CHEST PAIN
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18
Cardiovascular Problems in Emergency Medicine: A discussion-based review, First Edition.
Edited by Shamai A. Grossman and Peter Rosen.
© 2011 John Wiley & Sons, Ltd. Published 2011 by John Wiley & Sons, Ltd.
Non-ST segment elevation
myocardial infarction
David Plitt
1
& William J. Brady
2
1
Department of Medicine, University of Virginia School of Medicine, Charlottesville,
VA, USA
2
Vice Chair, Department of Emergency Medicine, Professor of Emergency Medicine
and Medicine, University of Virginia Health System, Charlottesville, VA, USA
2
Section I: Case presentation
A 58-year-old woman presented to the emergency
department (ED) with chest pain. The patient had a
history of myocardial infarction, hypertension, and
diabetes mellitus. The chest pain had its onset 12 hours
prior to presentation while the patient was at rest;
the patient noted that the discomfort was similar to
her past cardiac pains. The physical examination was
notable for marked hypertension and mild diaphore-
sis; her vital signs were otherwise unremarkable. The
12-lead electrocardiogram (EKG) demonstrated non-
specifi c ST-segment and T wave abnormalities. While
awaiting laboratory results, the patient received aspi-
rin and nitrates. The chest radiograph demonstrated
mild pulmonary congestion. The serum troponin
value was 0.09 mg/dl (normal ⬍0.02 mg/dl).
An acute coronary syndrome (ACS) was diagnosed.
Plans were made for hospital admission while serial
troponin testing was performed; the second value
was 1.9 mg/dl. Heparin was added along with clopi-
dogrel. A repeat 12-lead EKG demonstrated progres-
sive ST-segment depression in the inferior leads. Mild
pulmonary congestion was considered a relative con-
traindication to intravenous beta-blockade.
The patient was admitted to the hospital for serial
troponin testing. Approximately 18 hours after pre-
sentation, the serum troponin value was 11.1 mg/dl;
continued ST depression was noted in the right
precordial leads. The patient was taken to the cardiac
catheterization laboratory for coronary angiography.
While on-call to the laboratory, the patient received
a glycoprotein inhibitor. At catheterization, right and
circumfl ex coronary arterial occlusions were noted,
and both were successfully stented; inferior and pos-
terior hypokinesis were noted as well. The patient
was ultimately diagnosed with a non-ST-segment
elevation myocardial infarction with congestive heart
failure; the serum troponin peaked at 19.6 mg/dl.
Section II: Case discussion
Dr Peter Rosen: This is not a subtle case in terms of
the problems that physicians often have in recog-
nizing coronary ischemic syndromes in women, but
the real question is: What are your triggers for man-
agement and admission? When would you be com-
fortable defi ning a patient like this as stable angina
for whom not much has to be done, as opposed to
unstable angina where a different strategy has to be
undertaken?
Dr David Brown: To start, we should consider the
differential diagnosis, with an acute coronary syn-
drome being the fi rst, but not the only, item on the
list. Could this also be an aortic dissection, as this is
someone with a history of hypertension? We would
also consider some other cause of chest pain, such as
NON-ST SEGMENT ELEVATION MYOCARDIAL INFARCTION
19
unit. The next step, for a patient with an elevation of
troponin, probably wouldn’t be provocative testing;
it would be cardiac catheterization in a non-emergent
but urgent fashion, such as the next morning, assum-
ing she remained in stable condition over night.
WB: To reiterate, this patient has elevated biomark-
ers with an early rising pattern concerning for ACS
with myocardial injury. Such patients, as identifi ed
with positive biomarkers, are at high risk for acute
and subacute cardiovascular complications, including
death. These patients always should be admitted to
the hospital.
PR: What would you do with this patient with an
elevated troponin level if you were in an institution
that didn’t have a catheterization laboratory, or did
not have someone doing angioplasty?
Dr Amal Mattu: Traditionally, these patients would
be managed conservatively. Assuming they continued
to be pain and symptom free, they tended to do pretty
well with conservative management and medical
treatment, and did not need an immediate trip to the
catheterization laboratory unless there were compli-
cations or recurrent pain. This strategy is referred to
as a “selective invasive approach.”
DB: The TACTICS trial looked at this, although it’s
a few years old now. In 2001, this study looked at
conservative versus aggressive management, in a time
frame similar to the current era, with the signifi cant
addition of the use of antiplatelet therapy. The authors
conclude that conservative management is inferior to
more aggressive management. This conclusion means
that in non-STEMIs, the group of patients managed
with urgent but not emergent catheterization, followed
by revascularization, does better. This strategy was
proven by performing cardiac catheterization on all the
non-STEMI patients, not just those with an abnormal
post-MI stress test.
WB: If you are working in the ED of an institution
without coronary angiography, you should consider
transfer of such patients, assuming that logistical
issues are acceptable, including a safe, appropriate
EMS transport staff and vehicle; a reasonable dis-
tance to a receiving hospital; and favorable weather,
to name only a few issues. In a patient who is stable,
it is not unreasonable to consider admission to the
noninvasive hospital with transfer the next day. In the
pericarditis, myocarditis, pneumothorax, or pneumo-
nia. Then, we would obtain, in addition to the EKG, a
chest X-ray study and cardiac markers, whichever type
are done in this particular ED, including a troponin
level. Assuming we reasonably exclude the diagnoses
I mentioned, we would not need to do more in fi nd-
ing an alternative diagnosis. Nevertheless, in a patient
who presents like this with typical ischemic chest pain
that occurred at rest, as well as with a history of myo-
cardial infarction, there is a need to have, at the very
least, even with negative initial markers, some sort of
risk stratifi cation and a period of monitoring.
Dr William Brady: The use of biomarkers is not indi-
cated in all adult chest pain patients. This testing
modality should only be used in patients where the
clinical suspicion includes ACS.
DB: If we are 12 hours out from the onset of the symp-
toms, a single set of markers might be reasonable. We
still will require some sort of risk stratifi cation to see
whether this pain represents a provocable ischemia.
I can’t imagine a scenario in which this particular
patient will be sent directly home from the ED.
WB: The patient under discussion clearly needs admis-
sion to the hospital. Recurrent chest discomfort with
progressively rising biomarkers identifi es this patient
at high risk, requiring additional therapy and further
diagnostic evaluation.
Dr Shamai Grossman: You have several options as far
as admission. At some institutions, this patient might
require a full admission, while in others an observa-
tion unit stay might be available; regardless, she will
need serial testing and probably some form of stress
imaging.
DB: Much will depend on the results of the fi rst set
of markers in the ED. If she has a normal EKG and a
normal troponin, along with being 12 hours out from
the onset of symptoms that sound like ischemic chest
pain, then an observation admission and provocative
testing would be reasonable. This testing, depending
on the institution, might be an exercise tolerance test
with or without nuclear imaging or stress echo. On
the other hand, if the troponin level is positive, then
she should not go to an observation unit. She would,
by defi nition, have met criteria for a non-ST elevated
myocardial infarction (NSTEMI or non-STEMI) and
should be admitted, at least, to a cardiac step-down
CHAPTER 2
20
to be transferred to a tertiary care center. The issues
with starting someone in the community hospital on
a glycoprotein inhibitor concern a possible prolonga-
tion of stay in the transferring department, as well as
possibly having more complications if the transferring
physician is unfamiliar with the use of platelet inhibi-
tors. One must consider very carefully when you’re
in the community whether you want to be the person
to start the glycoprotein inhibitor, or whether that
should be started in the tertiary care facility where the
procedure will be performed, and whether the incre-
mental benefi t of having a glycoprotein inhibitor on
board for a brief period of time—for the 30 minutes
to an hour of transport time—will allow this agent to
actually help preserve the person’s myocardium or put
that patient at greater risk for an adverse outcome.
DB: I think we’re combining several issues. The fi rst
is: can the drug be safely given in the community by
doctors and nurses who are going to be relatively
unfamiliar with this drug? The second question is:
will the patient will be going directly for catheteriza-
tion? I don’t think that’s likely to happen for patients
with a non-STEMI. They are more likely to be trans-
ferred to a facility where they could be catheterized,
but it’s usually the next business day. Then the ques-
tion becomes: does 12 or even 24 hours of coverage
with a glycoprotein inhibitor while someone’s evolv-
ing a non-STEMI before revascularization make a
difference or not? These patients are not comparable
to STEMI patients being transferred directly to the
catheterization laboratory, for whom you can strongly
argue that it doesn’t make much difference whether the
glycoprotein inhibitor is given in the ED or in the cath-
eter laboratory. But this is a different group of patients.
These patients evolving a non-STEMI are going to wait
for 12 hours or more, in a coronary care unit (CCU) or
perhaps even in an ED observation unit, and will not
have an immediate revascularization procedure. There
is no evidence to help answer that question right now.
PR: I believe that one of your obligations required in
arranging a transfer is to fi nd out what your accepting
physician wants done. There is great virtue in shar-
ing responsibility in these cases. I worry less about
the ability to give a bolus or to run an infusion by
both emergency physicians and transferring EMTs or
fl ight nurses because I think that we now have enough
experience in the United States to show that it can be
done safely. To summarize, we have a patient with
more acute patient with progressive pathophysiology,
earlier transfer should be considered, assuming it is
possible in a practical sense.
SG: Based on this data, someone who comes to a com-
munity hospital and rules in for a non-STEMI ought
to have cardiac catheterization over the next day or so
to defi ne their anatomy, and revascularize whatever is
thought to be the culprit lesion or lesions.
PR: Assuming that you were going to transfer the
patient for that to be done, what would you use, med-
ically, to cover the patient while you’re arranging the
transfer?
DB: This decision depends on the patient. The patient
we are discussing has been pain free for 12 hours. I
think a patient like this can receive aspirin, nitrates,
and anti-coagulation; whether that’s low molecular
weight heparin or unfractionated heparin is still debat-
able, and probably not relevant. Whether the patient
should receive additional antiplatelet therapy beyond
aspirin is controversial. Some believe that anyone
with a positive troponin should receive a glycoprotein
inhibitor until such time as they undergo revascular-
ization, either in the catheterization laboratory or at
coronary artery bypass graft surgery (CABG). This
strategy is more compelling when a patient is show-
ing signs of progressive ACS or instability.
AM: If someone is having a non-STEMI, and the deci-
sion has been made for urgent cardiac catheterization,
I would place them on a glycoprotein inhibitor even
if they’ve been relatively asymptomatic for the past
nine to twelve hours. I think there’s good evidence to
indicate that these patients do better if they’re on the
glycoprotein inhibitor heading into the laboratory.
There is still debate about how long the glycoprotein
inhibitor needs to be on board prior to catheteriza-
tion, but I think they do better if it’s given when the
catheterization procedure begins.
WB: I agree. The ACS patients who are mechanically
managed (i.e., in the catheterization laboratory) likely
benefi t from glycoprotein inhibition. Other patient
groups that can benefi t are the ACS patients with
ongoing ischemia with positive biomarkers, an evolv-
ing EKG, or instability.
SG: Part of the question here is whether or not the
patient should actually have the glycoprotein inhibitor
started in the community hospital when they’re going
NON-ST SEGMENT ELEVATION MYOCARDIAL INFARCTION
21
PR: Let’s assume that this is a patient who has a nor-
mal fi rst set of biomarkers and either a normal EKG
or one with nonspecifi c changes. When would you try
to do a precatheterization laboratory stress test with
such a patient, knowing that this still is a patient who
had an ischemic coronary syndrome, perhaps a myo-
cardial infarction (MI) 2 years previously, and has
had some cardiac symptoms intermittently since?
SG: If the patient has a positive biomarker, and you’re
not going to take the patient to the catheterization
laboratory, you probably should wait about 5 days
before you put that patient back on a treadmill. Even
then, it’s controversial concerning how far you should
work the patient on the treadmill (whether you should
do a full Bruce Protocol, or some modifi cation), but I
don’t think anyone would immediately put a patient
who has positive biomarkers on a treadmill.
PR: What if the biomarkers are normal?
DB: Someone whose biomarkers are negative falls
into the moderate risk category, similar to patients
with a history of MI, a history of risk factors, and
an ischemic sounding event. At 12 hours with car-
diac markers that are negative, it’s a pretty good
bet that he or she didn’t have an MI. The decision
to obtain a stress test might depend somewhat on
what was known about the patient’s coronary artery
disease, and whether or not he or she had been hav-
ing symptoms over the past year that seemed to be
accelerating. If this was the fi rst episode since the MI,
whenever that was, it was 12 hours since the onset
of symptoms, the patient had a negative biomarker
and a nonspecifi c EKG, and continued to clinically
look well, then that’s a patient who I think benefi ts
from a stress imaging test to try to determine whether
that chest pain from yesterday was really angina or
whether it was from something else.
PR: How long is information that’s negative from
a stress test useful? For example, what if we have a
patient with a normal set of biomarkers and a normal
or nonspecifi c EKG but had an episode that sounds
clearly anginal? The patient had a stress test a year ago
that was negative. Does that make you want to repeat
the stress test, or is there a length of time during which
you feel that provides adequate negative information?
AM: Anecdotally, I would say that a negative stress
test is probably useful for about an hour. I’ve seen
an ischemic coronary syndrome who has an abnor-
mal set of biomarkers and who is pain free a number
of hours after the onset of pain. It sounds like there
is a controversy between routinely starting platelet
inhibition and waiting to have the cardiologist do so.
Where there is controversy, I think it becomes even
more important to fi nd out what the receiving cardi-
ologist wants done.
Let me ask a permutation of the question; let’s
assume now that the patient has a slight elevation
of the fi rst troponin and a normal or a nonspecifi c
abnormal EKG, but is having stuttering chest pain.
Would that alter your decision making about starting
platelet inhibition before transfer?
AM: I would still talk to the receiving cardiologist.
The practice patterns of cardiologists vary markedly,
even within a single institution, as to who likes gly-
coprotein inhibitor and who doesn’t. Even within the
group that likes the glycoprotein inhibitor, some want
eptifi batide while others want abciximab, some of
them don’t want either of these, and want clopidogrel
instead.
PR: I personally would rather start platelet inhibition
in somebody who is having stuttering symptoms than
in somebody who is pain free.
SG: Would you have used clopidogrel in this patient?
AM: This again would depend on what the spe-
cifi c cardiologist wanted. In the ED, we may not be
aggressive in using clopidogrel largely because car-
diac surgeons are highly concerned about periopera-
tive bleeding, should these patients ultimately require
operative revascularization. Nevertheless, some sur-
geons do not voice these concerns, and I would just
base my utilization of clopidogrel on the preferences
of the accepting cardiologist.
WB: With respect to clopidogrel, its use in the ACS
patient is most appropriate in those individuals who
will be managed conservatively (i.e., no percutaneous
coronary intervention [PCI]), and those persons who
will likely undergo PCI at least 6 hours beyond the
administration time of this platelet inhibitor. In other
words, clopidogrel most often benefi ts patients who
are managed medically for at least the initial phase
of their care. Using clopidogrel urgently and early in
a patient who is undergoing urgent PCI for STEMI is
likely of little benefi t.
CHAPTER 2
22
That patient will remain with a relatively high post-
test probability of cardiac ischemia. One approach
suggests that if a patient has a negative stress test, and
has another presentation with chest discomfort that is
either the same or different, one might try to use a dif-
ferent imaging modality. Such a situation is where a
coronary computed tomography angiogram (CTA) in
a younger patient with no history of coronary disease,
or adding imaging to a stress test that was previously
done without imaging, might be particularly useful.
DB: I don’t imagine that anyone would risk-stratify a
patient with known coronary disease and accelerat-
ing symptoms with just a plain treadmill stress test.
If the pretest probability is so high that the current
event represents coronary ischemia, in my institution
we would obtain a stress test with sestamibi imag-
ing. In some institutions, one might obtain a stress
echocardiogram. The patient today would not be a
candidate for a coronary CT because she has known
coronary artery disease (CAD). The CT scan is an
anatomic study that isn’t going to show whether
the known CAD seen on the scan is related to the
symptoms of this particular event. I think nonimag-
ing treadmill testing has a role in patients in whom
the pretest probability is low, and who have a normal
EKG. In that situation, we have to be careful to tell
the patients that we’re not excluding coronary artery
disease, we’re just doing a functional test to evaluate
whether walking on a treadmill provokes symptoms
or fi ndings on the EKG that suggest coronary artery
disease. If it does not, then the patient is generally safe
to be discharged, with further work-up as an outpa-
tient dictated by whoever manages the ongoing care.
Where we can run into trouble, is if we unthinkingly
and uniformly tell these patients, “You’re fi ne. Your
stress test was negative. You don’t have coronary
artery disease.” This is overstating and overestimat-
ing the ability of the test.
On the other hand, I don’t believe that someone
who has been pain free for 12 hours and has a nega-
tive set of biomarkers should automatically be taken
for cardiac catheterization, even if the presenting his-
tory is suggestive of cardiac ischemia. In this patient
today, we don’t really know what the etiology of
yesterday’s chest pain was. She has a worrisome his-
tory from an ischemic standpoint, but the markers are
negative and the EKG is unchanged or nonspecifi c in
its fi ndings. If she has a cardiac catheterization, you
people with a negative stress test and then a week,
or even 3 days, later have a STEMI. In one case,
a patient went into ventricular tachycardia (VT)
3 days after a completely negative stress test, and
then ruled in. I don’t think there’s reliable evidence
that says that if you get a stress test then you don’t
need to worry about cardiac ischemia for 3 months,
6 months, or a year. To be reasonable, you are not
going to keep stressing a patient over and over. So
generally we assume that if a patient had a negative
stress test within the past few months, and they’re
returning with the exact same symptoms that led
to the fi rst stress test, the exact intensity, radiation,
associated symptoms, then we would feel a lot more
comfortable, though perhaps still not 100%, that
the stress test is reliable. In almost all the cases where
I’ve seen patients have MIs after a recent stress test,
they experienced some change in their symptoms.
Thus, if a patient returns with a change in symp-
toms, this change, I believe, excludes the utility of
the prior stress test. Anecdotally, we’ve seen at least
a dozen cases in the past fi ve years where patients
coming back with a change in symptoms have ended
up ruling in, even though they’ve had negative stress
tests, again, anywhere from 3 days out to within the
prior 6 months.
WB: Although simple exercise stress testing is of lim-
ited value in ruling out signifi cant coronary obstruc-
tive lesions, the addition of a nuclear scan to this
testing modality markedly increases its ability to iden-
tify patients who would benefi t from a more aggres-
sive diagnostic evaluation.
PR: My personal prejudice is that stress tests only
have utility when they’re positive, and that negative
stress tests have no meaning whatsoever. A common
practice in the United States is to observe patients
overnight, perform a stress test in the morning, and
if it is negative, discharge the patient home. However,
if they have symptoms suggesting accelerating angina,
I personally wouldn’t be comfortable with anything
but a coronary angiogram.
SG: In truth, a test’s results are only as good as the
test itself. When Diamond fi rst published data in the
1970s on stress testing, it was predicated on pretest
and posttest probabilities, so that even a completely
normal stress test, in a patient with a high pretest
probability, did not rule out ischemic heart disease.
NON-ST SEGMENT ELEVATION MYOCARDIAL INFARCTION
23
that hyperglycemia may have some causal association
with increased morbidity and mortality in this form
of ischemic cardiac disease.
WB: Regarding the hyperglycemia, while it is a poten-
tial marker of a less-than-optimal outcome, extremely
tight control in the ED is not recommended. This con-
trol can be achieved during inpatient hospitalization.
AM: In terms of the hypertension, if she’s having
pain, my fi rst choice would be to go with nitrates. It
is probable that nitrates as well as pain control will
bring down the blood pressure. If she’s pain free and
still hypertensive, then I’d initially give her either her
regular blood pressure medication, or perhaps a small
dose of a beta-blocker; however, I tend to use early
beta-blockers less in ACS unless they have intractable
hypertension.
WB: Elevated blood pressures must be watched
closely. Yet, the mere presence of an elevated blood
pressure itself does not require immediate antihyper-
tensive therapy. Rather, the clinician must consider
the presence or absence of acute end-organ dysfunc-
tion among other issues; if present, antihyperten-
sive therapy is warranted. In fact, the patient with
an elevated blood pressure and no acute end-organ
malfunction should be observed. The use of antihy-
pertensive agents can cause morbidity, particularly
in the elderly patient with long-term blood pressure
elevations and less ability to auto-regulate organ per-
fusion. The use of beta-blockers in suspected ACS
patients early in their course is now in question.
Earlier research had suggested that the MI patient
demonstrates benefi t when beta-blockers are given
early in their course resulting in smaller infarctions,
improved ejection fractions, and fewer acute cardio-
vascular complications (particularly malignant ven-
tricular dysrhythmias). In the contemporary setting,
we have many more options to offer the ACS patient,
including antiplatelet and anticoagulant therapies, as
well as more aggressive revascularization tools. More
recent research indicates that certain ACS patients
may not benefi t from early, intravenous beta-blocker
administration. In fact, certain patients experience
higher rates of symptomatic bradycardia, hypoten-
sion, and pulmonary congestion while only demon-
strating a marginal benefi t in reduced occurrence of
primary ventricular fi brillation. Thus, widespread use
of beta-blockers in the suspected ACS patient early
will fi nd CAD, of course, because we already know
she has it; however, you will not know whether, in
someone who has been pain free for 12 hours and has
a negative set of biomarkers, that it is this disease that
is causing her symptoms. I would favor a treadmill
test with imaging to see whether symptoms and perfu-
sion correlate with each other on the treadmill. If they
do, then proceed with an angiogram.
SG: Thus, the stress test would be particularly use-
ful if there were multiple lesions found on diagnostic
catheterization.
PR: Let me change directions for a minute to manage-
ment of two of her other medical problems. It sounds
like she was not being well controlled in terms of her
hypertension. I did not hear what antihypertensive
medication she was taking but, clearly, her blood
pressure was not in a desirable range during this visit.
What would you do in terms of management of her
hypertension in terms of hoping to end her coronary
ischemia? Secondly, how would you manage her dia-
betes during this phase? Many of these patients are
type II diabetics. There’s been some argument in the
literature about whether it’s safe to continue manag-
ing them as a type II, or whether they should be placed
on insulin while they’re having their acute ischemic
coronary syndrome.
AM: In terms of the hyperglycemia, let’s assume that
she was hyperglycemic from the start. Hyperglycemia
at the time of admission or poorly controlled hyper-
glycemia during the in-hospital stay is associated
with a marked increase in hospital mortality and
short-term mortality and morbidity. No one has defi -
nitely shown that hyperglycemia per se is causing the
morbidity; it may just be an association rather than
causal, but more and more of these studies are sug-
gesting that tight glucose control can improve mor-
bidity and mortality. I would be inclined to use insulin
in a patient who is hyperglycemic in the ED with an
acute coronary syndrome. The parameter that they
defi ne in these studies for hyperglycemia is a glucose
level of about 140 mg/dl—fairly tight glucose control.
I would make an effort to control the glucose level
early on, and expect that the admitting physicians
will use insulin as well to get improved glucose con-
trol. Of note, hyperglycemia has been associated with
worse outcomes in sepsis, stroke, and postcardiac
arrest syndrome, so I think it’s reasonable to assume
CHAPTER 2
24
or exclude a diagnosis. The clinician must under-
stand its limitations and make treatment decisions
accordingly.
Section III: Concepts
Background
Chest pain accounts for 6 to 8 million ED visits in
the United States each year,
1,2
and is the second most
common presenting complaint accounting for 5% of
all ED visits.
2,3
Approximately two-thirds of these
patients are felt to have a presentation consistent with
an acute coronary syndrome, and are admitted to the
hospital, but only one-half of these admitted patients
(one-third of all who present) receive a discharge
diagnosis of unstable coronary artery disease.
2,4,5
This
diagnostic discrepancy amounts to an annual esti-
mated cost of 6 billion dollars for false-positive admis-
sions.
2
However, approximately 2–8% of patients
who present to the ED with an ACS are inadvertently
or incorrectly sent home.
2,6–8
Factors associated with
such discharges include younger age, female gender,
non-Caucasian ethnicity, atypical symptoms, lack of
a prior coronary history, and nonspecifi c EKG fi nd-
ings. Furthermore, these patients have signifi cant
short-term morbidity and mortality that is equivalent
to or higher than those patients with an ACS who are
admitted.
7,8
Given the highly effective short- and long-
term therapies for unstable coronary artery disease,
the tremendous costs associated with inappropriate
hospital admissions, and the increased morbidity and
mortality associated with a missed diagnosis, acute
coronary syndromes remain a diffi cult problem to
effi ciently triage, diagnose, and treat.
The presenting symptoms of an ACS are well
known, and have been extensively studied in both
prospective and retrospective analyses. Chest pain is
the prototypical chief complaint, but up to 25% of
patients present atypically without signifi cant chest
discomfort.
3,9
Studies of patients presenting with
nontraumatic chest pain suggestive of an ACS fi nd
that such descriptive terms as “burning” and “indi-
gestion” are equally as predictive as the terms “pres-
sure” and “suffocating,” while the terms “sharp” and
“stabbing” or pain that is positional, reproducible,
or pleuritic make an ACS signifi cantly less likely.
4,10,11
New chest pain that is exertional, or radiates to one
or both arms, is a helpful predictor of an unstable
in their care should be reconsidered. These patients
can receive oral beta-blockers within the initial
24 hours of hospitalization; this “delayed” manage-
ment still provides physiologic benefi t, and meets
regulatory requirement to the appropriate ACS can-
didate as well.
SG: Any patient whose chest examination has rales
or rhonchi, and on chest X-ray study there is mild
pulmonary congestion, should not receive a beta-
blocker in the ED, and should probably not receive a
beta-blocker until they no longer have any evidence of
congestive heart failure. However, if one excludes all
diabetics from beta blockade, one would preclude a
very large segment of the coronary artery disease pop-
ulation from receiving beta-blockers that, as therapy
for cardiac ischemia, has a well established benefi t in
mortality reduction.
AM: The traditional relative contraindication for
beta-blockers and diabetes is that diabetics usu-
ally recognize that they are becoming hypoglycemic
because they get a catecholamine surge, and then
develop symptoms such as diaphoresis, or lighthead-
edness. If they are taking a beta-blocker, they may not
get this surge, and therefore may not feel themselves
becoming hypoglycemic. It has also been suggested
that the beta blockade has a direct lowering effect on
the blood sugar.
SG: As beta-blockers remain one of the few agents
that truly have long-term mortality benefi t, it may be
worth the risk of hypoglycemia to obtain their protec-
tion. Close monitoring of the blood glucose levels may
enable one to obtain the benefi ts of the beta-blockers
without the negative effects of hypoglycemia.
WB: The EKG must also be discussed in this case.
As seen in our patient today, the EKG can be normal
or minimally abnormal in the setting of an ACS pre-
sentation. In a simple majority of acute myocardial
infarction patients, the EKG will be diagnostically
abnormal at presentation, with obvious ST-segment
changes and T wave abnormalities. In the remain-
der of patients, the presenting EKG can be nonspe-
cifi cally abnormal or even normal. Also, patients can
demonstrate confounding EKG patterns such as left
bundle branch block, left ventricular hypertrophy, or
a ventricular paced rhythm. Thus, while the EKG is a
powerful tool used in the chest pain patient suspected
of ACS, it cannot be relied upon solely to include