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Background

Acute coronary syndrome (ACS) refers to a spectrum of clinical presentations ranging from
those for ST-segment elevation myocardial infarction (STEMI) to presentations found in non
ST-segment elevation myocardial infarction (STEMI) or in unsta!le angina" In terms of
pathology# ACS is almost al$ays associated $ith rupture of an atherosclerotic pla%ue and partial
or complete throm!osis of the infarct-related artery" (See Etiology")
In some instances# ho$ever# sta!le coronary artery disease (CA&) may result in ACS in the
a!sence of pla%ue rupture and throm!osis# $hen physiologic stress (eg# trauma# !lood loss#
anemia# infection# tachyarrhythmia) increases demands on the heart" The diagnosis of acute
myocardial infarction in this setting re%uires a finding of the typical rise and fall of !iochemical
mar'ers of myocardial necrosis in addition to at least ( of the follo$ing
)(*
(See +or'up"),
Ischemic symptoms
&evelopment of pathologic - $aves
Ischemic ST-segment changes on electrocardiogram (EC.) or in the setting of a coronary
intervention
The terms transmural and nontransmural (su!endocardial) myocardial infarction are no longer
used !ecause EC. findings in patients $ith this condition are not closely correlated $ith
pathologic changes in the myocardium" Therefore# a transmural infarct may occur in the a!sence
of - $aves on EC.s# and many --$ave myocardial infarctions may !e su!endocardial# as noted
on pathologic e/amination" 0ecause elevation of the ST segment during ACS is correlated $ith
coronary occlusion and !ecause it affects the choice of therapy (urgent reperfusion therapy)#
ACS-related myocardial infarction should !e designated STEMI or STEMI" (See +or'up")
Attention to the underlying mechanisms of ischemia is important $hen managing ACS" A simple
predictor of demand is rate-pressure product# $hich can !e lo$ered !y !eta !loc'ers (eg#
metoprolol or atenolol) and pain1stress relievers (eg# morphine)# $hile supply may !e improved
!y o/ygen# ade%uate hematocrit# !lood thinners (eg# heparin# II!1IIIa agents such as a!ci/ima!#
eptifi!atide# tirofi!an# or throm!olytics)# and1or vasodilators (eg# nitrates# amlodipine)" (See
Medications")
In 23(3# the American 4eart Association (A4A) pu!lished ne$ guideline recommendations for
the diagnosis and treatment of ACS"
)2*
Etiology
Acute coronary syndrome (ACS) is caused primarily !y atherosclerosis" Most cases of ACS
occur from disruption of a previously nonsevere lesion (an atherosclerotic lesion that $as
previously hemodynamically insignificant yet vulnera!le to rupture)" The vulnera!le pla%ue is
typified !y a large lipid pool# numerous inflammatory cells# and a thin# fi!rous cap"
Elevated demand can produce ACS in the presence of a high-grade fi/ed coronary o!struction#
due to increased myocardial o/ygen and nutrition re%uirements# such as those resulting from
e/ertion# emotional stress# or physiologic stress (eg# from dehydration# !lood loss# hypotension#
infection# thyroto/icosis# or surgery)"
ACS $ithout elevation in demand re%uires a ne$ impairment in supply# typically due to
throm!osis and1or pla%ue hemorrhage"
The ma5or trigger for coronary throm!osis is considered to !e pla%ue rupture caused !y the
dissolution of the fi!rous cap# the dissolution itself !eing the result of the release of
metalloproteinases (collagenases) from activated inflammatory cells" This event is follo$ed !y
platelet activation and aggregation# activation of the coagulation path$ay# and vasoconstriction"
This process culminates in coronary intraluminal throm!osis and varia!le degrees of vascular
occlusion" &istal em!oli6ation may occur" The severity and duration of coronary arterial
o!struction# the volume of myocardium affected# the level of demand on the heart# and the a!ility
of the rest of the heart to compensate are ma5or determinants of a patient7s clinical presentation
and outcome" (Anemia and hypo/emia can precipitate myocardial ischemia in the a!sence of
severe reduction in coronary artery !lood flo$")
A syndrome consisting of chest pain# ischemic ST-segment and T-$ave changes# elevated levels
of !iomar'ers of myocyte in5ury# and transient left ventricular apical !allooning (ta'otsu!o
syndrome) has !een sho$n to occur in the a!sence of clinical CA&# after emotional or physical
stress" The etiology of this syndrome is not $ell understood !ut is thought to relate to a surge of
catechol stress hormones and1or high sensitivity to those hormones"
Patient Education
8atient education of ris' factors is important# !ut more attention is needed regarding delays in
door-to-!alloon time# and one ma5or !arrier to improving this delay is patient education
regarding his or her symptoms" 9ac' of recognition of symptoms may cause tremendous delays
in see'ing medical attention"
Educate patients a!out the dangers of cigarette smo'ing# a ma5or ris' factor for coronary artery
disease (CA&)" The ris' of recurrent coronary events decreases :3; at ( year after smo'ing
cessation" 8rovide all patients $ho smo'e $ith guidance# education# and support to avoid
smo'ing" Smo'ing-cessation classes should !e offered to help patients avoid smo'ing after a
myocardial infarction" 0upropion increases the li'elihood of successful smo'ing cessation"
&iet plays an important role in the development of CA&" Therefore# prior to hospital discharge# a
patient $ho has had a myocardial infarction should !e evaluated !y a dietitian" 8atients should !e
informed a!out the !enefits of a lo$-cholesterol# lo$-salt diet" In addition# educate patients a!out
A4A dietary guidelines regarding a lo$-fat# lo$-cholesterol diet"
A cardiac reha!ilitation program after discharge may reinforce education and enhance
compliance"
The follo$ing mnemonic may useful in educating patients $ith CA& regarding treatments and
lifestyle changes necessitated !y their condition,
A < Aspirin and antianginals
0 < 0eta !loc'ers and !lood pressure (08)
C < Cholesterol and cigarettes
& < &iet and dia!etes
E < E/ercise and education
=or patients !eing discharged home# emphasi6e the follo$ing,
Timely follo$-up $ith primary care provider
Compliance $ith discharge medications# specifically aspirin and other medications used
to control symptoms
eed to return to the E& for any change in fre%uency or severity of symptoms
Diagnostic Considerations
As many as half of all cases of ACS are clinically silent in that they do not cause the classic
symptoms of this syndrome" Conse%uently# ACS goes unrecogni6ed !y the patient" Maintain a
high inde/ of suspicion for ACS# especially $hen evaluating $omen# patients $ith dia!etes#
older patients# patients $ith dementia# and those $ith a history of heart failure"
Although ST-segment and T-$ave changes are associated $ith CA&# alternative causes of these
findings are left ventricular aneurysm# pericarditis# 8rin6metal angina# early repolari6ation#
+olff-8ar'inson-+hite syndrome# and drug therapy (eg# $ith tricyclic antidepressants#
phenothia6ines)"
Increasing pu!lic a$areness of the typical and atypical presentations of ACS is of the utmost
importance for optimal and timely treatment" Many patients do not recogni6e that their
symptoms are cardiac in origin and therefore may delay see'ing medical help" .uidelines from
the European Society of Cardiology (ESC)1American College of Cardiology (ACC)1American
4eart Association (A4A) recommend that patients $ith esta!lished CA& call emergency
medical services if they have chest pain that does not resolve after they ta'e a su!lingual
nitroglycerin ta!let"
Differentials
An/iety
Aortic Stenosis
Asthma
Cardiomyopathy# &ilated
Esophagitis
.astroenteritis
4ypertensive Emergencies in Emergency Medicine
Myocardial Infarction
Myocarditis
8ericarditis and Cardiac Tamponade