1. Dr . M. Vinod Kumar.
M.D., D.M.(Cardiology)
Interventional Cardiologist

2.  Definition ,pathology and diagnosis
 Risk stratification
 Medical management
 Secondary prevention

3. Applying Classification of Recommendations
and Level of Evidence
Class I Class IIa Class IIb Class III
Benefit >>> Risk Benefit >> Risk Benefit ≥ Risk Risk ≥ Benefit
Additional studies with Additional studies with No additional studies
focused objectives broad objectives needed; needed
needed Additional registry data
would be helpful Procedure/Treatment
Procedure/ Treatment IT IS REASONABLE to should NOT be
SHOULD be perform Procedure/Treatment performed/administered
performed/ procedure/administer MAY BE CONSIDERED SINCE IT IS NOT
administered treatment HELPFUL AND MAY
BE HARMFUL
Level A: Recommendation based on evidence from multiple randomized trials or meta-analyses
Multiple (3-5) population risk strata evaluated; General consistency of direction and magnitude of effect
Level B: Recommendation based on evidence from a single randomized trial or non-randomized studies
Limited (2-3) population risk strata evaluated
Level C: Recommendation based on expert opinion, case studies, or standard-of-care
Very limited (1-2) population risk strata evaluated

4.  ST Elevation Myocardial infarction (STEMI) is a major
public health problem in both the developed and the
developing countries in the world.
 The incidence in the developing countries is now similar
to that in the developed countries.
 Approximately 3-4 per cent of Indians in rural areas and
8-10 per cent in urban areas have CAD.

5.  STEMI is fatal in about one third of the patients, with 50%
deaths occurring in the first hour from ventricular tachy
arrhythmias.
 Time to thrombolysis remains a key modifiable
determinant of mortality in STEMI.

6.  Rapid diagnosis and early risk stratification of patients
presenting with acute chest pain constitute the pillars of
success in STEMI management.
 An efficient regional system of care based on pre-hospital
diagnosis, triage and rapid transportation to the best
available facility holds the key to success of treatment
and significantly improves outcome.

7. Revised Definition of Myocardial Infarction
 Criteria for Acute, Evolving, or Recent MI
 Either of the following criteria satisfies the diagnosis for acute, evolving,
or recent MI:
1. Typical rise and/or fall of biochemical markers of myocardial necrosis
with at least one of the following:
a. Ischemic symptoms
b. Development of pathologic Q waves in the ECG
c. Electrocardiographic changes indicative of ischemia (ST-segment
elevation )
d. Imaging evidence of new loss of viable myocardium or new regional
wall motion abnormality
2. Pathologic findings of an acute myocardial infarction

8. 1. Spontaneous ( primary) myocardial infarction
2. Myocardial infarction secondary
3. Sudden unexpected cardiac death, including
cardiac arrest
4a . Myocardial infarction associated with PCI
4b. Myocardial infarction associated with stent
thrombosis
5. Myocardial infarction associated with CABG

9.  Almost all MIs result from coronary atherosclerosis.
 An ACS develops when the vulnerable or high-risk plaque
undergoes disruption of the fibrous cap.
 Disruption of the plaque is the stimulus for thrombogenesis.
 Following disruption of a vulnerable or high-risk plaque
reduction of flow through the affected epicardial coronary
artery.
 The flow reduction may be caused by a completely occlusive
thrombus leads to STEMI or subtotally occlusive thrombus
leads to UA/NSTEMI.

10. Acute Coronary Syndromes.
Anderson J L et al. Circulation 2011;123:e426-e579
Copyright © American Heart Association

11.  Symptoms such as anginal chest
pain, dyspnoe, palpitation, diaphoresis etc
 ECG: ST segment elevation or new onset LBBB
 Enzymes : CKMB, Trop T and I

12. Electrocardiogram
Show 12-lead ECG results to emergency physician
I IIa IIb III
within 10 minutes of ED arrival in all patients with
chest discomfort (or anginal equivalent) or other
symptoms of STEMI.
I IIa IIb III In patients with inferior STEMI, ECG leads should
also be obtained to screen for right ventricular
infarction.

13. I IIa IIb III Laboratory examinations should be performed as part of the
management of STEMI patients, but should not delay the
implementation of reperfusion therapy.
 Serum biomarkers for cardiac damage
 Complete blood count (CBC) with platelets
 International normalized ratio (INR)
 Activated partial thromboplastin time (aPTT)
 Electrolytes and magnesium
 Blood urea nitrogen (BUN)
 Creatinine
 Glucose
 Complete lipid profile

14. I IIa IIb III Cardiac-specific troponins should be used as the
optimum biomarkers for the evaluation of patients with
STEMI who have coexistent skeletal muscle injury.
For patients with ST elevation on the 12-lead ECG and
I IIa IIb III symptoms of STEMI, reperfusion therapy should be
initiated as soon as possible and is not contingent on a
biomarker assay.

15. 100
Multiples of the URL
50
Cardiac troponin-no reperfusion
20 Cardiac troponin-reperfusion
10 CKMB- no reperfusion
CKMB- reperfusion
5
2
Upper reference limit
1
0 1 2 3 4 5 6 7 8
URL = 99th %tile of
Days After Onset of STEMI Reference Control Group

18.  There is risk stratification within STEMI, but in general, STEMI
is high-risk.
 Important to select greater-risk patients who warrant more
aggressive strategies for prevention of future serious events
such as reinfarction or sudden death.

19.  Occurs in several stages
 Initial presentation
 In-hospital course (CCU, intermediate CU)
 At the time of hospital discharge

20.  Prior angina pectoris  ECG Criteria
 Prior MI  Markedly elevated cardiac
 Female gender enzymes
 Hypertension  Elevated BUN
 History of CHF  Complications
 Hyperlipidemia  VSR/PMD-rupture
 Diabetes  Myocardial rupture

21.  Anterior MI/ Persisting ST elevation
 Q waves in multiple leads
 RVMI + IWMI
 High sum of ST elevation
 Reciprocal ( anterior ) ST depression
 Persisting ST depression
 Prolonged QT
 Conduction defects/ heart block
 Sinus tachycardia/atrial fibrillation

22.  TIMI
 GRACE
 killips
 PURSUIT
 best used to supplement—not replace—clinical judgment
 less useful in atypical presentations, but indeed validated in an
ED population . . .

23. (David A et al. TIMI Risk Score for ………..: An Intravenous nPA for Treatment of Infarcting Myocardium Early II Trial Substudy.
Circulation 2000, 102:2031-2037)

24. CLASS CLINICAL FINDINGS 30 DAY
MORTALITY RATE
Class 1 No rales, no 3rd 2.8%
heart sound
Class 2 Rales in <1⁄2 lung 8.8%
field or presence of
a 3rd heart sound
Class 3 Rales in >1⁄2 lung 14.4%
field–pulmonary
edema
Class 4 Cardiogenic shock– 67%
determined
clinically

26.  The first goal for healthcare professionals is to diagnose in a
very rapid manner whether the patient is having an STEMI or
NSTEMI because therapy differs between the 2 types of
myocardial infarction.

27.  As a general rule, initial therapy for acute myocardial
infarction is directed toward restoration of perfusion as
soon as possible to salvage as much of the jeopardized
myocardium as possible.
 This may be accomplished through medical or mechanical
means, such as PCI or CABG.

28.  If STEMI is present, the decision as to whether the patient will
be treated with thrombolysis or primary PCI should be made
within the next 10 minutes.
 The goal for patients with STEMI should be to achieve a door-
to-drug time of within 30 minutes and a door-to-balloon time
of within 90 minutes.

29.  Critical factors that weigh into the selection of a
reperfusion strategy include the following:
 The time elapsed since the onset of symptoms
 The risk associated with STEMI
 The risk of administering a fibrinolytic
 The time required to initiate an invasive strategy .

30.  Further treatment is based on the following:
 Restoration of the balance between the oxygen supply
and demand to prevent further ischemia
 Pain relief
 Prevention and treatment of any complications that may
arise

31. 1. Airway, Breathing, Circulation (ABC)
2. Vital signs, general observation
3. Presence or absence of jugular venous distension
4. Pulmonary auscultation for rales
5. Cardiac auscultation for murmurs and gallops
6. Presence or absence of stroke

32.  MONA
 Morphine
 Oxygen
 Nitroglycerin
 Aspirin

33.  Pain contribute to the heightened sympathetic activity
 Management of STEMI patients in the emergency
department should aim to relieve pain.

34.  Control of cardiac pain typically uses a combination of
nitrates, analgesics (e.g., morphine), oxygen, and in
appropriately selected patients, beta-adrenergic blocking
agents.

35.  ANALGESICS.
 Although a wide variety of analgesic agents has been
used to treat the pain associated with STEMI, including
meperidine, pentazocine, and morphine.
 Morphine remains the drug of choice, except in patients
with well-documented morphine hypersensitivity.

36.  A dose of 4 to 8 mg intravenously.
 Doses of 2 to 8 mg repeated at intervals of 5 to 15
minutes
 Toxicity —hypotension, depression of respiration, or
severe vomiting.
 Morphine has unequivocal beneficial effects in patients
with pulmonary edema because of peripheral arterial and
venous dilation .

37. Morphine sulfate (2 to 4 mg intravenously with
I IIa IIb III
increments of 2 to 8 mg intravenously repeated at 5 to
15 minute intervals) is the analgesic of choice for
management of pain associated with STEMI.

38.  OXYGEN.
 Hypoxemia results from ventilation-perfusion abnormalities are
sequelae of left ventricular failure.
 Oxygen should be administered to patients with STEMI when
arterial hypoxemia is clinically evident or can be documented by
measurement (e.g., Sao2 < 90%).
 The delivery of 2 to 4 liters/min of 100% oxygen by mask or nasal
prongs for 6 to 12 hours is satisfactory for most patients with mild
hypoxemia.

39.  Oxygen
Arterial oxygen desaturation (SaO2 < 90%)
Class I(B)
Uncomplicated STEMI during the first 6 hours
Class IIa(c)

40.  NITRATES.
 Ability to enhance coronary blood flow by coronary
vasodilation
 Decrease ventricular preload by increasing venous
capacitance.

41. I IIa IIb III Patients with ongoing ischemic discomfort should receive
sublingual NTG (0.4 mg) every 5 minutes for a total of 3
doses, after which an assessment should be made about
the need for intravenous NTG.
I IIa IIb III Intravenous NTG is indicated for relief of ongoing ischemic
discomfort that responds to nitrate therapy, control of
hypertension, or management of pulmonary congestion.

42. Nitroglycerin
I IIa IIb III Nitrates should not be administered to patients with:
• systolic pressure < 90 mm Hg or ≥ to 30 mm Hg
below baseline
• severe bradycardia (< 50 bpm)
• suspected RV infarction.
I IIa IIb III
Nitrates should not be administered to patients who have
received a phosphodiesterase inhibitor for erectile
dysfunction within the last 24 hours (48
hours for tadalafil).

43.  Long-acting oral nitrate preparations should be avoided
in the early course of STEMI because of the frequently
changing hemodynamic status of the patient.

44.  In patients with a prolonged period of waxing and waning
chest pain, intravenous nitroglycerin may help to control
symptoms and correct ischemia, but requires frequent
monitoring of blood pressure.

45.  Relieve ischemic pain, reduce need for analgesics, reduce
infarct size and life-threatening arrhythmias
 Reduce heart rate, decrease myocardial oxyzen demand .

46.  Avoid early intravenous beta blockade in patients
presenting in Killip class II or higher.

47.  Favorable effects with metoprolol, atenolol, carvedilol
and timolol.
 Beta blockers with intrinsic sympathomimetic activity
probably should not be chosen.
 Trial of esmolol in the presence of relative
contraindications.

48. Effects of Metoprolol
COMMIT (N = 45,852) Totality of Evidence (N = 52,411)
Death
13%
P=0.0006
ReMI
30% relative
22%
increase in
P=0.0002
*cardiogenic
shock
VF
15%
P=0.002
Lancet. 2005;366:1622.
*Risk factors for cardiogenic shock :heart failure, age > 70 , systolic blood
pressure < 120, sinus tachycardia > 110 or heart rate < 60, increased time since
onset of STEMI symptoms

49. Beta-Blockers
Oral beta-blocker therapy should be administered promptly
to those patients without a contraindication, irrespective of
concomitant fibrinolytic therapy or performance of primary
PCI. contraindications
1) signs of heart failure,
2) evidence of a low output state,
I IIa IIb III 3) increased risk for cardiogenic shock, or
4) relative contraindications to beta blockade
 1AVB > 0.24 sec,
 2nd- or 3rd-degree heart block
 reactive airway disease

50.  It is reasonable to administer intravenous beta-blockers
promptly to STEMI patients without contraindications,
especially if a tachyarrhythmia or hypertension is present.
 contraindications
signs of heart failure,
evidence of a low output state,
increased risk for cardiogenic shock, or
I
I IIa IIb III
IIa IIb III
relative contraindications to beta blockade
1AVB > 0.24 sec,
2nd- or 3rd-degree heart block
reactive airway disease

51. Beta-Blockers
Recommendations - Class III (A)
• IV beta blockers SHOULD NOT be administered to
STEMI patients who have any of the following:
1) signs of heart failure
2) evidence of a low output state
3) increased risk for cardiogenic shock
4) relative contraindications to beta blockade
 1AVB > 0.24 sec,
 2nd- or 3rd-degree heart block
 reactive airway disease

52.  Aspirin
 Aspirin is useful for the primary prevention of vascular
events
 Effective across the entire spectrum of acute coronary
syndromes
 Part of the initial management strategy for patients with
suspected STEMI.

53.  In a dose of 162 mg or more, aspirin produces a rapid
clinical antithrombotic effect caused by immediate and
near-total inhibition of thromboxane A2 production.
 ISIS-2-->ASA led to 23% reduction in mortality.

54.  Because low doses (40 to 80 mg) take several days to achieve
full antiplatelet effect, at least 162 to 325 mg should be
administered acutely in the emergency department.
 To achieve therapeutic blood levels rapidly, the patient should
chew the tablet to promote buccal absorption rather than
absorption through the gastric mucosa.

55. I IIa IIb III
Aspirin should be chewed by patients who have not
taken aspirin before presentation with STEMI. The
I IIa IIb III
initial dose should be 162 mg (Level of Evidence: A) to
325 mg (Level of Evidence: C)
Although some trials have used enteric-coated aspirin for initial
dosing, more rapid buccal absorption occurs with non–enteric-
coated formulations.

56. Aspirin
A daily dose of aspirin (initial dose of 162 to 325 mg
I IIa IIb III
orally; maintenance dose of 75 to 162 mg) should
be given indefinitely after STEMI to all patients
without a true aspirin allergy.

59. Reperfusion
The medical system goal is to facilitate rapid recognition and
treatment of patients with STEMI such that door-to- needle
(or medical contact–to-needle) time for initiation of
fibrinolytic therapy can be achieved within 30 minutes or that
door-to-balloon (or medical contact–to- balloon) time for PCI
can be kept within 90 minutes.

61. Reperfusion Options for STEMI Patients
Select Reperfusion Treatment.
If presentation is < 3 hours and there is no delay to an invasive
strategy, there is no preference for either strategy.
Fibrinolysis generally preferred
 Early presentation ( ≤ 3 hours from symptom
onset and delay to invasive strategy)
 Invasive strategy not an option
 Cath lab occupied or not available
 Vascular access difficulties
 No access to skilled PCI lab
 Delay to invasive strategy
 Prolonged transport
 Door-to-balloon more than 90 minutes
 > 1 hour vs fibrinolysis (fibrin-specific agent) now

62. Reperfusion Options for STEMI Patients
Select Reperfusion Treatment.
If presentation is < 3 hours and there is no delay to an invasive strategy, there is no
preference for either strategy.
Invasive strategy generally preferred
 Skilled PCI lab available with surgical backup
 Door-to-balloon < 90 minutes
• High Risk from STEMI
 Cardiogenic shock, Killip class ≥ 3
 Contraindications to fibrinolysis, including
increased risk of bleeding and ICH
 Late presentation
 > 3 hours from symptom onset
 Diagnosis of STEMI is in doubt

63. Symptom Onset to Balloon Time and Mortality
in Primary PCI for STEMI
6 RCTs of Primary PCI by Zwolle Group 1994 – 2001
N = 1791
12 P < 0.0001
One-year mortality, %
10
8
6
4
RR = 1.08 [1.01 – 1.16] for each 30 min delay
2 (P = 0.04)
0 0 60 120 180 240 300 360
Symptoms to balloon inflation (minutes)
DeLuca et al. Circulation 2004;109:1223.

64. PCI vs Fibrinolysis for STEMI:
Short Term Clinical Outcomes
35
30 PCI P < 0.0001
Fibrinolysis
Frequency (%)
25
21
20 P < 0.0001
15 P=0.0002 13
P=0.0003 P < 0.0001 P=0.032
9 8
10 7 7 7 7
P=0.0004
6 P < 0.0001 5
4.5
5 2.2
1 2 0 1
0
Death Death, Recurr. Recurr. Total Hemorrh. Major Death
no MI Ischemia Stroke Stroke Bleed MI
SHOCK
data CVA
N = 7739
Keeley et al. The Lancet 2003;361:13.

65.  Fibrinolysis
 The principal goal of fibrinolysis is prompt restoration of full
IRA patency.
 Promote conversion of plasminogen to plasmin, which
subsequently lyses fibrin thrombi.

66.  Fibrinolysis
 Recanalizes thrombotic occlusion associated with STEMI
 Restoration of coronary flow reduces infarct size
 Improves myocardial function.
 Improves survival over the short and the long term.

67.  INTRACORONARY FIBRINOLYSIS.
 In current practice, patients are more likely to be treated
by PCI.
 This has reopened the concept of delivering fibrinolytic
agents via the intracoronary route, but such efforts at
present are largely restricted to adjunctive use during
complicated PCI procedures.

68.  INTRAVENOUS FIBRINOLYSIS
 Streptokinase , tPA,, TNK, rPA
 TNK and rPA - bolus fibrinolytics

69.  WP-4 hr. t-PA is the preferred treatment
 streptokinase t-PA equivalent choices -risk of death is low
, and increased risk of ICH .
 WP-4 to 12 hr . streptokinase and t-PA are equivalent
options, but streptokinase is probably preferable to t-PA
because of cost considerations

70. (Antman EM et al: ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction. Circulation
110:e82, 2004.)
PARAMETER STREPTOKINASE ALTEPLASE RETEPLASE TNK t-PA
Up to 100 mg in 10 U ? 2 (30 min
30-50 mg based
Dose 1.5 MU in 30-60 min 90 min (based on apart) each over
on weight
weight) 2 min
Bolus administration No No Yes Yes
Antigenic Yes No No No
Allergic reactions
hypotension most Yes No No No
common
Systemic fibrinogen
Marked Mild Moderate Minimal
depletion
90-min patency rates (%) ≈50 ≈75 ≈75 ≈75
TIMI grade 3 flow (%) 32 54 60 63
Cost per dose (Rs) 2500 39375 (50mg)

71. GISSI-1: Streptokinase 18% reduction in mortality at 21 d
GUSTO-1: tPA. 15% reduction in 30-day mortality compared
to Streptokinase
GUSTO-3: Reteplase had no benefit over tPA but is easier to
use (double bolus)
ASSENT: TNKase is similar to tPA but with less non-cerebral
bleeding and better mortality with symptoms>4 hrs: Single
bolus, fibrin selective, resistance to PAI-1
*Overall risk of ICH is 0.7%; Strokes occurred in 1.4%

72. Fibrinolysis
In the absence of contraindications, fibrinolytic
I IIa IIb III
therapy should be administered to STEMI patients
with symptom onset within the prior 12 hours and
new or presumably new left bundle branch block
(LBBB).

73. Fibrinolysis
In the absence of contraindications, it is reasonable to
I IIa IIb III
administer fibrinolytic therapy to STEMI patients with
symptom onset within the prior 12 hours and 12-lead
ECG findings consistent with a true posterior MI.
In the absence of contraindications, it is reasonable to
administer fibrinolytic therapy to patients with
symptoms of STEMI beginning in the prior 12 to 24
hours who have continuing ischemic symptoms and ST
elevation > 0.1 mV in ≥ 2 contiguous precordial leads
or ≥ 2 adjacent limb leads.

74. Fibrinolysis
I IIa IIb III Fibrinolytic therapy should not be administered to
asymptomatic patients whose initial symptoms of
STEMI began more than 24 hours earlier.
I IIa IIb III Fibrinolytic therapy should not be administered to
patients whose 12-lead ECG shows only ST-segment
depression, except if a true posterior MI is suspected.

75. Contraindications and Cautions
for Fibrinolysis in STEMI
Any prior intracranial hemorrhage
Absolute
Contraindications Known structural cerebral vascular lesion
(e.g., arteriovenous malformation)
Known malignant intracranial neoplasm (primary
or metastatic)
Ischemic stroke within 3 months EXCEPT acute
ischemic stroke within 3 hours
Suspected aortic dissection
Active bleeding or bleeding diathesis (excluding
menses)
Significant closed-head or facial trauma within 3
months

76. Contraindications and Cautions
for Fibrinolysis in STEMI
Relative • History of chronic, severe, poorly controlled
Contraindications hypertension
• Severe uncontrolled hypertension on
presentation (SBP > 180 mm Hg or DBP > 110
mm Hg)
• History of prior ischemic stroke greater than 3
months, dementia, or known intracranial
pathology not covered in contraindications
• Traumatic or prolonged (> 10 minutes) CPR or
major surgery (< 3 weeks)

77. Contraindications and Cautions
for Fibrinolysis in STEMI
Relative • Recent (< 2 to 4 weeks) internal bleeding
Contraindications • Noncompressible vascular punctures
• For streptokinase/anistreplase: prior exposure (>
5 days ago) or prior allergic reaction to these
agents
• Pregnancy
• Active peptic ulcer
• Current use of anticoagulants: the higher the
INR, the higher the risk of bleeding

78.  Fibrinolytics given between 12 and 24 hours
 No mortality benefit - LATE and EMERAS trials
 Increases risk of cardiac rupture (elderly population)
 Preferable to restrict late fibrinolytic administration to
patients younger than 65 years with ongoing
ischemia, especially those with large anterior infarctions.

79.  Delays in the administration of thrombolysis often occur
because of the following factors:
 Delay in obtaining an ECG
 Interpretation
 Lack of immediate availability of thrombolytic agents

80.  EFFECT OF FIBRINOLYTIC THERAPY ON MORTALITY.
 Early intravenous fibrinolysis undoubtedly improves survival.
 The gretest benefit when administered as early as possible.
 Most dramatic results when given less than 2 hours after
symptoms begin.
 18% - 25% reduction in short-term mortality.

81.  Hazards of fibrinolysis
 Stroke (0.9–1.0%) - firstday after treatment, Largely
attributable to cerebral haemorrhage.
 Advanced age, lower weight, female gender, prior
cerebrovascular disease, and systolic and diastolic
hypertension on admission are significant predictors of
intracranial haemorrhage.
 Major non-cerebral bleeds (bleeding complications requiring
blood transfusion or that are life-threatening) occur in 4–13%
of the patients treated.

82.  Streptokinase may be associated with hypotension, but
severe allergic reactions are rare.
 Re-administration of streptokinase should be avoided
because of antibodies, which can impair its activity, and
because of the risk of allergic reactions.

83. Primary PCI for STEMI:
General Considerations
Patient with STEMI (including posterior MI) or MI with
new or presumably new LBBB
PCI of infarct artery within 12 hours of symptom onset
Balloon inflation within 90 minutes of presentation
I IIa IIb III
Skilled personnel available (individual performs > 75
procedures per year)
Appropriate lab environment (lab performs > 200
PCIs/year of which at least 36 are primary PCI for
STEMI)
Cardiac surgical backup available

84. Primary PCI for STEMI:
Specific Considerations
Primary PCI should be performed in patients less than
I IIa IIb III 75 years old with ST elevation or LBBB who develop
shock within 36 hours of MI and are suitable for
revascularization that can be performed within 18
hours of shock.

85. Primary PCI for STEMI:
Specific Considerations
Primary PCI is reasonable in selected patients 75 years or
I IIa IIb III older with ST elevation or LBBB who develop shock within
36 hours of MI and are suitable for revascularization that
can be performed within 18 hours of shock.

86. Primary PCI for STEMI:
Specific Considerations
It is reasonable to perform primary PCI for patients
with onset of symptoms within the prior 12 to 24
hours and 1 or more of the following:
a. Severe CHF
I IIa IIb III
b. Hemodynamic or electrical instability
c. Persistent ischemic symptoms.

89. PCI After Fibrinolysis
I IIa IIb III
It is reasonable to perform routine PCI in patients with
left ventricular ejection fraction (LVEF) ≤ 0.40, CHF, or
serious ventricular arrhythmias.
I IIa IIb III
It is reasonable to perform PCI when there is
documented clinical heart failure during the acute
episode, even though subsequent evaluation shows
preserved LV function (LVEF > 0.40).
I IIa IIb III
Routine PCI might be considered as part of an
invasive strategy after fibrinolytic therapy.

90. Assessment of Reperfusion
I IIa IIb III
It is reasonable to monitor the pattern of ST elevation,
cardiac rhythm and clinical symptoms over the 60 to 180
minutes after initiation of fibrinolytic therapy.
Noninvasive findings suggestive of reperfusion include:
 Relief of symptoms
 Maintenance and restoration of hemodynamic and/or
electrical instability
 Reduction of ≥ 50% of the initial ST-segment elevation
pattern on follow-up ECG 60 to 90 minutes after initiation of
therapy.

91.  Flow in the IRA angiographically
 Gd. 0, complete Occlussion
 Gd. 1, some penetration
 Gd.2, entire vessel with
Impaired flow
 Gd.3, entire vessel with
Normal flow

92. Rescue PCI
It is reasonable to perform rescue PCI
for patients with one or more of the following:
Hemodynamic or electrical instability
Persistent ischemic symptoms or
Fibrinolytic therapy has failed (ST-segment
elevation < 50%, resolved after 90 minutes
following initiation of fibrinolytic therapy in the lead
showing the worst initial elevation),
A moderate or large area of myocardium at risk
(Class II; LOE -B).

93.  Coronary artery bypass graft surgery should be
considered when recurrent ischemia occurs in patients
with STEMI whose coronary artery anatomy is not
suitable for PCI. This is a class I level b indication

94.  Coronary angiography should not be performed in
patients following fibrinolytic therapy with extensive
comorbidities in whom the risks of revascularization are
likely to outweigh the benefits (Class III; LOE, C).

95.  Establishing & maintaining patency of IRA.
 For prevention of
 DVT
 pulmonary embolism
 ventricular thrombus
 cerebral embolization

96. • Anticoagulant regimens with established efficacy include:
UFH
Enoxaparin
Fondaparinux
• Patients undergoing reperfusion with fibrinolytics should
receive anticoagulant therapy for a minimum of 48 hours
(Class IIa; C)
• Preferably for the duration of the index hospitalization,
up to 8 days when using regimens other than
unfractionated heparin (UFH) (Class IIa; A).

97.  Trials shown that more prolonged anticoagulant therapy
is beneficial (duration of index hospitalization) in patients
receiving thrombolytic therapy

98.  Recommendations for Anticoagulant Therapy
ANTICOAGULATION WITH FIBRINOLYSIS.
 A regimen of UFH bolus at 60 U/kg to a maximum of 4000
U, followed by an initial infusion of 12 U/kg/hr to a maximum
of 1000 U/hr given for 48 hours.
 Administration of enoxaparin or fondaparinux is preferred
when administration of an anticoagulant for longer than 48
hours is planned for patients with STEMI treated with a
fibrinolytic.

99. ADJUNCTIVE ANTICOAGULATION FOR PRIMARY
PERCUTANEOUS INTERVENTION.
 UFH is recommended for patients undergoing primary PCI .
PATIENTS TREATED WITHOUT REPERFUSION THERAPY.
 In STEMI patients not receiving reperfusion
therapy, fondaparinux reduces the composite of death or
recurrent MI without an increase in severe bleeding as
compared with placebo or UFH

101.  Recommendations for Antiplatelet Therapy
 During the maintenance phase of antiplatelet therapy
following STEMI, the dose of aspirin should be reduced to 75
to 162 mg to minimize bleeding risk.
 If true aspirin allergy is present, other antiplatelet agents such
as clopidogrel (loading dose, 300 to 600 mg; maintenance
dose, 75 mg/day) or ticlopidine (loading dose, 500 mg;
maintenance dose, 250 mg twice daily) can be substituted.

102.  The addition of a P2Y12 inhibitor to aspirin is warranted for most
patients with STEMI.
 Based on the results of the COMMIT and CLARITY-TIMI 2 trials,
 Clopidogrel at 75 mg/day orally is an alternative for all patients with
STEMI, regardless of whether they receive fibrinolytic therapy,
undergo primary PCI, or do not receive reperfusion therapy. (Class I;
lOE, B).
 The available data suggest that a loading dose of 300 mg of
clopidogrel should be given to patients younger than 75 years of age
who receive fibrinolytic therapy.

104. In patients for whom PCI is planned, clopidogrel should be started
and continued:
• ≥ 1 month after bare-metal stent
• ≥ 3 months after sirolimus-eluting stent
• ≥ 6 months after paclitaxel-eluting stent
• Up to 12 months in absence of high risk for
bleeding.

105. Thienopyridines
In patients taking clopidogrel in whom CABG is
I IIa IIb III planned, the drug should be withheld for at least 5
days, and preferably for 7 days, unless the urgency
for revascularization outweighs the risk of excessive
bleeding.

106. Glycoprotein IIb/IIIa Inhibitors
I IIa IIb III It is reasonable to start treatment with abciximab
as early as possible before primary PCI (with or
without stenting) in patients with STEMI.
I IIa IIb III Treatment with tirofiban or eptifibatide may be
considered before primary PCI (with or without
stenting) in patients with STEMI.

107.  Favorable impact on
 ventricular remodeling
 Improvement in hemodynamics
 Reductions in congestive heart failure
 Angiotensin-converting enzyme inhibitors
 Angiotensin II receptor blockers
 Aldosterone blockade

108.  For high-risk patients following STEMI
 EF ≤40%,
 clinical HF
 DM(Class I; lOE, A).
 EPHESUS trial
 Eplerenone, 25 mg/day titrated to 50 mg/day
 Mean follow-up 16 months, there was a 15% reduction in the
RR of mortality.

109. ACE/ARB: Within 24 Hours
I IIa IIb III
An ACE inhibitor should be administered orally
within the first 24 hours of STEMI to the following
patients without hypotension or known class of
contraindications:
• Anterior infarction
 Pulmonary congestion
 LVEF < 0.40
I IIa IIb III
An ARB should be given to ACE-intolerant patients with
either clinical or radiological signs of HF or LVEF < 0.40.

110. ACE/ARB: Within 24 Hours
I IIa IIb III An ACE inhibitor administered orally can be useful within
the first 24 hours of STEMI to the following patients
without hypotension or known class contraindications:
 Anterior infarction
 Pulmonary congestion
 LVEF < 0.40.
I IIa IIb III
An intravenous ACE inhibitor should not be given to
patients within the first 24 hours of STEMI because of the
risk of hypotension (possible exception: refractory
hypotension).

111.  Immediate-release preparation of nifedipine increased risk of in-
hospital mortality
 Verapamil & diltiazem can be given for relief of ongoing ischemia
or slowing of a rapid ventricular response in AF in patients with
contraindication to beta blockers.
 INTERCEPT trial compared 300 mg of diltiazem with placebo and
Diltiazem did not reduce cardiac death, nonfatal
reinfarction, during a 6-month follow-up

112.  Statins
 Statins should be used in the secondary prevention of patients with
CAD.
 In addition to lowering low-density lipoprotein (LDL)
cholesterol, statins also improve endothelial function, have
antiplatelet effects, and reduce inflammation.
 Data are not clear regarding the benefits of early statin use.
 STEMI patients are more likely to be on statin therapy in the post MI
period if treatment is initiated during the index hospitalization.
 An LDL goal of less than 70 mg/dL should be achieved.

113.  It is reasonable to use an insulin based regimen to achieve and
maintain glucose levels less than 180 mg/dl while avoiding
hypoglycemia for patients with STEMI with either a
complicated or uncomplicated course
Class IIa(B)

114. GENERAL MEASURES.
 A calm, quiet atmosphere allay anxiety and reduce
sympathetic tone, ultimately leading to a reduction in
hypertension, tachycardia, and arrhythmias.
 During the first 4 to 12 hours after admission patients should
receive nothing by mouth or a clear liquid diet.
 The diet should be enriched in foods that are high in
potassium, magnesium, and fiber but low in sodium.

115.  Haloperidol, a butyrophenone, can be used safely in patients
with STEMI, beginning with a dose of 2 mg intravenously for
mildly agitated patients and 5 to 10 mg for progressively more
agitated patients.
 Hypnotics, such as temazepam, 15 to 30 mg, or an equivalent,
should be provided as needed for sleep.
 Stool softener should be used to prevent constipation and
straining.

116.  Physical Activity
 In the absence of complications, patients with STEMI need not
be confined to bed for more than 12 hours and, unless they
are hemodynamically compromised.
 Progression of activity should be individualized depending on
the patient’s clinical status, age, and physical capacity.

117.  Myocardial dysfunction frequently occurs during the
acute and subacute phases following STEMI.
 Cardiogenic shock complicates 6–10% of all cases of
STEMI and remains a leading cause of death, with
hospital mortality rates approaching 50%.

118.  Heart failure
 Hypotension
 Pulmonary congestion
 Low output states
 Cardiogenic shock
 The diagnosis of heart failure is based on typical symptoms
such as dyspnoea, signs such as sinus tachycardia, a third heart
sound or pulmonary rales, and some objective evidence of
cardiac dysfunction, such as LV dilatation and reduced ejection
fraction.

122.  Mechanical Causes of Heart Failure
 Free wall rupture.
 Rupture of the interventricular septum.
 Rupture of a papillary muscle.

124.  first day and as late as 6 weeks after STEMI
 Radiation of the pain to either trapezius ridge.
 Treatment consists of aspirin doses of 650 mg orally every
4 to 6 hours may be necessary.
 NSAIDs and steroids should be avoided

125.  Anticoagulation- heparin to elevate the aPTT to 1.5 to 2
times that of control, followed by a minimum of 3 to 6
months of warfarin in the following clinical situations:
 An embolic event has already occurred or
 The patient has a large anterior infarction whether or not a
thrombus is visualized echocardiographically

126. CATEGORY ARRHYTHMIA OBJECTIVE OF TREATMENT THERAPEUTIC OPTIONS
Ventricular Correction of electrolyte deficits and Potassium and magnesium
premature beats increased sympathetic tone solutions, beta blocker
Ventricular Prophylaxis against ventricular fibrillation, Antiarrhythmic agents;
tachycardia restoration of hemodynamic stability cardioversion/defibrillation
Electrical Ventricular Defibrillation; bretylium
instability Urgent reversion to sinus rhythm
fibrillation tosylate
Accelerated Increase sinus rate (atropine,
Observation unless hemodynamic function
idioventricular atrial pacing); antiarrhythmic
is compromised
rhythm agents
Atrial overdrive pacing;
Nonparoxysmal Search for precipitating causes (e.g.,
antiarrhythmic agents;
atrioventricular digitalis intoxication); suppress arrhythmia
cardioversion relatively
junctional only if hemodynamic function is
contraindicated if digitalis
tachycardia compromised
intoxication present

127. CATEGORY ARRHYTHMIA OBJECTIVE OF TREATMENT THERAPEUTIC OPTIONS
Antipyretics; analgesics; consider beta
Reduce heart rate to blocker unless congestive heart failure
Sinus
diminish myocardial present; treat latter if present with
tachycardia
oxygen demands anticongestive measures (diuretics,
afterload reduction)
Pump failure,
excessive
sympathetic Verapamil, digitalis glycosides;
stimulation Atrial fibrillation Reduce ventricular rate; anticongestive measures (diuretics,
and/or atrial
restore sinus rhythm afterload reduction); cardioversion;
flutter
rapid atrial pacing (for atrial flutter)
Paroxysmal Vagal maneuvers; verapamil, cardiac
Reduce ventricular rate;
supraventricular glycosides, beta-adrenergic blockers;
restore sinus rhythm
tachycardia cardioversion; rapid atrial pacing

128. CATEGORY ARRHYTHMIA OBJECTIVE OF TREATMENT THERAPEUTIC OPTIONS
Acceleration of heart rate only if
Sinus bradycardia hemodynamic function is Atropine; atrial pacing
compromised
Bradyarrhyth
mias and
conduction Acceleration of sinus rate only if
disturbances Junctional escape loss of atrial “kick” causes Atropine; atrial pacing
rhythm
hemodynamic compromise
Atrioventricular
block and
Insertion of pacemaker
intraventricular
block

129. At time of discharge patient should be on:
 ASA unless contra-indication
 Clopidogrel if PCI/NSTEMI (duration minimum1 year)
 Longer duration of clopidogrel if DES in critical location or
complex lesion
 -blocker unless contra-indication
 ACE inhibitor for CHF or LV dysfunction
 All for vascular protection?
 Statin for LDL to < 70mg%(minimum 50% reduction)

130.  High Risk  Complicated MI
 extensive ECG changes  CHF/ flash pulmonary
 anterior/ infero-posterior/ edema
prior MI
 shock
 heart block
 Residual ischaemia
 post MI angina
 RBBB
 positive TMT/ perfusion scan  sustained ventricular
 non-Q MI arrhythmias
 ischaemia at a distance
 Anxiety/ physical labor/
young age

131.  Exercise Testing
 Performed either in the hospital or early after discharge in
patients not selected for cardiac catheterization and without
high-risk features to assess the presence and extent of
inducible ischemia Class I (B)
 Exercise testing might be considered before discharge of
patients recovering from STEMI to guide the post discharge
exercise prescription or to evaluate the functional
significance of a coronary lesion previously identified at
angiography Class IIb (C)

132.  Sub maximal protocol
Target workload =5 METS, 70 % MPHR or symptom
limited
 Predictors of poor outcome
Ischemic ST depression > 1 mm is inconsistent
predictor of mortality
poor exercise tolerance < 3 minutes doubles one
year mortality ( 7% to14%)
Inability to exercise or contra-indication to TMT
identifies High Risk patient.

133. Late Risk Stratification - 4 to 8 weeks
(Assessment of residual ischaemia)
 TMT
 Stress echocardiography
 Adenosine/Dipyridamole Perfusion imaging
 Un-interpretable ECG
 Equivocal TMT
 Inability to exercise

135.  Smoking Goal: Complete Cessation
 With in 2yrs risk of nonfatal MI falls to normal
 Blood pressure control:
 Goal: < 140/90 mm Hg or <130/80 mm Hg if chronic kidney
disease or diabetes
 Physical activity:
 Minimum goal: 30 minutes 3 to 4 days per week;
 Optimal daily

136.  Weight management:
 Goal: BMI 18.5 to 24.9 kg/m2
 Waist circumference: Women < 35 in. Men: < 40 in.
 Diabetes management:
 Goal: HbA1c < 7%
 Lipid management: Primary goal: LDL-C <70mg%
 Start dietary therapy in all patients (< 7% of total calories as saturated
fat and < 200 mg/d cholesterol). Promote physical activity and weight
management. Encourage increased consumption of omega-3 fatty
acids.
 Assess fasting lipid profile in all patients, preferably within 24 hours of
STEMI.

137.  Hormone therapy:
 It is recommended that not starting hormone therapy with
estrogen plus progestin after STEMI and discontinuing it in
postmenopausal women after STEMI.
Class III (A)
 Antioxidant vitamins:
 Such as vitamin E and/or vitamin C supplements should not
be prescribed to patients recovering from STEMI to prevent
cardiovascular disease

138.  Psychosocial status of the patient should be
evaluated, including inquiries regarding symptoms of
depression, anxiety, or sleep disorders and the social support
environment. Class I (C)
 Treatment with cognitive-behavioral therapy and selective
serotonin reuptake inhibitors can be useful for STEMI patients
with depression that occurs in the year after hospital
discharge. Class IIa (A)

139. ( Yusuf, S. Two decades of progress in preventing vascular disease. Lancet 2002; 360: 2-3).
RRR 2yr Event Rate
None 8%
ASA 25% 6%
-Blockers 25% 4.5%
Lipid lowering 30% 3.0%
ACE-inhibitors 25% 2.3%
Cumulative relative risk reduction if all four drugs are used is about 75%

141. THANK YOU