ACUTE CORONARY

SYNDROMES:
Acute MI and Unstable Angina

Tintinalli Chapter 50
September 20, 2005
 Acute Coronary Syndrome
(ACS)
 Ischemic heart disease accounts for
500,000 deaths annually in the U.S.
 CAD and myocardial ischemia contribute
to > 5 million ER visits yearly for chest
pain
 15% of pts with chest pain will have
acute MI and 25-30% will have unstable
angina
ACS
 a term used to describe pts with acute CP
and other symptoms of myocardial
ischemia
 During the initial exam, often not possible to
determine whether permanent damage to
the myocardium has occurred
– Only in retrospect after serial ECGs or cardiac
markers can the distinction b/w AMI or UA be
made
Pathophysiology
 ACS is caused by secondary reduction
in myocardial blood flow due to
– coronary arterial spasm
– disruption of atherosclerotic plaques
– platelet aggregation or thrombus formation
at site of atherosclerotic lesion
Thrombus formation
 Atherosclerotic plaque formation occurs
through repetitive injury to vessel wall
 When plaque ruptures, potent
thrombogenic substances are exposed to
platelets
 These platelets respond by adhesion,
activation, and aggregation thus initiating
thrombus formation in the coronary vessels
 The extent of O2 deprivation and thus
clinical presentation of ACS depend on
the limitation of O2 delivery by thrombus
adhering to fixed, fissured, or eroded
plaques
Stable Angina
 Ischemia occurs only when activity
induces O2 demands beyond the supply
restrictions imposed by a partially
occluded coronary vessel
 occurs at a relatively fixed and predictable
point and changes slowly over time
 atherosclerotic plaque has not ruptured
thus there is little superimposed thrombus
ACS
 Atherosclerotic plaque rupture and
platelet-rich thrombus develop
 Degree and duration of O2 supply-
demand mismatch determines whether
reversible myocardial ischemia w/o
necrosis (unstable angina) or
myocardial ischemia w/ necrosis
(myocardial infarction)
Clinical Features
 Main symptom of ischemic heart
disease is chest pain
– need to characterize its severity, location,
radiation, duration, and quality
– ask about associated symptoms: N/V,
diaphoresis, dyspnea, lightheadedness,
syncope, palpitations
 Reproducible chest wall tenderness is
not uncommon
 Patients with ACS may complain of easy
fatigability
 Usually an AMI is accompanied by more
prolonged and severe chest discomfort
and more prominent associated
symptoms
Angina Pectoris
 Exercise, stress, or cold environment
classically precipitates angina
 duration of symptoms typically < 10
minutes, occasionally lasting up to 20
minutes
 usually improves within 2-5 minutes
after rest or nitroglycerin
ACS
 Up to 30% of patients with AMI are
clinically unrecognized
– Some of these patients have had atypical
symptoms for which they didn’t pursue
medical advice
– Worse prognosis for pts who have atypical
symptoms at the time of their infarction
– women and elderly most likely to have
atypical symptoms
Cardiac Risk Factors
 Age over 40  High cholesterol
 male  truncal obesity
 postmenopausal  sedentary lifestyle
females  diabetes
 family history  previous cardiac hx
 cigarette smoking
 hypertension
Cardiac Risk Factors
 Risk factors are modestly predictive of
CAD is asymptomatic patients
 In the ER, risk factors are poor predictors
of cardiac risk for MI or other ACS
– In males, only DM and family history are
weakly predictive
– Cardiac risk factors are not predictive of ACS
in female ER chest pain pts
Physical Examination
 Not helpful in distinguishing pts with
ACS from those with non cardiac
etiologies
 Pts may appear deceptively will without
distress or be uncomfortable, pale,
cyanotic, and in respiratory distress.
Vital Signs
 Bradycardic rhythms are more common
with inferior wall MI
– in the setting of anterior wall MI,
bradycardia or heart block is very poor
prognostic sign
 Extremes of blood pressures are
associated with worse prognosis
Heart Sounds
 S1 and S2 are often diminished due to poor
myocardial contractility
 S3 is present in 15-20% of pts with AMI
– implies a failing myocardium
 S4 is common in pts with long standing HTN or
myocardial dysfunction
 Presence of new systolic murmur is an ominous sign
– signifies papillary m. dysfunction, flail leaflet of mitral
valve, or VSD
ECG
 12 lead is single best test to identify pts
with AMI upon presentation to ER
 Current guidelines state that the initial 12
lead ECG must be obtained and
interpreted within 10 minutes of patient
presentation
 Yet ECG has a relatively low sensitivity
for detection of AMI
ECG
 ST segment is elevated on the initial
ECG in approximately 50% of pts with
AMI
– most other AMI pts will have ST depression
and/or T wave inversions
 Only 1-5% of pts with AMI have an
entirely normal initial ECG
ECG criteria and AMI
 Anteroseptal -->  QS deflections in V1-
V3, possibly V4
 Anterior -->
 rS defection in V1, Q
waves V2-4 or decr
in amplitude of initial
R wave in V1-V4

 anterolateral -->  Q waves in V4-6, I,

aVL
ECG Criteria and AMI
 Lateral -->  Q waves in I, aVL
 inferior -->  Q waves II, III, aVF
 inferolateral -->  Q waves II, III, aVF,
and V5-V6
 true posterior -->
 Initial R waves in V1-
V2 >0,04s and R/S
ratio > 1
 Q waves II, III, aVF &
 right ventricular --> ST elevation rV4
ECG
 In distributions previously described:
– ST elevation suggests acute transmural injury
– ST depression suggests subendocardial
ischemia
 All inferior wall MI should have right sided
ECG
– ST elevation in rV4 indicates right ventricular
infarction
ECG
 Reciprocal ST segment changes
predict:
– a larger infarct distribution
– an increased severity of underlying CAD
– more severe pump failure
– a higher likelihood of cardiovascular
complications
– increased mortality
Difficult ECG interpretations
 ST elevation in absence of AMI
– early repolarization
– LVH
– pericarditis/myocarditis
– Left ventricular aneurysm
– Hypertropic cardiomyopathy
– hypothermia
– ventricular paced rhythms
– LBBB
Difficult ECG interpretations
 ST depression in absence of ischemia
– hypokalemia
– digoxin effect
– cor pulmonale and right heart strain
– early repolarization
– LVH
– ventricular paced rhythms
– LBBB
Difficult ECG interpretations
 T wave inversions without ischemia
– persistent juvenile pattern
– seizures or Stokes Adams syncope
– post-tachycardia T wave inversion
– post-pacemaker T wave inversion
– Intracranial pathology (CNS hemorrhage)
– Mitral valve prolapse
– pericarditis
– primary or secondary myocardial disease
 T wave inversion without ischemia
– PE or cor pulmonale
– spontaneous PTX
– myocardial contusion
– LVH
– ventricular paced rhythms
– RBBB
– LBBB
AMI and LBBB
 In the setting of LBBB, the following are
indicative of AMI
– 1. ST elevation 1mm or greater and
concordant with the QRS complex
– 2. ST depression 1mm or more in leads
V1, V2, or V3
– 3. ST elevation 5mm or greater and
discordant with the QRS complex
Cardiac Enzymes
 Serial measurements are more
sensitive and accurate than initial single
measurement
 serum markers have less utility in the
diagnosis of UA, only about 50% will
have elevated troponins
CK-MB
 Most commonly used marker in ACS
 a serial rise to above 5 times baseline followed
by fall back to baseline is considered diagnostic
for AMI
 peaks at 12-24 hours, with fall back to baseline
in 2-3 days
 useful in detecting recurrent infarction after the
initial 24-48 hours by noting a repeat elevation
in the level
Conditions Associated
with Elevated CK-MB
 Unstable angina  Cardiac surgery
 acute coronary ischemia  skeletal m. trauma
 inflammatory heart  dermatomyositis,
disease polymyositis
 cardiomyopathies
 myopathic disorders
 circulatory failure &
 muscular dystrophy
shock  vigorous exercise
 DTs  malignant hyperthermia
 Rhabdomyolysis
 Ethanol poisoning
(chronic)
Troponin
 Main regulatory protein for the actin-myosin
myofibrils
 3 subunits:
– inhibitory subunit (Trop I)
– tropomyosin binding subunit (Trop T)
– calcium binding subunit (Trop C)
 Trop I has not been identified in skeletal m.
during any stage of develop therefore specific to
myocardium
Troponin
 Peak level in 12 hours
 prolonged elevation for 7 to 10 days before
returning to baseline
– thus making trop of no use in detecting recurrent
infarctions during this time
 Rise in serum Trop I or T is considered diagnostic
for AMI
 Low level elevations in Trop correlate with risk for
CV complications in UA, CAD, and renal failure
Myoglobin
 Rises within 2-3 hours of symptoms
onset
 peaks within 4 to 24 hours
 more sensitive than CK and CK-MB but
not specific for cardiac muscle
 there is a high false-positive rate due to
its presence in all muscle tissue
Complications of MI
 1. Dysrhythmias and conduction
disturbances
 2. Cardiac failure
 3. Mechanical complications
 4. Pericarditis
 5. Right Ventricular Infarction
 6. Other
Dysrhythmias
 Occurs in 72-100% of AMI pts treated in
coronary care unit
 PVCs are common in AMI
– occur in >90% of AMI patients
 Atrial premature contractions are also
common
– occur in up to 50% of AMI patients
– not associated with increased mortality
Dysrhythmias
 Early in AMI, pts often show increased
autonomic nervous system activity
– sinus brady, AV block, hypotension occur
from increased vagal tone
 Later, increased sympathetic activity results
in incr catecholamine release
– thus creates electrical instability: PVCs, Vtach,
Vfib, accelerated idioventricular rhythms, AV
junctional tachycardia
Dysrhythmias
 Hemodynamic consequences of
dysrhythmias are dependent on
ventricular function
– Normal hearts have a loss of 10-20% of left
ventricular output when atrial kick is
eliminated
– Reduced left ventricular compliance can
result in 35% reduction in stroke volume when
the atrial systole is eliminated
Dysrhythmias
 Persistant tachycardia is associated with
poor prognosis
– due increase myocardial oxygen use
 When Vtach occurs late in AMI course,
usually associated with transmural
infarct and left ventricular dysfunction
– induces hemodynamic deterioration
– mortality rate approaches 50%
Conduction Disturbances
 First degree and Mobitz I (Wenckebach)
– more common with inferior AMI
– intermittent during the first 72 hrs after infarction
– rarely progresses to complete block or
pathologic rhythm
 Mobitz II
– usually associated with anterior AMI
– does progress to complete heart block
Conduction Disturbances
 Complete Heart Block
– occurs in setting of inferior MI
– usually progresses from less AV blocks
– this form is usually stable & should resolve
– Mortality is 15% in absence of RV involvement
& increases to 30% when RV is affected
 Complete block in setting of anterior MI
results in grave prognosis
Conduction Disturbance
 New RBBB
– occurs in approximately 2% of AMI pts
– associated with anteroseptal AMI
– associated with increased mortality
because often leads to complete AV block
Conduction Disturbance
 New LBBB
– occurs in 5% of pts with AMI
– associated with high mortality
– Left posterior hemiblock associated with
higher mortality than isolated anterior
hemiblock
• represents larger area of infarction
Cardiac Failure
 15-20% of AMI pts present in some
degree of CHF
 More severe the degree of left ventricular
dysfunction, the higher the mortality
– dependent on the net effect of prior
myocardial dysfunction, baseline myocardial
hypertrophy, acute myocardial necrosis, &
acute reversible dysfunction (“stunned
myocardium”)
Cardiac Failure
 B-type natriuretic peptide
– useful for risk stratification of pts with non
ST elevation MI and UA
– elevated levels of BNP early in the hospital
course predict a worse outcome at 30 days
Mechanical Complications
of AMI
 Sudden decompensation of previously
stable AMI pt should raise concern of the
“mechanical” complication
 Free wall rupture
– occurs in 10% of AMI fatalities, usually 1 to 5
days after infarction
– rupture of LV free wall usually leads to
pericardial tamponade and death (>90% of
cases)
Mechanical Complications
of AMI
 NSAIDs, steroids, and late
administration of thrombolytics have
been linked to an increased likelihood of
cardiac rupture
– however, studies remain contradictory

 LV hypertrophy appears to be protective

Mechanical Complications
of AMI
 Rupture of interventricular septum
– is more often detected clinically than
ventricular wall rupture
– pts have chest pain, dyspnea, sudden
appearance of new holosystolic murmur
• murmur often associated with palpable thrill and
best heard at lower left sternal border
– more common in pts with anterior wall MI
and pts with extensive (3 vessel) CAD
Mechanical Complications
of AMI
 Papillary Muscle Rupture
– occurs in 1% of pts with AMI
– more common with inferior wall MI
– usually occurs 3 to 5 days after AMI
– occurs with a small to modest sized MI
– posteromedial m. commonly ruptured
• receives blood from only one coronary a.
– present with acute dyspnea, increasing CHF, and new
holosystolic murmur consistent with mitral
regurgitation
Pericarditis
 Occurs in 10-20% of post-AMI pts
 more common with transmural MI
 usually occurs 2-4 days after AMI
 Pericardial friction rubs detected more
often with inferior wall and right ventricular
infarcts
 Pericardial effusions may also be present;
may take months to resorb
 Dressler Syndrome
– post AMI syndrome
– occurs 2 to 10 weeks after AMI
– pts presents with chest pain, fever, and
pleuropericarditis
Right Ventricular Infarction
 Usually seen as a complication of an
inferior infarction
– approximately 30% of inferior wall MI
involve the RV
 Presence of RV infarction is associated
with significant increase in mortality and
cardiovascular complications
Other Complications
 Left ventricular thrombus formation
 arterial embolization
 venous thrombus
 pulmonary embolism
 postinfarction angina
 infarct extension
– **these are diagnoses to think about when a pt
presents to the ER after recent discharge from the
hospital
Postprocedure Chest Pain
 Pts who present with symptoms of ACS
shortly after angioplasty or stent placement
should be assumed to have abrupt vessel
closure
 Subacute thrombotic occlusion after stent
placement occurs in approximately 4% of
pts 2 to 14 days after procedure
– this less common than closure after angioplasty
 Pts with chest pain syndromes after
CABG
– may have abrupt vessel closure
– symptoms of recurrent ischemia can be
confused with post-AMI pericarditis
Disposition
 All patients with acute chest pain need
to be evaluated for the possibility of
ACS
– pts are admitted to appropriate level of
care depending on their risks
 Results of prior cardiac catheterization
are very useful for risk stratification
Cardiac Cath Results
– pts with previously documented minimal stenosis
(<25%) or normal coronary arteriograms have
excellent long-term prognosis
• more than 90% of these pts are free from MI 10
yrs later
– a recent cardiac cath (within last 2 yrs) with
normal or minimally diseased vessels almost
eliminates the possibility of ACS due to
atherosclerosis
• doesn’t eliminate vasospasm or small vessel dz
Stress Tests Results
 When pts complete all stages of the
stess protocol, have no ECG changes
and normal imaging studies, exercise
testing can r/o acute ischemic
syndromes with sensitivities b/w 80-
90%
 If all criteria are not met, stress test
have poor sensitivity
QUESTIONS?
 1. Which of the following is false about
new RBBB?
– a. Occurs in 2% of AMI pts
– b. Occurs most commonly with inferior
wall MI
– c. Often leads to complete AV block
– d. Associated with increased mortality
QUESTIONS?
 2. True or False: Inferior wall MI can
result from occlusion of left circumflex a.
or RCA

 3. True or False: Left ventricular free

wall rupture occurs in 10% of AMI
fatalities usually 3-4 weeks after initial
infarct
QUESTIONS?
 4. True or False: B type natriuretic
peptide has a high specificity in
diagnosing CHF

 5. True or False: Reproducible chest

wall pain rules out ACS.

 Answers: B, true, false, false, false

References
 Tintinalli, J. “Emergency Medicine: A
Comprehensive Study Guide.” 6th edition.
pg. 343-351.
 Ma, O.J. and David Cline. “Emergency
Medicine: Just the facts.” 2nd edition. pg.
91-97.
 Rivers, C. “Preparing for the Written Board
Exam in Emergency Medicine.” 4th edition.
pg. 60-76.