Coronary artery disease (CAD) is a major cause of death in India. Atherosclerosis underlies most CAD cases. Unstable angina and NSTEMI are types of acute coronary syndrome (ACS) caused by a reduction in oxygen supply to the heart. The clinical presentation of ACS can include chest pain and other symptoms. Diagnosis involves ECG, cardiac biomarkers, and risk stratification. Treatment focuses on anticoagulation, antiplatelet therapy, and revascularization. Myocardial infarction (MI or heart attack) occurs when an atherosclerotic plaque ruptures completely blocking a coronary artery. This leads to necrosis of heart muscle cells. Diagnosis of MI requires specific ECG changes and elevated cardiac

2. EPIDEMIOLGY
• Main cause of death
• The highest rate is in south India.
• It has been estimated that India had
the highest number of deaths in the
world due to CAD in 2002, nearly 1.5
million and which is expected to
double by 2015.
• Atherosclerosis remains the major
cause of death and premature
disability

3. MEANING
• Atherosclerosis :
athere=fatty
mush, skleros =
hard.
• Atherosclerosis
= “hardening of
the arteries”

4. MEANING
ACS
no ST
elevation
Unstable
angina
NSTEMI
ST
elevation
MI

6. Coronary circulation

7. Coronary circulation

8. Risk factors

9. Non modifiable Risk Factors
• Heredity
• Age
• Personality factors
• Gender

10. Modifiable Risk Factors
• Smoking
• Hypertension
• Elevated serum cholesterol level
• Diabetes
• Obesity
• Physical Inactivity

11. Contributing Risk Factors
• Response to stress
• Homocysteine Level
• Inflammatory Level
• Menopause
• Type A Behavioural Patterns, TABP
• Hemostatic factors

12. Novel risk factors
• Homocysteine
• CRP
• Plasma fibrinogen
• Fibrin D dimer
• Lipoprotein

13. CAUSES OF ACS
• Decrease in the oxygen
available to the myocardium
– Nonobstructive clot on an
atherosclerotic plaque.
– Coronary vasospasm.
– Atherosclerotic obstruction
without clot or vasospasm.
– Inflammation or infection.
– Unstable angina due to a non
cardiac cause.
– Thrombus formation with
subsequent coronary artery
occlusion

14. CAUSES OF ACS
• Increase in the oxygen
demand

15. PATHOPHYSIOLOGY
• Initiation of Atherosclerosis
• Leukocyte Recruitment
• Foam-Cell Formation
• Atheroma Evolution and Complications
• Microvessels
• Calcification
• Plaque Evolution

19. Deterioration of a stable
atherosclerotic plaque
Exposing the intima to blood
Stimulating platelet aggregation
Local vasoconstriction
Thrombus formation
Partially occluded by the thrombus
(manifesting UA/NSTEMI) or totally
occluded by a thrombus (STEMI)
A
C
S
A
C
S

22. Criteria for diagnosis of ACS
Major criteria Minor criteria
A diagnosis of ACS can be
made if one or more of the
following major criteria are
present:
 ST elevation or LBBB in
the setting of recent
(<24hrs) or ongoing
angina
 New or presumably new,
ST segment depression
(≥0.05mV) or T wave
inversion (≥ 0.2mV)
with rest symptoms
 Elevated serum markers
of myocardial damage
(ie, Troponin I, T and
CK-MB)
In the absence of a major criterion, a diagnosis of ACS requires
the presence of at least one item from both column 1 and 2
1 2
 Prolonged (ie, >20mts)
chest, arm/shoulder,
neck or epigastric
discomfort
 New onset chest, arm/
shoulder, neck, or
epigastric discomfort at
rest , minimal exertion or
ordinary activity
 Previously documented
chest, arm/ shoulder,
neck, or epigastric
discomfort which has
become distinctly more
frequent or longer in
duration
 Typical/ atypical angina
 Male> 40yrs or
female>60yrs
 Known CAD
 HF, hypotension or
transient mitral valve
regurgitation by
examination
 DM
 Extracardiac disease
 Pathologic Q wave on
ECG
 Abnormal ST segment or
T wave abnormalities
not known to be new

23. NSTE ACS

24. Definition
Stable angina pectoris is
characterized by chest or arm
discomfort that may not be
described as pain but is
reproducibly associated with
physical exertion or stress and is
relieved within 5–10 minutes by
rest and/or sublingual
nitroglycerin.

25. Unstable Angina is defined as angina
pectoris or equivalent ischemic
discomfort with at least one of three
features:
(1) it occurs at rest (or with minimal
exertion), usually lasting >10
minutes;
(2) it is severe and of new onset (i.e.,
within the prior 4–6 weeks); and/or
(3) it occurs with a crescendo pattern

26. The diagnosis of NSTEMI is
established if a patient with the
clinical features of UA develops
evidence of myocardial necrosis,
as reflected in elevated cardiac
biomarkers.

27. Canadian Cardiovascular
Society - Classification of
Angina
CLASS
ACTIVITY
EVOKING
ANGINA
LIMITS TO
ACTIVITY
I
II
III
IV
Prolonged
exertion
Walking>2
blocks
Walking<2
blocks
Minimal or rest
None
Slight
Marked
Severe

28. Pathophysiology
A reduction in oxygen supply and/or
by an increase in myocardial
oxygen demand superimposed on
a lesion that causes coronary
arterial obstruction, usually an
atherothrombotic coronary plaque

29. (1) plaque rupture or erosion with a
superimposed nonocclusive thrombus 
NSTEMI may occur with downstream
embolization of platelet aggregates and/or
atherosclerotic debris;
(2) dynamic obstruction [e.g., coronary spasm,
as in Prinzmetal's variant angina (PVA)
(3) progressive mechanical obstruction [e.g.,
rapidly advancing coronary atherosclerosis
or restenosis following percutaneous
coronary intervention (PCI)]
(4) UA secondary to increased myocardial
oxygen demand and/or decreased supply
(e.g., tachycardia, anemia).

30. Clinical Presentation
• Typical chest and associated
symptoms (not related to trauma):

31. Atypical symptoms
• Neck, throat, jaw or tooth discomfort
• Shoulder or arm pain
• Numbness or tingling in the chest or related area
• Fullness or burning in the chest
• Epigastric discomfort which is described as indigestion
• Discomfort between scapula or in the midback region
• Dizziness/ light headedness with or without syncope
• Fatigue or weakness not related to neurologic problems
• Palpitation of new onset with no history of dysrhythmia
• Mid back pain (not related to degenerative joint
diseases)

32. Diagnostic Pathways
• Clinical history
• ECG
• Cardiac markers
• Stress testing (coronary imaging is
an emerging option).

33. Clinical history

34. Electrocardiogram

35. Electrocardiogram

36. Biochemical cardiac markers
• Creatine kinase (CK-MB)
• Troponin I and T and/ or
• Myoglobulin

37. Medical Treatment
• Bed rest
• Continuous ECG monitoring for ST-
segment deviation and cardiac
arrhythmias.
• Ambulation is permitted if the
patient shows no recurrence of
ischemia and does not develop a
biomarker of necrosis for 12–24 h.

43. TREATMENT
Medical
therapy
Anti-ischemic
treatment
Antithrombotic
treatment.

44. Anti-ischemic treatment
• To provide relief and prevention of
recurrence of chest pain
• Initial treatment should include
– bed rest
– nitrates, and
– beta blockers

45. Antithrombotic Therapy:
• Other main component of treatment
for UA/NSTEMI
• Initial treatment should begin with the
platelet cyclooxygenase inhibitor
aspirin.
• The typical initial dose is 325 mg/d,
with lower doses (75–162 mg/d)
recommended for long-term therapy.

46. Anticoagulant therapy
• Unfractionated heparin (UFH
• The low-molecular-weight heparin
(LMWH), enoxaparin
• The indirect Factor Xa inhibitor,
fondaparinux
• Bivalirudin

47. Unstable Angina Risk
Stratification
o Low risk
– New-onset exertional angina
– Minor chest pain during exercise
– Pain relieved promptly by nitroglycerine
o Management
– Can be managed safety as an outpatient
(assuming close follow-up and rapid
investigation)

48. Unstable Angina Risk
Stratification
o Intermediate risk
– Prolonged chest pain
– Diagnosis of rule-out MI
o Management
– Observe in the ER or Chest Pain Unit
– Monitor clinical status and ECG
– Obtain cardiac enzyme (troponin T or I) every
8 to 12 hours

49. Unstable Angina Risk
Stratification
o High risk
– Recurrent chest pain
– ST-segment change
– Hemodynamic compromise
– Elevation in cardiac enzyme
o Management
– Monitor in the coronary Care Unit

50. Risk Stratification by ECG
The risk of death or MI at 30 days is
stongly related to the ECG at the
time of chest pain
• ST depression 10 %
• T-wave inversion 5 %
• No ECG changes 1~2 %

51. PRINZMETAL'S VARIANT
ANGINA (PVA)
• A syndrome of severe ischemic
pain that occurs at rest but not
usually with exertion and is
associated with transient ST-
segment elevation.
• This syndrome is due to focal
spasm of an epicardial coronary
artery, leading to severe
myocardial ischemia

52. Clinical and Angiographic
Manifestations

53. Treatment of PVA
• Nitrates and calcium channel
blockers
• Aspirin may actually increase the
severity of ischemic episodes,
possibly as a result of the exquisite
sensitivity of coronary tone to
modest changes in the synthesis of
prostacyclin.
• The response to beta blockers is
variable.
• Coronary revascularization

54. MYOCARDIAL INFARCTION
(STEMI)

55. DEFINITION
• A dynamic process by which one
or more regions of the heart
experience a severe and prolonged
decrease in oxygen supply because
of insufficient coronary blood flow;
subsequently, necrosis or death•to
the myocardial tissue occurs.

56. Pathophysiology
slowly developing high
grade stenosis of
epicardial coronary
arteries
complete occlusion ,
but do not precipitate
MI
Development of
collateral circulation
atherosclerotic plaque
rupture
exposure of substances
that promote platelet
activation and
aggregation
thrombin generation
thrombus formation
interrupt blood supply
and leads imbalance
between O2 demand
and supply
myocardial necrosis
contractile function of
the heart stops at
necrotic area

57. • The coronary plaques prone to
disruption are those with a rich
lipid core and a thin fibrous cap.
disrupted plaque
Formation of an
initial platelet
monolayer
activation of various
agonists
promote platelet
activation
release of
thromboxane A2
further platelet
activation
potential resistance
to fibrinolysis
develops.

58. Platelet activation
change in the glycoprotein IIb/IIIa
receptor
develops a high affinity for soluble
adhesive proteins (i.e., integrins)
such as fibrinogen
platelet cross-linking and
aggregation

59. Disrupted plaque
exposure of tissue
factor in damaged
endothelial cells at the
site
coagulation cascade is
activated
Factors VII and X are
activated
the conversion of
prothrombin to
thrombin
converts fibrinogen to
fibrin
autoamplification
reaction
further activation of
the coagulation
cascade
Artery is occluded by a
thrombus containing
platelet aggregates and
fibrin strands.

60. The amount of myocardial
damage caused by coronary
occlusion depends on
(1) the territory supplied by the affected vessel
(2) whether or not the vessel becomes totally
occluded
(3) the duration of coronary occlusion
(4) the quantity of blood supplied by collateral vessels
to the affected tissue
(5) the demand for oxygen of the myocardium whose
blood supply has been suddenly limited
(6) endogenous factors that can produce early
spontaneous lysis of the occlusive thrombus, and
(7) the adequacy of myocardial perfusion in the
infarct zone when flow is restored in the occluded
epicardial coronary artery.

61. Location of Infarction
Location of MI Primary siteof occlusion
Inferior MI RCA (80-90%), LCX (10-
20%)
Inferolateral MI LCX
Posterior MI RCA/ LCX
Anterior MI LAD
Anterior septal
MI
LAD
Lateral MI LAD/LCX
Right ventricular RCA

62. KILLIPS CLASSIFICATION
Killip class
I
Individuals with no clinical signs of
heart failure
Killip class
II
Individuals withrales or crackles in the
lungs , an S3, and elevated JVP
Killip class
III
Individuals with frank acute pulmonary
edema
Killip class
IV
Individuals with cardiogenic shock/
hypotension and evidence of peripheral
vasoconstriction (oliguria, cyanosis or
sweating)

63. DEGREES OF DAMAGE

64. Involved layers of heart
muscle
– Transmural (Q wave) infarction - area
of necrosis occurs throughout the
entire thickness of the heart muscle.
– Subendocardial (nontransmural/non
Q-wave) infarction area of necrosis is
confined to the innermost layer of
the heart lining the chambers.

65. Clinical features
• Chest pain

66. Clinical features
• Diaphoresis, cool clammy skin, facial
pallor.
• Hypertension or hypotension and
Bradycardia or tachycardia
• Premature ventricular and/or atrial
beats
• Palpitations, severe anxiety, dyspnea
• Disorientation, confusion,
restlessness
• Fainting, marked weakness
• Nausea, vomiting, hiccups

68. Atypical symptoms
• Epigastric or abdominal distress
• dull aching or tingling sensations
• shortness of breath
• extreme fatigue

70. Physical Signs
• Fourth and third heart sounds
• Decreased intensity of the first
heart sound
• Paradoxical splitting of the second
heart sound
• A pericardial friction rub
(transmural STEMI)
• Temperature elevations up to
38°C.

71. Diagnostic Evaluation
(1) ECG
(2) serum cardiac biomarkers
(3) cardiac imaging
(4) nonspecific indices of tissue
necrosis and inflammation

72. Physical Examination
• muffling of sounds
• presence of gallop
• arrhythmia, and
• accentuation of pulmonary second
sound

73. WHO criteria for diagnosis of
MI:
It requires atleast two of the
following three elements
• A history of ischemic type chest
discomfort
• Evolutionary changes on serially
obtained ECG tracing
• Typical rise and fall in serum
cardiac markers

74. ECG Changes
– ST segment depression and T wave
inversion indicate a pattern of
ischemia.
– ST elevation indicates an injury
pattern.
– Q waves indicate tissue necrosis and
are permanent

75. Location of MI Primary siteof
occlusion
Primary ECG changes Complications
Inferior MI RCA (80-90%)
LCX (10-20%)
L II,III, aVF First and second degree
AV block, right
ventricular infarct
Inferolateral MI LCX L II, III, aVF, V5,V6 Third degree heart block,
left HF, CMP, left
ventricular rupture
Posterior MI RCA/ LCX No lead truly looks at
posterior surface. Look for
reciprocal changes in V1
and V2- tall, broad R
waves; ST depression and
tall T waves. Posterior
leads V7,V8 and V9 may
be recorded and evaluated
First, second, and third
degree heart block, HF,
bradydysrhythmias
Anterior MI LAD V2- V4 Third degree heart block,
HF, bundke branch block
Anterior septal
MI
LAD V1-V3 Second and third degree
heart block
Lateral MI LAD/LCX V5, V6, I, aVL HF
Right
ventricular
RCA V4R
Right precordial leads
V1R – V6R may be
recorded and evaluated
Increased RAP, decreased
CO, bradydysthymias,
heart blocks, hyptension,
cardiogenic shock

76. ECG leads showing changes Location of
infarct
V1-V3 Anteroseptal
V4- V6, L1 and aVL Anterolateral
aVF,L2 and L3, ST depression in
V1 and V2
Inferior wall
Presence of tall R wave and
upright T waves in V1 and V2
True posterior
infarct
ST elevation in Rt sided chest
leads and Q waves (V3R, V4R)
Right ventricular
infarct

77. Cardiac Markers
• Nonspecific markers
– lactate dehydrogenase
– aspartate aminotransferase
– myoglobin
• Specific cardiac markers
– Troponin (troponin C, troponin I and
troponin T).
– Creatine kinase (CK)

78. Marker Rise in
serum
level from
onset
Peak level Time to
return to
normal
Time for
blood
collection
SGOT (5-
40u/l)
8-12 hrs 18-36hrs 3-4 days Once n
12hrs
LDH (20-
220IU/L)
10hrs 24-48hrs 10- 14
days
24hrs
CK-MB 3-12hrs 24hrs 48-72 hrs Every
12hrs for 3
days
C TnT 3-12hrs 12hrs-2
days
5-14 days Once
atleast
every 12
hrs
C TnI 3-12hrs 24hrs 5-10days Once
atleast
every 12
hrs

80. • Chest xray: Prominent pulmonary
vascular markings on x ray indicate
left ventricular failure. Chest film
helps to exclude other causes of
chest pain such as pneumothorax,
pulmonary infarction with effusion,
aortic dissection and skeletal
fractures.
• Echocardiogram:
– used to evaluate ventricular function.
– used to assist in diagnosing an MI,
especially when the ECG is
nondiagnostic.

82. • CT Scan: to reveal cavity
dimensions, wall thickness,
aneurysms and intracardiac
thrombi.
• Nuclear imaging : to study nature
of myocardial lesion, its viability
and prognosis
• MRI scan: to assess the perfusion
of infracted and noninfarcted
tissue as well as the state of
reperfused myocardium

83. Other Findings
• Elevated CRP and lipoprotein
• Abnormal coagulation studies
• Elevated white blood cell (WBC) count
and sedimentation rate
• Radionuclide imaging allows recognition
of areas of decreased perfusion.
• PET determines the presence of
reversible heart muscle injury and
irreversible or necrotic tissue; extent to
which the injured heart muscle has
responded to treatment can also be
determined.

84. Management
• Prehospital care:
1) recognition of symptoms by the patient and
prompt seeking of medical attention;
(2) rapid deployment of an emergency medical
team capable of performing resuscitative
maneuvers, including defibrillation;
(3) expeditious transportation of the patient to
a hospital facility that is continuously staffed
by physicians and nurses skilled in managing
arrhythmias and providing advanced cardiac
life support; and
(4) expeditious implementation of reperfusion
therapy

87. Emergency department
• Goals:
– control of cardiac discomfort,
– rapid identification of patients who
are candidates for urgent reperfusion
therapy,
– triage of lower-risk patients to the
appropriate location in the hospital,
and
– avoidance of inappropriate discharge
of patients with STEMI.

88. • Aspirin : Rapid
inhibition of
cyclooxygenase-1 in
platelets followed
by a reduction of
thromboxane A2
• Supplemental O2:
when hypoxemia is
present, O2 should
be administered by
nasal prongs or face
mask (2–4 L/min)
for the first 6–12 h
after infarction

89. Control of Discomfort
• Sublingual nitroglycerin
• Morphine
• Intravenous beta blockers

90. Management Strategies:
Initial 12-lead ECG  ST-segment
elevation of at least 2 mm in 2
contiguous precordial leads and 1
mm in 2 adjacent limb leads is
present  a patient should be
considered a candidate for
reperfusion therapy
• Gold hour = first 60 mts. Total
ischemic time : 120 mts

91. Primary Percutaneous
Coronary Intervention
• PCI, usually angioplasty and/or
stenting without preceding
fibrinolysis, referred to as primary
PCI
• It is effective in restoring perfusion
in STEMI when carried out on an
emergency basis in the first few
hours of MI.

92. • Advantage:
– patients who have contraindications to fibrinolytic
therapy
– More effective than fibrinolysis in opening
occluded coronary arteries

93. PCI
• Indication:
– When the diagnosis is in doubt
– Cardiogenic shock is present
– Bleeding risk is increased, or
– Symptoms have been present for at
least 2–3 h when the clot is more
mature and less easily lysed by
fibrinolytic drugs.

95. Fibrinolysis
• Ideally initiated within 30 min of
presentation (door-to-needle time
30 min).
• Goal of fibrinolysis is prompt
restoration of full coronary arterial
patency.

96. Fibrinolytic agents
• Tissue plasminogen activator (tPA),
streptokinase, tenecteplase (TNK), and
reteplase (rPA)
– First generation drugs- streptokinase,
urokinase
– Second generation- TPA, anioylated
plasminogen streptokinase
– Third generation- reteplase, TNK
• These drugs are promoting the
conversion of plasminogen to plasmin,
which subsequently lyses fibrinthrombi.

97. Thrombolysis in myocardial
infarction (TIMI) grading
system
• Grade 0 - Complete occlusion of the
infarct-related artery
• Grade 1 - Some penetration of the
contrast material beyond the point of
obstruction but without perfusion of the
distal coronary bed;
• Grade 2 - Perfusion of the entire infarct
vessel into the distal bed, but with flow
that is delayed compared with that of a
normal artery
• Grade 3 - Full perfusion of the infarct
vessel with normal flow

98. CONTRAINDICATIONS OF
FIBRINOLYSIS
• History of cerebrovascular
hemorrhage, a nonhemorrhagic
stroke or other cerebrovascular
event within the past year
• Suspicion of aortic dissection
• Active internal bleeding (excluding
menses).
• Advanced age associated with an
increase in hemorrhagic disorders

99. Relative contraindications:
• Current use of anticoagulants (INR- 2)
• A recent (<2 weeks) invasive or surgical procedure
or prolonged (>10 min) cardiopulmonary
resuscitation
• Known bleeding disorders
• Pregnancy
• A hemorrhagic ophthalmic condition (e.g.,
hemorrhagic diabetic retinopathy)
• Active peptic ulcer disease
• A history of severe hypertension that is currently
adequately controlled.
• Because of the risk of an allergic reaction, patients
should not receive streptokinase if that agent had
been received within the preceding five days to
two years.

100. Hospital Management
• Coronary Care Units
• Diet
• Bowel Management
• Sedation

101. Interventional Cardiology:
• Percutaneous transluminal
coronary angioplasty
• Intracoronary stent

102. Surgical Revascularization
• Coronary Artery Bypass Graft
• Minimal Invasive Coronary Artery
Surgery
• Transmyocardial revascularization

103. Cardiac Rehabilitation
• Medically supervised program
consisting of exercise training,
education on heart healthy living,
and counseling to reduce stress
and help patients return to an
active lifestyle and recover more
quickly

104. Components
• Physician-prescribed
exercise
• Cardiac risk factor
modification (education,
counseling and
behavioral intervention)
• Psychosocial assessment
• Outcomes assessment
• Individualized treatment
plan

105. Complications
• Ventricular Dysfunction and
Congestive Heart Failure
STEMI
left ventricle begins
to dilate results from
expansion of the
infarct
resulting in
disproportionate
thinning and
elongation of the
infarct zone
lengthening of the
noninfarcted
segments occurs
overall chamber
enlargement
HEART FAILURE

106. EARLY COMPLICATIONS
• Hypovolemia
• Cardiogenic Shock
• Right Ventricular Infarction
• Arrhythmias
• Ventricular Premature Beats
• Ventricular Tachycardia and
Fibrillation
• Sinus Bradycardia

107. LATE COMPLICATIONS
• Left Ventricular Aneurysm
• Dressler’s syndrome
• Shoulder hand syndrome

108. Nursing Management of MI

109. Nursing Assessment
• Gather information regarding the patient's chest
pain:
• Evaluate cognitive, behavioral, and emotional
status.
• Prior health status with emphasis on current
medications, allergies
• Analyze information for contraindications for
thrombolytic therapy and PCI.
• Gather information about presence or absence of
cardiac risk factors.
• Identify patient's social support system and
potential caregivers.
• Identify significant other's reaction to the crisis
situation.

110. • Acute pain related to decreased
blood supply to the myocardium

111. • Ineffective tissue perfusion :
cardiopulmonary related to
reduced coronary blood flow from
coronary thrombus and
atherosclerotic plaque

112. • Anxiety related to pain and fear of
death

113. • Risk for decreased cardiac output
related to decrease in LV function

114. • Activity intolerance related to
imbalance between oxygen
demand and supply

115. • Ineffective coping related to life
threatening diagnosis

116. • Risk for bleeding

117. HEALTH EDUCATION

118. BIBLIOGRAPHY
• Braunwald, Fauci,Kasper,Hauser,
Longo,Jameson. Harrison’s Principles of
Internal Medicine. 15th ed. Vol 1. New
York:McGraw-Hill;2001
• K.V Krishnadas. Textbook of Medicine. 5th
ed. Delhi: Jaypee brothers;2008
• Bonow. Mann. Zipes, Libby. Braunwald’s
Heart disease. 9th ed. India; Elsevier
publication; 2011.
• Joyce M Black, Jane Hokanson Hawks.
Medical Surgical Nursing. 8th ed. Vol-2.
India: Saunders Elsevier publishers; 2010