slSTEMI

1. DCARD STUDENT, DMCH

2. Coronary Artery Disease
 Atherosclerotic
 Non-atherosclerotic
1. Congenital anomalies
2. Embolus
3. Dissection
4. Spasm
5. Trauma
6. Arteritis
7. Metabolic disorders
8. Intimal proliferation
9. External compression
10. Thrombosis without underlying atherosclerotic plaque
11. Substance abuse
12. Myocardial oxygen demand-supply disproportion
13. Intramural coronary artery disease (small-vessel disease)

3. Acute Coronary Syndrome
Drill of the Month 3

4. Recognizing and Managing
Acute Coronary Syndrome
Overview:
 Definitions
 Causes
 Risk Factors
 Symptoms
 Assessment and care
Drill of the Month 4

5. Drill of the Month 5
Acute Coronary Syndrome:
Definition
 Acute coronary syndrome
 Umbrella term: includes group of clinical
symptoms of AMI( ST elevated or Non-ST
elevated) and Unstable angina

6. ACS PATHOPHYSIOLOGY
 Disruptions of coronary artery
plaque -> platelet
activation/aggregation
/activation of coagulation
cascade -> endothelial
vasoconstriction ->intraluminal
thrombus/embolisation ->
obstruction -> ACS
 Severity of coronary vessel
obstruction & extent of
myocardium involved
determines characteristics of
clinical presentation

8. Drill of the Month 8
Acute Coronary Syndrome: Causes
 Causes: Plaque
 Made up of lipids, accumulates in arteries
 Narrows arteries and blocks blood flow
 Pain from restricted blood flow causes
angina
 Breaks away from arterial wall, blocks artery
or causes a clot resulting in heart attack

9. Universal definition of myocardial
infarction
 A combination of criteria is required to meet the diagnosis of acute
MI, namely the detection of an increase and/or decrease of a cardiac
biomarker, preferably high-sensitivity cardiac troponin, with at least
one value above the 99th percentile of the upper reference limit and
at least one of the following:
(1) Symptoms of ischaemia.
(2) New or presumed new significant ST-T wave changes or left
bundle branch block on 12-lead ECG.
(3) Development of pathological Q waves on ECG.
(4) Imaging evidence of new or presumed new loss of viable
myocardium or regional wall motion abnormality.
(5) Intracoronary thrombus detected on angiography or autopsy.

10. Types
 Type 1 MI
Type 1 MI is characterized by atherosclerotic plaque
rupture, ulceration, fissure, erosion or dissection
with resulting intraluminal thrombus in one or more
coronary arteries leading to decreased myocardial
blood flow and/or distal embolization and
subsequent myocardial necrosis.

11.  Type 2 MI
Type 2 MI is myocardial necrosis in which a
condition other than coronary plaque instability
contributes to an imbalance between myocardial
oxygen supply and demand. Mechanisms include
coronary artery spasm, coronary endothelial
dysfunction, tachyarrhythmias, bradyarrhythmias,
anaemia, respiratory failure, hypotension and
severe hypertension, injurious effects of
pharmacological agents and toxins.

13. Definition
 STEMI is a clinical syndrome defined by
characteristic symptoms of myocardial
ischemia in association with persistent
electrocardiographic (ECG) ST elevation
and subsequent release of biomarkers of
myocardial necrosis.

14. Epidemiology
 At present, STEMI comprises approximately
25% to 40% of MI presentations.

15. MI Classifications
 MI’s can be subcategorized by anatomy
and clinical diagnostic information.
Anatomic
 Transmural and Subendocardial
Diagnostic
 ST elevations (STEMI) and non ST
elevations (NSTEMI).

16. Risk Factors
 The presence of any risk factor is
associated with doubling the risk of an
MI.
Non Modifiable
 Age
 Gender
 Family history

17. Risk Factors
Modifiable
 Smoking
 Diabetes
 Hypertension
 Hyperlipidemia
 Obesity
 Physical Inactivity

18. symptoms
 The most common initial manifestation is
chest pain or discomfort of typical
charrecteristics.
 Anxiety or fear of impending death
 Nausea/vomiting
 Breathlessness
 Collapse/syncope

19. signs
 Signs of sympathetic activation-
pallor,sweating,tachycardia
 Signs of vagal activation-
vomiting,bradycardia
 Signs of impaired myocardial function-
hypotension,oliguria,cold periphery.
Narrow pulse pressure
raisedJVP
third heart sound
lung crepitation
 Sign of tissue damage-
Fever
 Complications-
murmur
Pericardial rub

20. Diagnosis:
 It is based on :
Symptoms
Classical ECG finding
Raising titre of cardiac enzymes
 The classic ECG findings: ST segment
elevation, followed by T wave inversion
and Q waves.

21. STEMI
 Diagnostic ST elevation in the absence
of left ventricular (LV) hypertrophy or left
bundle-branch block (LBBB) is defined
as:
new ST elevation at the J point in at least 2
contiguous leads of 2 mm (0.2 mV) in men
or 1.5 mm (0.15 mV) in women in leads V2–
V3 and/or of 1 mm (0.1 mV) in other
contiguous chest leads or the limb leads.

22.  The majority of patients will evolve ECG
evidence of Q-wave infarction.
 New LBBB at presentation interfere with
ST-elevation analysis, and not a
diagnostic criteria of AMI in isolation.

23. STEMI
 ST segment elevations
 T wave changes
 Q wave development
 Enzyme elevations
 Reciprocals

24.  The laboratory diagnosis of myocardial
infarction:
 Cardiac Troponin-are the most sensitive and
specific marker of myocardial necrosis.
 CK-MB
 myoglobin

26. •Blood tests: used to evaluate kidney and thyroid
function as well as to check cholesterol levels and the
presence of anemia.
•Chest X-ray: shows the size of heart and whether
there is fluid build up around the heart and lungs.
•Echocardiogram: shows a graphic outline of the
heart’s movement
•Ejection fraction (EF): determines how well heart
pumps with each beat.
Other Tests

27. Community Preparedness and
System Goals for Reperfusion
Therapy

28. Reperfusion Therapy for
Patients with STEMI

31. 1) Primary PCI in STEMI

32. Primary PCI in STEMI

34. 2) Aspiration Thrombectomy and
recent advances

35. Aspiration Thrombectomy
Current ACCF/AHA guidelines recommend routine
thrombus aspiration before primary PCI in STEMI
(Class IIa) based on the available evidence
supporting this therapy.
I IIa IIb III

37. 3) Antiplatelet Therapy to Support
Primary PCI for STEMI and recent
advances

38. Antiplatelet drugs
Oral Intravenous
 Aspirin
 Clopidogrel/prasuegrel/ticagre
lor
 Abciximab
 Eptifibatide
 Tirofiban

39. Antiplatelet Therapy
 Class I
1. Aspirin 162 to 325 mg should be given before
primary PCI. (LOE: B)
2. After PCI, aspirin should be continued
indefinitely.(81 to 325 mg daily maintenance dose)
(LOE: A)
3. A loading dose of a P2Y12 receptor inhibitor should
be given as early as possible or at time of primary
PCI to patients with STEMI. Options include:
a. Clopidogrel 600 mg (LOE: B); or
b. Prasugrel 60 mg(LOE: B); or
c. Ticagrelor 180 mg. (LOE: B)

40. Antiplatelet Therapy
4. P2Y12 inhibitor therapy should be given for 1
year to patients with STEMI who receive a stent
(BMS or DES) during primary PCI using the
following maintenance doses:
a. Clopidogrel 75 mg daily (Level of Evidence:
B);or
b. Prasugrel 10 mg daily (Level of Evidence: B);
or
c. Ticagrelor 90 mg twice a day. (Level of
Evidence: B)

41.  Class III: Harm
1. Prasugrel should not be
administered to patients with a
history of prior stroke or transient
ischemic attack. (LOE: B)

42. 5) Anticoagulant Therapy to Support Primary
PCI And recent advances

43. Commonly used anticoagulants
 Unfractionated heparin
 Bivaluridin
 fondaparinux

44. Anticoagulant Therapy to Support Primary
PCI: Recommendations
 Class I
1. For patients with STEMI undergoing primary PCI,
the following supportive anticoagulant regimens
are recommended:
a. UFH, with additional boluses administered as
needed to maintain therapeutic activated clotting
time levels, taking into account whether a GP
IIb/IIIa receptor antagonist has been administered
(LOE: C); or
b. Bivalirudin with or without prior treatment with
UFH.(LOE: B)

45. Anticoagulant Therapy to Support Primary
PCI: Recommendations
 Class IIa
1. In patients with STEMI undergoing PCI who are
at
high risk of bleeding, it is reasonable to use
bivalirudin monotherapy in preference to the
combination of UFH and a GP IIb/IIIa receptor
antagonist.
(Level of Evidence: B)
 Class III: Harm
1. Fondaparinux should not be used as the sole
anticoagulant to support primary PCI because
of the risk of catheter thrombosis.304 (Level of
Evidence: B)

46. Residual risk and use of oral
anticoagulants
 Patients with ACS remain at a significant risk
of recurrent ischemic events after initial
revascularization despite optimal medical
therapy and aggressive risk factor
modification.
 1 in 10 patients experiences a significant
atheroembolic event (cardiac death,
myocardial infarction or stroke) within a year
of the first ACS episode.

47.  This is felt to be secondary to a persistent
thrombogenic state that extends well beyond the
initial ACS event.
 New oral anticoagulants have emerged in the
last decade with the potential to minimize
residual risk ie. Rivaroxaban

48. 1) Fibrinolytic Therapy When There Is an
Anticipated Delay to Performing Primary PCI
Within 120 Minutes of FMC

49. Indications for Fibrinolytic
Therapy When There Is a >120-
Minute Delay From FMC to
Primary PCI

50. Fibrinolytic drugs
 Tenecteplase
Alteplase
Reteplase
 streptokinase

51. Fibrinolytic Agents
Fibrin specific:
1.Tenecteplase(TNK-tPA)
Dose: single I/V weight based bolus. 30mg for <60kg;
35mg for 60-69kg;40mg for 70-79kg; 45mg for 80-
89kg; 50mg for >90kg
2.Reteplase(rPA)
Dose: 10U + 10U I/V bolus given 30 min apart
3.Alteplase(tPA)
Dose: bolus 15mg, infusion 0.75mg/kg for 30 min(max
50mg), then 0.5mg/kg(max 35mg) over next 60 min(
total dose not to exceed 100 mg)
Non-Fibrin specific:
1. Streptokinase
Dose: 1.5 million unit I/V given over 30-60 min

52. Contraindications and Cautions for
Fibrinolytic
Therapy in STEMI
Absolute contraindications
 Any prior ICH
 Known structural cerebral vascular lesion (eg, arteriovenous
 malformation)
 Known malignant intracranial neoplasm (primary or metastatic)
 Ischemic stroke within 3 mo
EXCEPT acute ischemic stroke within 4.5 h
 Suspected aortic dissection
 Active bleeding or bleeding diathesis (excluding menses)
 Significant closed-head or facial trauma within 3 mo
 Intracranial or intraspinal surgery within 2 mo
 Severe uncontrolled hypertension (unresponsive to emergency
therapy)
 For streptokinase, prior treatment within the previous 6 mo

53. Contraindications and Cautions for Fibrinolytic
Therapy in STEMI
Relative contraindications
 History of chronic, severe, poorly controlled hypertension
 Significant hypertension on presentation (SBP 180 mm Hg or DBP
 110 mm Hg)
 History of prior ischemic stroke 3 mo
 Dementia
 Known intracranial pathology not covered in absolute
contraindications
 Traumatic or prolonged (10 min) CPR
 Major surgery (3 wk)
 Recent (within 2 to 4 wk) internal bleeding
 Noncompressible vascular punctures
 Pregnancy
 Active peptic ulcer
 Oral anticoagulant therapy

54. 2) Adjunctive Antithrombotic
Therapy With Fibrinolysis

55. Aspirin (162- to 325-mg loading dose)
and clopidogrel (300-mg loading dose for
patients ≤75 years of age, 75-mg dose for
patients >75 years of age) should be
administered to patients with STEMI who
receive fibrinolytic therapy.
I IIa IIb III

56. • aspirin should be continued indefinitely
and
In patients with STEMI who receive fibrinolytic
therapy:
I IIa IIb III
• clopidogrel (75 mg daily) for at least
14 days
• and up to 1 year
I IIa IIb III
I IIa IIb III

57. Adjunctive Antiplatelet Therapy With
Fibrinolysis
It is reasonable to use aspirin 81 mg per
day in preference to higher maintenance
doses after fibrinolytic therapy.
I IIa IIb III

58. 3) Adjunctive Anticoagulant Therapy With
Fibrinolysis

59. I IIa IIb III
Patients with STEMI undergoing
reperfusion with fibrinolytic therapy
should receive anticoagulant therapy for
a minimum of 48 hours, and preferably
for the duration of the index
hospitalization, up to 8 days or until
revascularization if performed.

60. a.UFH adm. as a weight-adjusted
intravenous bolus and infusion to obtain
an aPTT time of 1.5 to 2.0 times control,
for 48 hours or until revascularization;
b.Enoxaparin adm. a/c to age, weight, and
creatinine clearance, given as an i.v
bolus, followed in 15 min. by s/c inj. for
the duration of the index hospitalization,
up to 8 days or until revascularization; or
I IIa IIb III
I IIa IIb III
Recommended regimens include:

61.  Fondaparinux administered with initial i.v
dose, followed in 24 hrs by daily s/c inj. if
the estimated creatinine clearance is
greater than 30 mL/min, for the duration of
the index hospitalization, up to 8 days or
until revascularization.
I IIa IIb III

62. Enoxaparin:
● If age 75 y: 30-mg IV bolus, followed in 15 min by 1 mg/kg
subcutaneously every 12 h (maximum 100 mg for the first 2
doses)
● If age 75 y: no bolus, 0.75 mg/kg subcutaneously every 12 h
(maximum 75 mg for the first 2 doses)
● Regardless of age, if CrCl 30 mL/min: 1 mg/kg
subcutaneously every 24 h
● Duration: For the index hospitalization, up to 8 d or until
revascularization

63. Coronary Angiography in Patients Who
Initially Were Managed With Fibrinolytic
Therapy or Who Did Not Receive
Reperfusion

64. Indications for Coronary Angiography in Patients
Who Were Managed With Fibrinolytic Therapy or
Who Did Not Receive Reperfusion Therapy

65. CABG in Patients With
STEMI

66. Urgent CABG is indicated in patients with
STEMI and coronary anatomy not
amenable to PCI who have ongoing or
recurrent ischemia, cardiogenic shock,
severe HF, or other high-risk features.
CABG is recommended in patients with
STEMI at time of operative repair of
mechanical defects.
I IIa IIb III
I IIa IIb III

71. Other modalities
 Monoclonal antibodies-Inclacumab
 Stem cell therapy

72. Complications of AMI:
Within minutes to 3 days of onset:
. Arrythmias :75-95% i) ventricular
fibrillation ; ii) block of A-V bundles and its
branches causing acute heart failure.
. Cardiogenic shock 10-15%(usually in
large infarct) causing acute heart failure.
. Thrombotic complication- 15-40% mural
thrombus over infarct area or Atrial
thrombus, causing embolism to brain,
kidney etc.
.Rupture of heart.

73.  3-14 days:
. Rupture
Site of rupture is ventricular wall, papillary
muscle & interventricular septum.
. Acute fibrinous or hemorrhagic pericarditis
- over infarct area.
After weeks or months:
. Chronic heart failure
. Cardiac aneurysm, which may rupture
producing hemopericardium and death.

74. . Dressler’s syndrome
autoimmune pericarditis, pericardial
friction rub and pleurisy.

76.  Treatment of Cardiogenic Shock:
 Recommendations Class I
1. Emergency revascularization with either PCI or CABG is
recommended in suitable patients with cardiogenic shock due
to pump failure after STEMI irrespective of the time delay from
MI onset.
2. In the absence of contraindications, fibrinolytic therapy
should be administered to patients with STEMI and
cardiogenic shock who are unsuitable candidates for either
PCI or CABG
 Class IIa 1. The use of intra-aortic balloon pump (IABP)
counterpulsation can be useful for patients with cardiogenic
shock after STEMI who do not quickly stabilize with
pharmacological therapy
 Class IIb 1. Alternative LV assist devices for circulatory
support may be considered in patients with refractory
cardiogenic shock.

77. Severe heart failure
 Diurertics
 Vasodilators
 Inotropes
 ACEi/ARB
 Beta blocker

78. arrythmia
Ventricular arrythmias
AF and other
supraventricular arrythmia
 Immediate defibrillation
or cardioversion in VF or
pulseless sustained VT
 Antiarrythmic drugs for
VT with pulse
 Correction of electrolytes
and acid base imbalance
 ICD before discharge(in
selected pt.)
Antiarrythmic drugs
 If hemodynamically unstable or
unsuccesful medical treat ment-
synchronised DC cardioversion
Bradycardia ,AV
block,intraventricular
conduction defect
medical treatment ;if non
responsive then temporary
pacing

79. mechanical
 Mitral regurgitation
if due to rupture-urgent surgery
If due to ischemia-timely reperfusion,diuretics,afterload
reduction
 Ventriclar septal rupture- urgent surgery
 Free wall rupture --urgent surgery

80. Posthospitalization Plan of Care:
1. Posthospital systems of care designed to prevent hospital readmissions
should be used to facilitate the transition to effective, coordinated outpatient
care for all patients with STEMI.
2. Exercise-based cardiac rehabilitation/secondary prevention programs are
recommended for patients with STEMI
3. A clear, detailed, and evidence-based plan of care that promotes medication
adherence, timely follow-up with the healthcare team, appropriate dietary
and physical activities, and compliance with interventions for secondary
prevention should be provided to patients with STEMI.
4. Encouragement and advice to stop smoking and to avoid secondhand
smoke should be provided to patients with STEMI.