ACUTE CORONARY SYNDROMES: Acute MI and Unstable Angina

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ACUTE CORONARY SYNDROMES Acute MI and Unstable
Angina

• Tintinalli Chapter 50
• September 20, 2005

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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

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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

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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

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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

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• 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

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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

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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)

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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

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• 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

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Angina Pectoris

• Exercise, stress, or cold environment classically
  precipitates angina
• duration of symptoms typically occasionally lasting up to 20 minutes
• usually improves within 2-5 minutes after rest or
  nitroglycerin

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ACS

• Up to 30 of patients with AMI are clinically
  unrecognized
• Some of these patients have had atypical symptoms
  for which they didnt 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

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Cardiac Risk Factors

• Age over 40
• male
• postmenopausal females
• family history
• cigarette smoking
• hypertension

• High cholesterol
• truncal obesity
• sedentary lifestyle
• diabetes
• previous cardiac hx

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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

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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.

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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

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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

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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

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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

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ECG criteria and AMI

• Anteroseptal --
• Anterior --
• anterolateral --

• QS deflections in V1-V3, possibly V4
• rS defection in V1, Q waves V2-4 or decr in
  amplitude of initial R wave in V1-V4
• Q waves in V4-6, I, aVL

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ECG Criteria and AMI

• Lateral --
• inferior --
• inferolateral --
• true posterior --
• right ventricular --

• Q waves in I, aVL
• Q waves II, III, aVF
• Q waves II, III, aVF, and V5-V6
• Initial R waves in V1-V2 0,04s and R/S ratio 1
• Q waves II, III, aVF ST elevation rV4

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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

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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

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Difficult ECG interpretations

• ST elevation in absence of AMI
• early repolarization
• LVH
• pericarditis/myocarditis
• Left ventricular aneurysm
• Hypertropic cardiomyopathy
• hypothermia
• ventricular paced rhythms
• LBBB

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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

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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

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• T wave inversion without ischemia
• PE or cor pulmonale
• spontaneous PTX
• myocardial contusion
• LVH
• ventricular paced rhythms
• RBBB
• LBBB

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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

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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

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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

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Conditions Associated with Elevated CK-MB

• Unstable angina
• acute coronary ischemia
• inflammatory heart disease
• cardiomyopathies
• circulatory failure shock
• DTs
• Rhabdomyolysis

• Cardiac surgery
• skeletal m. trauma
• dermatomyositis, polymyositis
• myopathic disorders
• muscular dystrophy
• vigorous exercise
• malignant hyperthermia
• Ethanol poisoning (chronic)

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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

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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

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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

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Complications of MI

• 1. Dysrhythmias and conduction disturbances
• 2. Cardiac failure
• 3. Mechanical complications
• 4. Pericarditis
• 5. Right Ventricular Infarction
• 6. Other

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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

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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

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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

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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

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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

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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

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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

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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

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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)

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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

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Mechanical Complicationsof 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)

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Mechanical Complicationsof 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

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Mechanical Complicationsof 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

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Mechanical Complicationsof 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

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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

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• Dressler Syndrome
• post AMI syndrome
• occurs 2 to 10 weeks after AMI
• pts presents with chest pain, fever, and
  pleuropericarditis

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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

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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

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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

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• Pts with chest pain syndromes after CABG
• may have abrupt vessel closure
• symptoms of recurrent ischemia can be confused
  with post-AMI pericarditis

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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

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Cardiac Cath Results

• pts with previously documented minimal stenosis
  (
  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
• doesnt eliminate vasospasm or small vessel dz

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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

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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

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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

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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

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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.