Acute Myocardial Infarction

1. Myocardial InfarctionMyocardial Infarction

3. Definitions
• Acute coronary syndrome is defined as
myocardial ischemia due to myocardial
infarction (NSTEMI or STEMI) or unstable
angina
• Unstable angina is defined as angina at rest,
new onset exertional angina (<2 months),
recent acceleration of angina (<2 months),
or post revascularization angina

4. Sponsored
Medical Lecture Notes – All Subjects
USMLE Exam (America) – Practice

6. ACS-STEMIACS-STEMI
ACUTE CORONARY SYNDROMES
No ST elevation ST elevation
Unstable
angina
NSTEMI STEMIStable
angina

8. BackgroundBackground
Myocardial Infarction if the rapidMyocardial Infarction if the rapid
development of myocardial necrosis by adevelopment of myocardial necrosis by a
critical imbalance between oxygen supplycritical imbalance between oxygen supply
and demand to the myocardiumand demand to the myocardium

9. ClassificationClassification
Anatomic or morphologicAnatomic or morphologic
Transmural= Full thicknessTransmural= Full thickness
Non-transmural= Partial thicknessNon-transmural= Partial thickness
ECGECG
Q wave MIQ wave MI
Non Q wave MINon Q wave MI
Does not distinguish transmural from a non-Does not distinguish transmural from a non-
transmural MI as determined by pathologytransmural MI as determined by pathology

10. Diagnosis
• Dx of acute coronary syndrome is based on
history, physical exam, ECG, cardiac enzymes
• Patients can then be divided into several groups
– Non-cardiac chest pain (i.e., Gastrointestinal,
musculoskeletal, pulmonary embolus)
– Stable angina
– Unstable angina
– Myocardial infarction (STEMI or NSTEMI)
– Other cardiac causes of chest pain (i.e., aortic
dissection, pericarditis)

11. HistoryHistory
Chest Pain- anterior precordium tightnessChest Pain- anterior precordium tightness
Pain may radiate to jaw, neck andPain may radiate to jaw, neck and
epigastriumepigastrium
Dyspnea- angina equivalent, poor LVDyspnea- angina equivalent, poor LV
functionfunction
Nausea/abdominal pain with posterior MINausea/abdominal pain with posterior MI
AnxietyAnxiety

13. Differential Diagnosis of
Chest Pain
Cardiac
Ischemic
 Angina
 Unstable angina
 AMI
Non-ischemic
Pericarditis
Aortic dissection
Valvular
Myositis

14. Differential Diagnosis of
Chest Pain
Non-cardiac
Gastroesophageal Causes
 GERD
 Esophageal spasm
 PUD
 Boerhaave’s Syndrome
 Cholecystitis

15. Differential Diagnosis of
Chest Pain
Non-cardiac
Non-gastroesophageal
 Pneumothorax
 Pulmonary embolism
 Musculoskeletal
 Somatoform disorders

16. Chest Pain-Diagnosis
History and Physical
ECG
Cardiac serum markers

17. HistoryHistory
Nausea with and without vomitingNausea with and without vomiting
Diaphoresis or sweatingDiaphoresis or sweating
Syncope or near syncopeSyncope or near syncope
Elderly present with MS changes, fatigue,Elderly present with MS changes, fatigue,
syncope or weaknesssyncope or weakness
As many as half of MI are clinically silentAs many as half of MI are clinically silent

18. PhysicalPhysical
The physical exam can often beThe physical exam can often be
unremarkableunremarkable
HypertensionHypertension
HypotensionHypotension
Acute valvular dysfunction may be presentAcute valvular dysfunction may be present
RalesRales
Neck vein distentionNeck vein distention

19. PhysicalPhysical
Third heart sound may be presentThird heart sound may be present
A fourth heart sound poor LV complianceA fourth heart sound poor LV compliance
DysrhythmiasDysrhythmias
Low grade feverLow grade fever

20. CausesCauses
Most frequent cause is rupture of anMost frequent cause is rupture of an
atherosclerotic lesion within coronary wallatherosclerotic lesion within coronary wall
with subsequent spasm and thrombuswith subsequent spasm and thrombus
formationformation
Coronary artery vasospasmCoronary artery vasospasm
Ventricular hypertrophyVentricular hypertrophy
HypoxiaHypoxia
Coronary artery emboliCoronary artery emboli

21. CausesCauses
CocaineCocaine
ArteriesArteries
Coronary anomaliesCoronary anomalies
Aortic dissectionAortic dissection
Pediatrics Kawasaki disease, TakayasuPediatrics Kawasaki disease, Takayasu
arteritisarteritis
Increased afterload which increasesIncreased afterload which increases
myocardial demandmyocardial demand

22. Risk factors for atherosclerosisRisk factors for atherosclerosis
AgeAge
Male genderMale gender
SmokingSmoking
Hypercholesterolemia and triglyceridemiaHypercholesterolemia and triglyceridemia
Diabetes MellitusDiabetes Mellitus
Poorly controlled hypertensionPoorly controlled hypertension

23. Risk factors for atherosclerosisRisk factors for atherosclerosis
Family HistoryFamily History
Sedentary lifestyleSedentary lifestyle

24. Mechanisms of Myocardial damageMechanisms of Myocardial damage
The severity of an MI is dependent of threeThe severity of an MI is dependent of three
factorsfactors
The level of the occlusion in the coronaryThe level of the occlusion in the coronary
The length of time of the occlusionThe length of time of the occlusion
The presence or absence of collateralThe presence or absence of collateral
circulationcirculation

25. Cardiac BiomarkersCardiac Biomarkers
Cardiac biomarkers are protein moleculesCardiac biomarkers are protein molecules
released into the blood stream fromreleased into the blood stream from
damaged heart muscledamaged heart muscle
Since ECG can be inconclusive ,Since ECG can be inconclusive ,
biomarkers are frequently used tobiomarkers are frequently used to
evaluate for myocardial injuryevaluate for myocardial injury
These biomarkers have a characteristicThese biomarkers have a characteristic
rise and fall patternrise and fall pattern

26. Troponin T and ITroponin T and I
These isoforms are very specific forThese isoforms are very specific for
cardiac injurycardiac injury
Preferred markers for detectingPreferred markers for detecting
myocardial cell injurymyocardial cell injury
Rise 2-6 hours after injuryRise 2-6 hours after injury
Peak in 12-16 hoursPeak in 12-16 hours
Stay elevated for 5-14 daysStay elevated for 5-14 days

27. Creatinine Kinase ( CK-MB)Creatinine Kinase ( CK-MB)
Creatinine Kinase is found in heart muscleCreatinine Kinase is found in heart muscle
(MB), skeletal muscle (MM), and brain(MB), skeletal muscle (MM), and brain
(BB)(BB)
Increased in over 90% of myocardialIncreased in over 90% of myocardial
infractioninfraction
However, it can be increased in muscleHowever, it can be increased in muscle
trauma, physical exertion, post-op,trauma, physical exertion, post-op,
convulsions, and other conditionsconvulsions, and other conditions

28. Creatine Kinase (MB)Creatine Kinase (MB)
Time sequence after myocardial infarctionTime sequence after myocardial infarction
Begins to rise 4-6 hoursBegins to rise 4-6 hours
Peaks 24 hoursPeaks 24 hours
returns to normal in 2 daysreturns to normal in 2 days
MB2 released from heart muscle andMB2 released from heart muscle and
converted to MB1.converted to MB1.
A level of MB2 > or = 1 and a ratio ofA level of MB2 > or = 1 and a ratio of
MB2/MB1 > 1.5 indicates myocardialMB2/MB1 > 1.5 indicates myocardial
injuryinjury

29. MyoglobinMyoglobin
Damage to skeletal or cardiac muscleDamage to skeletal or cardiac muscle
release myoglobin into circulationrelease myoglobin into circulation
Time sequence after infarctionTime sequence after infarction
Rises fast 2hoursRises fast 2hours
Peaks at 6-8 hoursPeaks at 6-8 hours
Returns to normal in 20-36 hoursReturns to normal in 20-36 hours
Have false positives with skeletal muscleHave false positives with skeletal muscle
injury and renal failureinjury and renal failure

30. Renal Failure and RenalRenal Failure and Renal
TransplantationTransplantation
Diagnostic accuracy of serum markers ofDiagnostic accuracy of serum markers of
cardiac injury are altered in patients withcardiac injury are altered in patients with
renal failurerenal failure
Cardiac troponins decreased diagnosticCardiac troponins decreased diagnostic
sensitivity and specificity in patientssensitivity and specificity in patients
receiving renal replacement therapyreceiving renal replacement therapy
Current data show levels of troponin I areCurrent data show levels of troponin I are
unaltered while levels of troponin T mayunaltered while levels of troponin T may
be elevatedbe elevated

31. CBCCBC
Leukocytosis may be observed withinLeukocytosis may be observed within
several hours after myocardial injury andseveral hours after myocardial injury and
returns returns to levels within thereturns returns to levels within the
reference range within one weekreference range within one week

32. Chemistry ProfileChemistry Profile
Potassium and magnesium levels shouldPotassium and magnesium levels should
be monitored and correctedbe monitored and corrected
Creatinine levels must be consideredCreatinine levels must be considered
before using contrast dye for coronarybefore using contrast dye for coronary
angiography and percutanousangiography and percutanous
revascularizationrevascularization

33. C-reactive Protein (CRP)C-reactive Protein (CRP)
C- reactive protein is a marker of acuteC- reactive protein is a marker of acute
inflammationinflammation
Patients without evidence of myocardialPatients without evidence of myocardial
necrosis but with elevated CRP are atnecrosis but with elevated CRP are at
increased risk of an eventincreased risk of an event

34. Chest X-RayChest X-Ray
Chest radiography may provide clues toChest radiography may provide clues to
an alternative diagnosis ( aortic dissectionan alternative diagnosis ( aortic dissection
or pneumothorax)or pneumothorax)
Chest radiography also revealsChest radiography also reveals
complications of myocardial infarctioncomplications of myocardial infarction
such as heart failuresuch as heart failure

36. EchocardiographyEchocardiography
Use 2-dimentional and M modeUse 2-dimentional and M mode
echocardiography when evaluating overallechocardiography when evaluating overall
ventricular function and wall motionventricular function and wall motion
abnormalitiesabnormalities
Echocardiography can also identifyEchocardiography can also identify
complications of MI ( eg. Valvular orcomplications of MI ( eg. Valvular or
pericardial effusion, VSD)pericardial effusion, VSD)

37. ElectrocardiogramElectrocardiogram
A normal ECG does not exclude ACSA normal ECG does not exclude ACS
High probability include ST segmentHigh probability include ST segment
elevation in two contiguous leads orelevation in two contiguous leads or
presence of q wavespresence of q waves
Intermediate probability ST depressionIntermediate probability ST depression
T wave inversions are less specificT wave inversions are less specific

40. Progression of wave changesProgression of wave changes
Hyperacute T wave changes - increased T waveHyperacute T wave changes - increased T wave
amplitude and width; may also see ST elevation.amplitude and width; may also see ST elevation.
Marked ST elevation with hyperacute T waveMarked ST elevation with hyperacute T wave
changes (transmural injury)changes (transmural injury)
Pathologic Q waves, less ST elevation, terminal TPathologic Q waves, less ST elevation, terminal T
wave inversion (necrosis) (Pathologic Q waveswave inversion (necrosis) (Pathologic Q waves
are usually defined as durationare usually defined as duration >>0.04 s or >25%0.04 s or >25%
of R-wave amplitude)of R-wave amplitude)
Pathologic Q waves, T wave inversion (necrosisPathologic Q waves, T wave inversion (necrosis
and fibrosis)and fibrosis)
Pathologic Q waves, upright T waves (fibrosisPathologic Q waves, upright T waves (fibrosis))

41. Current of Injury Patterns

42. Reciprocal Changes

43. Electrocardiographic evolution
of myocardial infarction.
After the first few minutes the T waves become tall,
pointed and upright and ST segment elevation develops
After the first few hours the T waves invert,
the R wave voltage is decreased and
Q waves develop.
After a few days the ST segment returns to normal.
After weeks or months the T wave may return
to upright but the Q wave remains.

45. This picture shows a normal sinus complex. The ST segment is on the iso-electric line.
At the onset of pain the ECG would be normal but the ST segment would soon start to
change. In this picture, the T wave has grown taller.
Within an hour the ST segment would be noticeably elevated, indicating the onset on
myocardial necrosis. (tissue death). This is the point at which we would be aiming
to administer the thrombolytic (clot-busting) drug.
If thrombolysis is administered, we would be looking for specific changes on the ECG.
A 50% reduction in ST segment elevation is a good indicator of success. In this
picture, the ST elevation has reduced by more than 50% from picture 2. We would
expect to see these changes within 90 minutes of administering thrombolysis. You can
also see the T wave invertion is much deeper. This is a good sign of reperfusion.
(blood flow returning to the damaged area.)
24 hours later, the ST segment may have returned to the iso-electric line. In this
picture you can see the ST segment is back on the iso-electric line but the T wave
remains inverted. It may stay inverted for days, weeks or months.
6. In some cases, after a few months the ECG looks relatively normal. Compare
picture 6 with picture 1. They look much the same but for the deep Q wave in picture
6. A deep Q wave is an indicator of myocardial tissue death and will remain on
the ECG. A "pathological" Q wave is not "time-specific". It may be there from a
previous heart attack and therefore is not part of the criteria for evaluating an Acute
Myocardial Infarction.

46. MIs can be locatedMIs can be located
in thein the
anterior,anterior,
septal,septal,
lateral,lateral,
posterior,posterior,
or inferior wallsor inferior walls
of the left ventricle.of the left ventricle.
LOCATION OF THE INFARCTIONLOCATION OF THE INFARCTION

47. Diagram of the coronary arteries arising from the aorta and encirclingDiagram of the coronary arteries arising from the aorta and encircling
the heart. Some of the coronary veins also are shown.the heart. Some of the coronary veins also are shown.

49. Inferior MIInferior MI
Pathologic Q waves and evolving ST-Pathologic Q waves and evolving ST-
T changes in leads II, III, aVF.T changes in leads II, III, aVF.
Q waves usually largest in lead III,Q waves usually largest in lead III,
next largest in lead aVF, and smallestnext largest in lead aVF, and smallest
in lead IIin lead II

50. Inferior MIInferior MI

51. Inferoposterior MIInferoposterior MI
ECG changes are seen in anterior precordial leadsECG changes are seen in anterior precordial leads
V1-3, but are theV1-3, but are the mirror imagemirror image of an anteroseptalof an anteroseptal
MI,MI,
Increased R wave amplitude and duration (i.e., aIncreased R wave amplitude and duration (i.e., a
"pathologic R wave" is a mirror image of a"pathologic R wave" is a mirror image of a
pathologic Q).pathologic Q).
R/S ratio in V1 or V2 >1 (i.e., prominent anteriorR/S ratio in V1 or V2 >1 (i.e., prominent anterior
forces).forces).
Hyperacute ST-T wave changes: i.e., STHyperacute ST-T wave changes: i.e., ST
depression and large, inverted T waves in V1-3.depression and large, inverted T waves in V1-3.
Late normalization of ST-T with symmetricalLate normalization of ST-T with symmetrical
upright T waves in V1-3.upright T waves in V1-3.
Often seen with inferior MI (i.e., "inferoposteriorOften seen with inferior MI (i.e., "inferoposterior
MI")MI")

52. Inferoposterior MIInferoposterior MI

53. Inferoposterior MIInferoposterior MI

54. Right Ventricular MIRight Ventricular MI
Right Ventricular MI (only seen withRight Ventricular MI (only seen with
proximal right coronary occlusion;proximal right coronary occlusion;
i.e., with inferior family MI's)i.e., with inferior family MI's)
ECG findings usually requireECG findings usually require
additional leads on right chest (V1Radditional leads on right chest (V1R
to V6R, analogous to the left chestto V6R, analogous to the left chest
leads)leads)
ST elevation,ST elevation, >>1mm, in right chest1mm, in right chest
leads, especially V4R.leads, especially V4R.

55. V3R,
V4R,
V5R,
V6R
right chest leads

56. Right Ventricular MIRight Ventricular MI

57. Anterior MIAnterior MI

58. High Lateral MIHigh Lateral MI

59. What is the diagnosis?What is the diagnosis?

60. MI plus LBBBMI plus LBBB
Q waves of any size inQ waves of any size in twotwo or more of leads I, aVL, V5, oror more of leads I, aVL, V5, or
V6 (See below: one of the most reliable signs and probablyV6 (See below: one of the most reliable signs and probably
indicatesindicates septalseptal infarction, because the septum is activatedinfarction, because the septum is activated
early from the right ventricular side in LBBB).early from the right ventricular side in LBBB).
Reversal of the usual R wave progression in precordialReversal of the usual R wave progression in precordial
leads.leads.
Notching of the downstroke of the S wave in precordialNotching of the downstroke of the S wave in precordial
leads to the right of the transition zone (i.e., before QRSleads to the right of the transition zone (i.e., before QRS
changes from a predominate S wave complex to achanges from a predominate S wave complex to a
predominate R wave complex); this may be a Q-wavepredominate R wave complex); this may be a Q-wave
equivalent.equivalent.

61. MI plus LBBBMI plus LBBB
Notching of the upstroke of the S wave in precordial leadsNotching of the upstroke of the S wave in precordial leads
to the right of the transition zone (another Q-waveto the right of the transition zone (another Q-wave
equivalent).equivalent).
rSR' complex in leads I, V5 or V6 (the S is a Q-waverSR' complex in leads I, V5 or V6 (the S is a Q-wave
equivalent occurring in the middle of the QRS complex)equivalent occurring in the middle of the QRS complex)
RS complex in V5-6 rather than the usual monophasic RRS complex in V5-6 rather than the usual monophasic R
waves seen in uncomplicated LBBB; (the S is a Q-wavewaves seen in uncomplicated LBBB; (the S is a Q-wave
equivalent).equivalent).
"Primary" ST-T wave changes (i.e., ST-T changes in the"Primary" ST-T wave changes (i.e., ST-T changes in the
same direction as the QRS complex rather than the usualsame direction as the QRS complex rather than the usual
"secondary" ST-T changes seen in uncomplicated LBBB);"secondary" ST-T changes seen in uncomplicated LBBB);
these changes may reflect an acute, evolving MI.these changes may reflect an acute, evolving MI.

62. Old MI plus LBBOld MI plus LBB

63. Non-Q wave MINon-Q wave MI
Recognized by evolving ST-T changes over time without theRecognized by evolving ST-T changes over time without the
formation of pathologic Q waves (in a patient with typical chestformation of pathologic Q waves (in a patient with typical chest
pain symptoms and/or elevation in myocardial-specific enzymes)pain symptoms and/or elevation in myocardial-specific enzymes)
Although it is tempting to localize the non-Q MI by the particularAlthough it is tempting to localize the non-Q MI by the particular
leads showing ST-T changes, this is probably only valid for the STleads showing ST-T changes, this is probably only valid for the ST
segment elevation pattern.segment elevation pattern.
Evolving ST-T changes may include any of the following patterns:Evolving ST-T changes may include any of the following patterns:
Convex downward ST segment depression only (common)Convex downward ST segment depression only (common)
Convex upwards or straight ST segment elevation only.Convex upwards or straight ST segment elevation only.
Symmetrical T wave inversion only (common)Symmetrical T wave inversion only (common)

64. Non-Q wave MINon-Q wave MI

65. Differential MI patternDifferential MI pattern
WPW preexcitation (WPW preexcitation (negativenegative delta wavedelta wave
may mimic pathologic Q waves)may mimic pathologic Q waves)
IHSS (septal hypertrophy may makeIHSS (septal hypertrophy may make
normal septal Q waves "fatter" therebynormal septal Q waves "fatter" thereby
mimicking pathologic Q waves)mimicking pathologic Q waves)
LVH (may have QS pattern or poor R waveLVH (may have QS pattern or poor R wave
progression in leads V1-3)progression in leads V1-3)
RVH (tall R waves in V1 or V2 may mimicRVH (tall R waves in V1 or V2 may mimic
true posterior MI)true posterior MI)
Complete or incomplete LBBB (QS wavesComplete or incomplete LBBB (QS waves
or poor R wave progression in leads V1-3)or poor R wave progression in leads V1-3)

66. Differential MI patternDifferential MI pattern
Pneumothorax (loss of right precordial R waves)Pneumothorax (loss of right precordial R waves)
Pulmonary emphysema and cor pulmonale (lossPulmonary emphysema and cor pulmonale (loss
of R waves V1-3 and/or inferior Q waves withof R waves V1-3 and/or inferior Q waves with
right axis deviation)right axis deviation)
Left anterior fascicular block (may see small q-Left anterior fascicular block (may see small q-
waves in anterior chest leads)waves in anterior chest leads)
Acute pericarditis (the ST segment elevation mayAcute pericarditis (the ST segment elevation may
mimic acute transmural injury)mimic acute transmural injury)
Central nervous system disease (may mimic non-Central nervous system disease (may mimic non-
Q wave MI by causing diffuse ST-T wave changesQ wave MI by causing diffuse ST-T wave changes

67. Localizing Infarcts on the 12 Lead ECG
anterior
Lateral - Cx
posterior
anterior
Inferior - RCA Inferior - RCA
Ant – sep - LAD
Ant – sep - LAD
septal
Anterior - LAD
anterior

68. ECG #1- 68 year old with chest pain for 3 daysECG #1- 68 year old with chest pain for 3 days

69. ECG #2- 66 year old man with 1 hour historyECG #2- 66 year old man with 1 hour history
of chest pressureof chest pressure

70. ECG #4 - 62 year old with profuse diaphoresisECG #4 - 62 year old with profuse diaphoresis
and vomitingand vomiting

71. ECG #6- 45 year old female with onset of chestECG #6- 45 year old female with onset of chest
discomfort 2 hours ago – PMH ?Cancerdiscomfort 2 hours ago – PMH ?Cancer

72. ECG #7 – 50 year old man with crushing
substernal chest pain for 30 minutes

73. ECG #8- 72 year old female with history ofECG #8- 72 year old female with history of
HTN found unconsciousHTN found unconscious

74. ECG #9- 67 year old man with PMH of MI inECG #9- 67 year old man with PMH of MI in
respiratory failure due to acute CHFrespiratory failure due to acute CHF

75. ECG #10- Chest pain radiating to the jaw inECG #10- Chest pain radiating to the jaw in
a 41 year old womana 41 year old woman

76. ECG #1- 32 year old with chest pain at a
party

77. Anterolateral MI

78. Anterolateral MI - II

79. Anterolateral MI - III

80. 65 year old with acute chest pain

81. Anterior MI

82. Acute Anterior MI

83. Acute Anteroseptal MI

84. Acute Anterior MI

85. Acute Anteroseptal MI

86. 53 year old with severe light headedness,
nausea, diaphoresis, and upper abdominal pain.
Bloods pressure 85/palp.
Acute Inferoposterior MI

87. R
R
R
R
R

88. Acute Lateral MI

89. ECG #4 - 62 year old with profuse
diaphoresis and vomiting

90. ECG #7 – Acute Posterior MI - Old inferior MI

91. Inferior MI

92. (MR# 866159) -77 year old male with chest pain
and palpitation

93. Anterior MI

94. LVH with ST-T Wave Changes

95. RBBB, Inferoposterior MI

96. RBBB+LAHB+
Anterolateral MI

97. RBBB+LPHB+
Anteroseptal

99. TherapyTherapy
The goals of therapy in AMIThe goals of therapy in AMI
are the expedient restorationare the expedient restoration
of normal coronary flow andof normal coronary flow and
the maximum salvage ofthe maximum salvage of
functional myocardiumfunctional myocardium

100. REPERFUSION STRATEGY

101. • Patients receiving fibrinolysis should be risk-stratified to identify need
for further revascularization with percutaneous coronary intervention
(PCI) or coronary artery bypass graft surgery (CABG).
• All patients should receive late hospital care and secondary
prevention of STEMI.
Fibrinolysis
Primary PCI
Noninvasive Risk
Stratification
Late
Hospital Care
and Secondary
Prevention
PCI or CABG
Not
PCI Capable
PCI Capable
Rescue Ischemia
driven
Options for Transport of Patients With STEMI andOptions for Transport of Patients With STEMI and
Initial Reperfusion TreatmentInitial Reperfusion Treatment

102. Treatments
 Oxygen
 Aspirin
 Nitroglycerin
 Morphine
 Beta - blocker
 Heparin/ Lovenox
 Clopidogrel
 Fibrinolytics
 Percutaneous Coronary Intervention (PCI)

103. Percutaneous transluminal coronary angioplasty (PTCA procedure)
is another important method of thrombolysis and reperfusion.

104. Balloon Angioplasty Illustration

105. Bypass surgery, is indicated in the
following situations associated with
myocardial infarction: PTCA procedure
failure (with persistent pain or
hemodynamic instability), PTCA risk
procedure due to the coronary anatomy
(left common trunk stenosis), coronary
occlusion occurred after catheterization,
cardiogenic shock.

106. Antiplatelet AgentsAntiplatelet Agents
Aspirin at lease 160mg immediatelyAspirin at lease 160mg immediately
Interferes with function of cyclooxygenaseInterferes with function of cyclooxygenase
and inhibits the formation of thromboxaneand inhibits the formation of thromboxane
ASA alone has one of the greatest impactASA alone has one of the greatest impact
on the reduction of MI mortality.on the reduction of MI mortality.
Clopidogrel, ticlopidine, have not beenClopidogrel, ticlopidine, have not been
shown in any large scal trail to be superiorshown in any large scal trail to be superior
to Aspirin in acute MIto Aspirin in acute MI

107. Supplemental OxygenSupplemental Oxygen
Because MI impairs the circulatoryBecause MI impairs the circulatory
function of the heart, oxygen extraction byfunction of the heart, oxygen extraction by
the heart and other tissues may bethe heart and other tissues may be
diminisheddiminished
Supplemental oxygen should beSupplemental oxygen should be
administered to patient with symptomsadministered to patient with symptoms
and or signs of pulmonary edema or pulseand or signs of pulmonary edema or pulse
oximetry readings less than 90%.oximetry readings less than 90%.

108. NitratesNitrates
IV nitrates to all patients with MI andIV nitrates to all patients with MI and
congestive heart failure, persistentcongestive heart failure, persistent
ischemia, hypertension, or large anteriorischemia, hypertension, or large anterior
wall MIwall MI
Primary benefit vasodilator effectPrimary benefit vasodilator effect
Metabolized to nitric oxide in the vascularMetabolized to nitric oxide in the vascular
endothelium, relaxes endotheliumendothelium, relaxes endothelium
Vasodilatation reduces myocardial oxygenVasodilatation reduces myocardial oxygen
demand and preload and afterloaddemand and preload and afterload

109. Beta-blockersBeta-blockers
Recommended within 12 hours of MIRecommended within 12 hours of MI
symptoms and continued indefinitelysymptoms and continued indefinitely
Reduces Myocardial mortality byReduces Myocardial mortality by
decreasing arrythmogenic deathdecreasing arrythmogenic death
Decrease the rate and force of myocardialDecrease the rate and force of myocardial
contraction and decreases overall oxygencontraction and decreases overall oxygen
demanddemand

110. Unfractionated heparinUnfractionated heparin
Forms a chemical complex withForms a chemical complex with
antithrombin III inactivates both freeantithrombin III inactivates both free
thrombin and factor Xathrombin and factor Xa
Recommended in patients with MI whoRecommended in patients with MI who
undergo PTCA or fibrinolytic therapy withundergo PTCA or fibrinolytic therapy with
alteplasealteplase

111. Low-molecular weight heparinLow-molecular weight heparin
Direct activity against factors Xa and IIaDirect activity against factors Xa and IIa
Proven to be effective in treating ACS thatProven to be effective in treating ACS that
are characterized by unstable angina orare characterized by unstable angina or
non ST- elevation MInon ST- elevation MI
Their fixed doses are easy to administerTheir fixed doses are easy to administer
and laboratory testing to measure theirand laboratory testing to measure their
therapeutic effect is not necessary makestherapeutic effect is not necessary makes
them attractive alternative of un-them attractive alternative of un-
fractionated heparinfractionated heparin

113. ThrombolyticsThrombolytics
Indicated with MI and ST segmentIndicated with MI and ST segment
elevation greater than 0.1mV in 2elevation greater than 0.1mV in 2
contiguous ECG leads, or new onsetcontiguous ECG leads, or new onset
LBBB, who present less than 12 hours butLBBB, who present less than 12 hours but
not more than 24 hours after symptomnot more than 24 hours after symptom
onsetonset
The most critical variable in achievingThe most critical variable in achieving
successful fibrinolysis is time formsuccessful fibrinolysis is time form
symptom onset to drug administrationsymptom onset to drug administration

116. ThrombolyticsThrombolytics
As a class the plasminogen activators haveAs a class the plasminogen activators have
been shown to restore coronary blood flow in 50-been shown to restore coronary blood flow in 50-
80% of patients80% of patients
Contraindication active intracranial bleeding,Contraindication active intracranial bleeding,
CVA 2months, CNS neoplasm, HTN,CVA 2months, CNS neoplasm, HTN,
coagulopathycoagulopathy
Retaplase slightly higher angiographic patencyRetaplase slightly higher angiographic patency
but did not translate into survival benefitbut did not translate into survival benefit
Intracranial bleed risk major drawbackIntracranial bleed risk major drawback

117. Glycoprotein IIb/IIIa AntagonistsGlycoprotein IIb/IIIa Antagonists
Potent inhibitors of platelet aggregationPotent inhibitors of platelet aggregation
Use during PCI and in patients with highUse during PCI and in patients with high
risk features ACS have been shown torisk features ACS have been shown to
reduce the composite end points of death,reduce the composite end points of death,
reinfraction and the need for target lesionreinfraction and the need for target lesion

118. Percutanous Coronary InterventionPercutanous Coronary Intervention
Alternative if performed by skilled operatorAlternative if performed by skilled operator
in an experienced centerin an experienced center
Standard is a “ door to balloon” time of 90Standard is a “ door to balloon” time of 90
minutesminutes
PCI can successfully restore coronaryPCI can successfully restore coronary
blood flow in 90 to 95% of MI patientsblood flow in 90 to 95% of MI patients
PCI definitive survival advantage overPCI definitive survival advantage over
fibrinolytics for MI patients who are infibrinolytics for MI patients who are in
cardiogenic shockcardiogenic shock

119. Surgical RevascularizationSurgical Revascularization
Emergent or surgical revascularization inEmergent or surgical revascularization in
setting of failed PTCA in patients withsetting of failed PTCA in patients with
hemodynamic instability and coronaryhemodynamic instability and coronary
anatomy amendable to surgical graftinganatomy amendable to surgical grafting
Also indicated of mechanicalAlso indicated of mechanical
complications of MI including VSD, freecomplications of MI including VSD, free
wall rupture, or acute MRwall rupture, or acute MR
Carries a higher risk of perioperativeCarries a higher risk of perioperative
mortality than elective CABGmortality than elective CABG

120. Lipid ManagementLipid Management
All post MI patients should be on AMAAll post MI patients should be on AMA
step II diet ( < 7% of calories fromstep II diet ( < 7% of calories from
saturated fats)saturated fats)
Post MI patients with LDL > 100 mg/dl arePost MI patients with LDL > 100 mg/dl are
recommended to be on drug therapy to tryrecommended to be on drug therapy to try
to lower levels to <100 mg/dlto lower levels to <100 mg/dl
Recent data indicate that all MI patientsRecent data indicate that all MI patients
should be on statin therapy, regardless ofshould be on statin therapy, regardless of
lipid levels or dietlipid levels or diet

121. Long term MedicationsLong term Medications
Most oral medications instituted in theMost oral medications instituted in the
hospital at the time of MI are continuedhospital at the time of MI are continued
long termlong term
Aspirin, beta blockers and statin areAspirin, beta blockers and statin are
continued indefinitelycontinued indefinitely
ACEI indefinitely in patients with CHF,ACEI indefinitely in patients with CHF,
ejection fraction <.40, hypertension, orejection fraction <.40, hypertension, or
diabetesdiabetes

122. 1st1st
24 h24 h
DuringDuring
HospHosp
Hosp DC +Hosp DC +
Long TermLong Term
Aspirin 162-325 mg
chewed
75-162
mg/d p.o.
75-162
mg/d p.o.
Fibrinolytic tPA,TNK,
rPA, SK
UFH
60U/kg (4000)
12 U/kg/h (1000)
aPTT 1.5 - 2 x C
aPTT
1.5 - 2 x C
Beta-blocker Oral daily Oral daily Oral daily
Summary of Pharmacologic Rx:Summary of Pharmacologic Rx: IschemiaIschemia
JACC 2004;44: 671
Circulation 2004;110: 588

123. 1st1st
24 h24 h
During HospDuring Hosp Hosp DC +Hosp DC +
Long TermLong Term
ACEI Anterior MI,
Pulm Cong., EF < 40 Oral
Daily
Oral
Daily
IndefinitelyARB ACEI intol.,
HF, EF < 40
Aldo
Blocker
No renal dysf,
K+
< 5.0 mEq/L
On ACEI,
HF or DM
Same as
during
Hosp.
Statin Start w/o lipid
profile
Indefinitely,
LDL << 100
Summary of Pharmacologic Rx:Summary of Pharmacologic Rx: LVD, Sec. Prev.,LVD, Sec. Prev.,
JACC 2004;44:671JACC 2004;44:671
Circ 2004;110:588Circ 2004;110:588

124. Vascular Complications
 Recurrent ischemia
 Recurrent infarction
Mechanical Complications
 Left ventricular free wall rupture
 Ventricular septal rupture
 Papillary muscle rupture with
acute mitral regurgitation
Myocardial Complications
 Diastolic dysfunction
 Systolic dysfunction
 Congestive heart failure
 Hypotension/cardiogenic
shock
 Right ventricular infarction
 Ventricular cavity dilation
 Aneurysm formation (true,
false)

125. Pericardial Complications
 Pericarditis
 Dressler’s syndrome
 Pericardial effusion
Thromboembolic
Complications
 Mural thrombosis
 Systemic thromboembolism
 Deep venous thrombosis
 Pulmonary embolism
Electrical
Complications
 Ventricular tachycardia
 Ventricular fibrillation
 Supraventricular
tachydysrhythmias
 Bradydysrhythmias
 Atrioventricular block
(first, second, or third
degree)

126. Thank You!Thank You!

127. Summary: pump failure and shock.
Diagnosis: chest X-ray, echocardiography, right heart catheterization.
Treatment of mild and moderately severe heart failure:
O2
furosemide: 20–40mg intravenously repeated at 1–4 hourly intervals if necessary
nitrates: if no hypotension
ACE inhibitors in the absence of hypotension, hypovolaemia or renal failure.
Treatment of severe heart failure:
O2
furosemide: cfr. supra
nitrates if no hypotension
inotropic agents: dopamine and/or dobutamine
haemodynamic assessment with balloon floating catheter
ventilatory support if inadequate oxygen tension
consider early revascularization.
Treatment of shock:
O2
haemodynamic assessment with balloon floating catheter
inotropic agents: dopamine and dobutamine
ventilatory support if inadequate oxygen tension
intraaortic balloon pump
consider left ventricular assist devices and early revascularization.