WHAT AN INTENSIVIST SHOULD KNOW FOR MANAGING ACUTE CORONARY SYNDROME PTS.

1. ACUTE CORONARY SYNDROME
Dr Abhinov K
MBBS DNB FNB

2. DEFINITION
Coronary artery disease (CAD), also known
as ischemic heart disease (IHD),is a group of
diseases that includes: stable
angina, unstable angina, myocardial
infarction, and sudden cardiac death.
ACS- ST elevation myocardial infarction (STEMI,
30%), non ST elevation myocardial
infarction (NSTEMI, 25%), or unstable
angina (38%).

3. • Stable angina- chest discomfort and associated
symptoms precipitated by some activity (running,
walking, etc.) with minimal or non-existent symptoms
at rest or after administration
of sublingual nitroglycerin.
• Unstable angina -is defined as angina that changes or
worsens. it occurs at rest (or with minimal exertion),
usually lasting more than 10 minutes
• it is severe and of new onset (i.e., within the prior 4–6
weeks)
• it occurs with a crescendo pattern (i.e., distinctly more
severe, prolonged, or frequent than before).

5. Pathophysiology

6. R

7. Diagnosis
History
ECG
Cardiac Biomarkers
Echocardiography

8. History
• Character of pain
• Onset and duration
• Location and radiation
• Aggravating and relieving factors
• Autonomic symptoms

10. NEW YORK HEART ASSOCIATION FUNCTIONAL CLASSIFICATION OF ANGINA
•
• Class 1- Patients with cardiac disease but without resulting
limitation of physical activity. Ordinary physical activity does not
cause undue fatigue, palpitation, dyspnea, or anginal pain.
• Class II- Patients with cardiac disease resulting in slight limitation
of physical activity. They are comfortable at rest. Ordinary physical
activity results in fatigue, palpitation, dyspnea, or anginal pain.
• Class III- Patients with cardiac disease resulting in marked
limitation of physical activity. They are comfortable at rest. Less
than ordinary activity causes fatigue, palpitation, dyspnea, or
anginal pain.
• Class IV- Patients with cardiac disease resulting in inability to carry
on any physical activity without discomfort. Symptoms of heart
failure or the anginal syndrome may be present even at rest. If any
physical activity is undertaken, discomfort is increased.

11. ECG
• All patients who present with a suspected ACS must have
an ECG within 10 minutes of first acute clinical contact
• A clinician with ECG expertise should review the ECG
• STEMI minimum criteria:
– STEMI is defined as presentation with clinical symptoms
consistent with ACS (generally of ≥ 20 minutes duration) with
persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads
of:
• ≥ 2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men
under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in
leads V2-3 in men over 40 years
• ≥ 1.5 mm ST elevation in V2-3 in women
• ≥ 1 mm ST elevation in other leads
• New LBBB (LBBB should be considered new unless there is evidence
otherwise)

12. • Findings in ACS
– may be normal
– classic changes in acute myocardial infarction
• peaked T waves with ST elevation
• gradual loss of R wave
• development of pathological Q wave and TWI
– anatomical localisation of ST elevation
• Anterior= LAD=V1-6
• Septal=LAD=V1-2
• lateral = LCx=I, aVL, V5-6
• Inferior = RCA(80%), LCx(20%)= II III aVf
• Posterior = LCx or PDA (off RCA) = V7-9

14. • Minimal S-T changes can be difficult to interpret,
especially in those with pre-existing CAD or other
significant CVS disease. In such cases:
– Comparison with old ECGs will be useful
– Modified Sgarbossa criteria can help if LBBB or paced:
• concordant ST elevation of > 1mm
• concordant ST depression of > 1mm in V1, V2 or V3
• discordant ST elevation of > 5mm
– In cases of LBBB urgent echocardiography may be
useful, if readily available, to detect wall motion
abnormalities (suggesting myocardial ischaemia) and
hence assist in decision making

16. STEMI
• The threshold values for ST-segment elevation
consistent with STEMI are J-point elevation of >1
mm in two or more contiguous leads except
V2V3.
• For V2V3 a diagnosis of STEMI is made when men
<40 years old have J-point elevations above 0.25
mV (2.5 mm), for men >40 years old the J-point
elevation threshold is above 0.2 mV (2.0 mm) and
for women above 0.15 mV (1.5 mm).

17. Ischemia modified albumin

18. Biomarkers

19. Case Study 1
A patient presented with chest pain and
exacerbation of heart failure as a result of fluid
overload. Serum type B natriuretic peptide level was
1280 pg/mL (reference range, 0.00-99.0 pg/mL), and
the cTn level was 0.08 ng/mL (reference range, 0.00-
0.06 ng/mL). The patient described the pain as a
nonradiating chest pressure that was completely
relieved with sublingual nitroglycerin. The ECG showed
atrial flutter and ST-segment depression in the anterior
and low lateral leads. Subsequent serial cTn levels at 6
and 12 hours were 0.10 and 0.09 ng/mL, respectively.

20. Case Study 2
A patient with end-stage renal disease
experienced several episodes of hypotension
during dialysis. The cTn level was 0.12 ng/mL,
and the ECG showed a pattern of global ST-
segment elevation and PR segment depression
(interpreted as acute pericarditis). Subsequent
serial cTn levels were 0.10 and 0.11 ng/mL.

21. • Case Study 3
A 45-year-old male patient with diabetes
presented with new-onset chest pressure
relieved with sublingual nitroglycerin. The ECG
finding was normal, there was a family history of
MI, and the patient had dyslipidemia. The
patient’s cTn level in the emergency department
was 0.06 ng/mL. Subsequent serial cTn levels
were 3.0 and 1.5 ng/mL. The patient received
heparin and platelet inhibitors and was sent to
the cardiac catheterization laboratory.

22. • Case Study 4
A 60-year-old male patient was recovering on
postoperative day 2 following coronary artery
bypass surgery and valve repair. The
postoperative ECG showed T-wave
abnormalities, and cTn levels were 3.78 ng/mL
at 9:00 am and 3.11 ng/mL at 4:00 pm . A
bedside echocardiogram showed normal
ventricular wall motion.

23. • Case Study 5
A rapid response alert was called on the surgical unit
when a general surgery patient (postoperative day 2)
was found to have an irregular tachycardia. The patient
was transferred to the intensive care unit where he was
found to have an initial cTn level of 0.16 ng/mL and a
hematocrit of 26% (20% drop since admission).
Subsequent serial cTn levels were 2.10 and 1.30 ng/mL.
The patient was treated with heart rate control drugs,
and packed red cells were transfused.

26. Classification of MI
Type-1- Spontaneous MI
Spontaneous myocardial infarction related to atherosclerotic
plaque rupture, ulceration, erosion, or dissection with
resulting intraluminal thrombus in one or more of the
coronary arteries.
Type 2- MI secondary to ischaemic imbalance
Myocardial injury with necrosis where a condition other than
CAD contributes to an imbalance between myocardial oxygen
supply and/or demand.
Type 3- MI resulting in death when biomarker values are
unavailable
Cardiac death with symptoms suggestive of myocardial
ischemia and presumed new ischemic ECG changes or new
LBBB, but death occurring before blood samples could be
obtained, before cardiac biomarker could rise, or in cases
cardiac biomarkers were not collected
Type 4- MI related to PCI (3x)
Type 5- MI related to CABG (5x) five times the 99th percentile of the
normal reference range during the initial 72 hrs following CABG

27. New biomarkers
Copeptin - Copeptin (C-terminal pro-
vasopressin) which is released very early soon
after onset of symptoms and has
demonstrated myocardial damage within an
hour of symptom onset.

28. Echocardiography
• Echocardiography provides convenient
bedside assessment of left ventricular global
and regional function. This can help with the
diagnosis and management of infarction. It
has been used successfully to make judgments
about admission and management of patients
with suspected infarction, since normal wall
motion makes an infarction unlikely

30. DDx
•Acute Gastritis
•Acute Pericarditis
•Anxiety Disorders
•Aortic Dissection
•Aortic Stenosis
•Biliary Colic
•Cholecystitis
•Gastroesophageal Reflux Disease
•Pericarditis
•Costochondritis

31. Management of NSTEMI
• Pain relief is one of the most pressing needs of
the patient. In acute coronary ischaemia, the
increased heart rate, higher blood pressure or
high preload result in decreased myocardial
oxygen supply and increased myocardial
oxygen demand. This oxygen imbalance
results in ischaemic pain. The objective of
anti-ischaemic drugs is to reverse these
processes and secure pain relief.

32. • Nitrates- decreases Preload, Improves O2 delivery (C/I if pt is on
sildenafil)
• b-Blockers: Current recommendation includes introducing b-
blockers within 24-h of diagnosis in those without signs of low-
output heart failure or major risk factors for cardiogenic shock.
• Calcium Channel Blockers: These are for patients already on
nitrates/b-blockers, those for whom b-blockers are contraindicated
and those with coronary vasospasm.
• ACEI/ ARBs: Can be given within 24 h of presentation for NSTEMI
patients with pulmonary venous congestion or left ventricular
ejection fraction (LVEF) less than 40 % or in the absence of
hypotension.
• Morphine: Data from the CRUSADE registry demonstrated higher
mortality in patients requiring morphine.

33. Antiplatelets

34. Anti-Platelet Agents
• Aspirin, 325 mg loading f/b 150mg maintanence per oral should be
administered as soon as possible after presentation, provided no
contraindications (e.g., allergy, active bleeding, current peptic ulceration,
recent neurosurgery or haemorrhagic stroke) exist to its use. Efficacy is not
increased with higher maintenance doses, which carry a greater risk of
gastrointestinal intolerance.
• P2Y12 receptor antagonists- Ticlopidine- thrombotic thrombocytopenic
purpura (TTP) and neutropenia led to its relative non-use and replacement
by clopidogrel
• Clopidogrel, a pro-drug activated in the liver by the CYP2C19 isoenzyme of
cytochrome P450. Clopidogrel interacts with many drugs, especially
proton pump inhibitors (PPIs) (except possibly pantoprazole), phenytoin,
tamoxifen, tolbutamide, warfarin, heparin, enoxaparin, anistreplase,
dipyridamole, streptokinase, ticlopidine and urokinase. In November
2009, the FDA announced that clopidogrel should be used with caution in
patients on PPIs such as omeprazole and esomeprazole.

35. Double-dose (600 mg on day 1, 150 mg on days 2-7, then 75 mg daily)
versus standard-dose (300 mg on day 1 then 75 mg daily) clopidogrel
and high-dose (300-325 mg daily) versus low-dose (75-100 mg daily)
aspirin. The primary outcome was cardiovascular death, myocardial
infarction, or stroke at 30 days.
They found that Compared with the standard dose, double-dose
clopidogrel reduced the rate of the primary outcome (330 events
[3·9%] vs 392 events [4·5%]; (p=0·039) and definite stent thrombosis
(58 [0·7%] vs 111 [1·3%]; p=0·0001). High-dose and low-dose aspirin
did not differ for the primary outcome (356 [4·1%] vs 366 [4·2%];
p=0·76).

36. PLATO Trial
• The 2009 Platelet Inhibition and Patient Outcomes
(PLATO) trial randomized 18,624 patients with ACS
(37.5% with STEMI) to ticagrelor or clopidogrel, in
addition to standard care. At 12 months, the ticagrelor
group had lower rates of CV death, MI, or stroke than
clopidogrel (9.8% vs. 11.7%) and all-cause mortality
(4.5% vs. 5.9%). While there was no difference in major
bleeding, ticagrelor was associated with more non-
CABG-related bleeding (4.5% vs. 3.8%). The ticagrelor
group experienced a higher rate of dyspnea (13.8% vs.
7.8%) and a trend towards more bradycardia (4.4% vs.
4.0%), likely due to ticagrelor's close resemblance to
adenosine

37. Anti-coagulant Therapy
• Anticoagulation is recommended for all patients
presenting with NSTEMI, in addition to dual anti-
platelet therapy.
• UFH is given at a dose of 70–100 IU/kg body weight.
Dosing should be guided by measurements of activated
clotting times (ACT).
• LMWHs, however, can be administered subcutaneously
at a dose of 1 mg/kg every 12 h for at least 2 days until
clinical stabilization. Treatment may be continued for
up to 8 days.
• Factor Xa inhibitors otamixaban, fondaparinux can also
be considered in the treatment

38. UFH Vs LMWH
In aspirin-treated patients with acute coronary syndrome
without ST elevation, short-term unfractionated heparin or
LMWH halves the risk of myocardial infarction or death.
There is no convincing difference in efficacy or safety
between LMWH and unfractionated heparin. Long-term
LMWH has not been proven to confer benefit additional to
aspirin and there is no evidence to support its use after the
first 7 days.

39. Coronary Revascularization in NSTEMI
• Risk Stratification
• Those with low risk benefit from conservative management, while those
at high risk may require an invasive approach.
• The best timing for invasive evaluation in NSTEMI patients at extremely
high risk and who are haemodynamically unstable (those with ongoing
chest pain in spite of optimal medical therapy, severe heart failure or
lifethreatening arrhythmias) is generally immediately after presentation
(i.e., less than 2 h).
• For patients with at least one primary high-risk criterion(Primary criteria
for high-risk categorization includes relevant rise or fall in cardiac
biomarker levels, and/or dynamicST- or T-wave changes) and a GRACE risk
Score>140, an early invasive strategy within 24 h of presentation would be
advisable .
• In patients with at least one primary high-risk criterion and a GRACE risk
score <140, an invasive strategy is recommended within 72 h after first
presentation.

40. TIMI Risk Score* for NSTE-ACS
TIMI Risk
Score
All-Cause Mortality, New or Recurrent MI, or
Severe Recurrent Ischemia Requiring Urgent
Revascularization Through 14 d After
Randomization, %
0–1 4.7
2 8.3
3 13.2
4 19.9
5 26.2
6–7 40.9
*The TIMI risk score is determined by the sum of the presence of 7 variables at
admission; 1 point is given for each of the following variables: ≥65 y of age; ≥3
risk factors for CAD; prior coronary stenosis ≥50%; ST deviation on ECG; ≥2
anginal events in prior 24 h; use of aspirin in prior 7 d; and elevated cardiac
biomarkers.

41. GRACE Risk Model Nomogram

43. Prognosis: Early Risk Stratification
Recommendations COR LOE
In patients with chest pain or other symptoms suggestive of ACS,
a 12-lead ECG should be performed and evaluated for ischemic
changes within 10 minutes of the patient’s arrival at an
emergency facility.
I C
If the initial ECG is not diagnostic but the patient remains
symptomatic and there is a high clinical suspicion for ACS, serial
ECGs (e.g., 15- to 30-minute intervals during the first hour)
should be performed to detect ischemic changes.
I C
Serial cardiac troponin I or T levels (when a contemporary assay
is used) should be obtained at presentation and 3 to 6 hours after
symptom onset in all patients who present with symptoms
consistent with ACS to identify a rising and/or falling pattern of
values.
I A

44. Prognosis: Early Risk Stratification (cont’d)
Recommendations COR LOE
Additional troponin levels should be obtained beyond 6 hours
after symptom onset (see Section 3.4, Class I, #3
recommendation if time of symptom onset is unclear) in patients
with normal troponin levels on serial examination when changes
on ECG and/or clinical presentation confer an intermediate or
high index of suspicion for ACS.
I A
Risk scores should be used to assess prognosis in patients with
NSTE-ACS.
I A
Risk-stratification models can be useful in management. IIa B

45. Prognosis: Early Risk Stratification (cont’d)
Recommendations COR LOE
It is reasonable to obtain supplemental electrocardiographic
leads V7 to V9 in patients whose initial ECG is nondiagnostic and
who are at intermediate/high risk of ACS.
IIa B
Continuous monitoring with 12-lead ECG may be a reasonable
alternative in patients whose initial ECG is nondiagnostic and
who are at intermediate/high risk of ACS.
IIb B
Measurement of B-type natriuretic peptide or N-terminal pro–B-
type natriuretic peptide may be considered to assess risk in
patients with suspected ACS.
IIb B

46. Biomarkers: Diagnosis
Recommendations COR LOE
Cardiac-specific troponin (troponin I or T when a contemporary
assay is used) levels should be measured at presentation and 3 to
6 hours after symptom onset in all patients who present with
symptoms consistent with ACS to identify a rising and/or falling
pattern.
I A
Additional troponin levels should be obtained beyond 6 hours
after symptom onset in patients with normal troponins on serial
examination when electrocardiographic changes and/or clinical
presentation confer an intermediate or high index of suspicion
for ACS.
I A
If the time of symptom onset is ambiguous, the time of
presentation should be considered the time of onset for
assessing troponin values.
I A
With contemporary troponin assays, creatine kinase myocardial
isoenzyme (CK-MB) and myoglobin are not useful for diagnosis of
ACS.
III: No
Benefit
A

47. Biomarkers: Prognosis
Recommendations COR LOE
The presence and magnitude of troponin elevations are useful
for short- and long-term prognosis. I B
It may be reasonable to remeasure troponin once on day 3 or day
4 in patients with MI as an index of infarct size and dynamics of
necrosis.
IIb B
Use of selected newer biomarkers, especially B-type natriuretic
peptide, may be reasonable to provide additional prognostic
information.
IIb B

48. Oxygen
Recommendation COR LOE
Supplemental oxygen should be administered to patients with
NSTE-ACS with arterial oxygen saturation less than 90%,
respiratory distress, or other high-risk features of hypoxemia.
I C

49. Anti-Ischemic and Analgesic Medications:
Nitrates
Recommendations COR LOE
Patients with NSTE-ACS with continuing ischemic pain should
receive sublingual nitroglycerin (0.3 mg to 0.4 mg) every 5
minutes for up to 3 doses, after which an assessment should be
made about the need for intravenous nitroglycerin if not
contraindicated.
I C
Intravenous nitroglycerin is indicated for patients with NSTE-ACS
for the treatment of persistent ischemia, HF, or hypertension. I B
Nitrates should not be administered to patients with NSTE-ACS
who recently received a phosphodiesterase inhibitor, especially
within 24 hours of sildenafil or vardenafil, or within 48 hours of
tadalafil.
III:
Harm
B

50. Anti-Ischemic and Analgesic Medications:
Analgesic Therapy
Recommendations COR LOE
In the absence of contraindications, it may be reasonable to
administer morphine sulfate intravenously to patients with NSTE-
ACS if there is continued ischemic chest pain despite treatment
with maximally tolerated anti-ischemic medications.
IIb B
Nonsteroidal anti-inflammatory drugs (NSAIDs) (except aspirin)
should not be initiated and should be discontinued during
hospitalization for NSTE-ACS because of the increased risk of
MACE associated with their use.
III:
Harm
B

51. Treated With an Initial Invasive or Ischemia-Guided Strategy
Recommendations COR LOE
Non–enteric-coated, chewable aspirin (162 mg to 325 mg) should
be given to all patients with NSTE-ACS without contraindications
as soon as possible after presentation, and a maintenance dose
of aspirin (81 mg/d to 162 mg/d) should be continued
indefinitely.
I A
In patients with NSTE-ACS who are unable to take aspirin
because of hypersensitivity or major gastrointestinal intolerance,
a loading dose of clopidogrel followed by a daily maintenance
dose should be administered.
I B

52. Treated With an Initial Invasive or Ischemia-Guided Strategy (cont’d)
Recommendations COR LOE
A P2Y12 inhibitor (either clopidogrel or ticagrelor) in addition to
aspirin should be administered for up to 12 months to all patients
with NSTE-ACS without contraindications who are treated with
either an early invasive or ischemia-guided strategy. Options
include:
• Clopidogrel: 300-mg or 600-mg loading dose, then 75 mg daily
• Ticagrelor║: 180-mg loading dose, then 90 mg twice daily
I
B
B

53. Treated With an Initial Invasive or Ischemia-Guided Strategy (cont’d)
Recommendations COR LOE
It is reasonable to use ticagrelor in preference to clopidogrel for
P2Y12 treatment in patients with NSTE-ACS who undergo an early
invasive or ischemia-guided strategy.
IIa B
In patients with NSTE-ACS treated with an early invasive strategy
and dual antiplatelet therapy (DAPT) with intermediate/high-risk
features (e.g., positive troponin), a GP IIb/IIIa inhibitor may be
considered as part of initial antiplatelet therapy. Preferred
options are eptifibatide or tirofiban.
IIb B

54. Initial Parenteral Anticoagulant Therapy in Patients With Definite NSTE-ACS
Recommendations COR LOE
In patients with NSTE-ACS, anticoagulation, in addition to
antiplatelet therapy, is recommended for all patients irrespective
of initial treatment strategy. Treatment options include:
• Enoxaparin: 1 mg/kg subcutaneous (SC) every 12 hours
(reduce dose to 1 mg/kg SC once daily in patients with
creatinine clearance [CrCl] <30 mL/min), continued for the
duration of hospitalization or until PCI is performed. An initial
intravenous loading dose is 30 mg.
I A

55. Initial Parenteral Anticoagulant Therapy in Patients With Definite NSTE-ACS
(cont’d)
Recommendations COR LOE
(cont’d)
• Bivalirudin: 0.10 mg/kg loading dose followed by 0.25 mg/kg
per hour (only in patients managed with an early invasive
strategy), continued until diagnostic angiography or PCI, with
only provisional use of GP IIb/IIIa inhibitor, provided the
patient is also treated with DAPT.
• Fondaparinux: 2.5 mg SC daily, continued for the duration of
hospitalization or until PCI is performed.
I
B
B

56. Initial Parenteral Anticoagulant Therapy in Patients With Definite NSTE-ACS
(cont’d)
Recommendations COR LOE
(cont’d)
• If PCI is performed while the patient is on fondaparinux, an
additional anticoagulant with anti-IIa activity (either UFH or
bivalirudin) should be administered because of the risk of
catheter thrombosis.
• UFH IV: initial loading dose of 60 IU/kg (maximum 4,000 IU)
with initial infusion of 12 IU/kg per hour (maximum 1,000
IU/h) adjusted per activated partial thromboplastin time to
maintain therapeutic anticoagulation according to the specific
hospital protocol, continued for 48 hours or until PCI is
performed.
I
B
B
In patients with NSTE-ACS (i.e., without ST elevation, true
posterior MI, or left bundle-branch block not known to be old),
intravenous fibrinolytic therapy should not be used.
III:
Harm
A

57. Algorithm for Management of Patients With Definite or Likely NSTE-ACS
NSTE-ACS:
Definite or Likely
Ischemia-Guided Strategy Early Invasive Strategy
Initiate DAPT and Anticoagulant Therapy
1. ASA (Class I; LOE: A)
2. P2Y12 inhibitor (in addition to ASA) (Class I; LOE: B) :
·Clopidogrel or
·Ticagrelor
3. Anticoagulant:
·UFH (Class I; LOE: B) or
·Enoxaparin (Class I; LOE: A) or
·Fondaparinux (Class I; LOE: B)
Initiate DAPT and Anticoagulant Therapy
1. ASA (Class I; LOE: A)
2. P2Y12 inhibitor (in addition to ASA) (Class I; LOE: B):
·Clopidogrel or
·Ticagrelor
3. Anticoagulant:
·UFH (Class I; LOE: B) or
·Enoxaparin (Class I; LOE: A) or
·Fondaparinux† (Class I; LOE: B) or
·Bivalirudin (Class I; LOE: B)
Medical therapy
chosen based on cath
findings
Can consider GPI in addition to ASA and P2Y12 inhibitor
in high-risk (e.g., troponin positive) pts
(Class IIb; LOE: B)
·Eptifibatide
·Tirofiban
Therapy
Ineffective
Therapy
Effective

58. PCI With Stenting
Initiate/continue antiplatelet and anticoagulant
therapy
1. ASA (Class I; LOE: B)
2. P2Y12 Inhibitor (in addition to ASA):
·Clopidogrel (Class I; LOE: B) or
·Prasugrel (Class I; LOE: B) or
·Ticagrelor (Class I; LOE: B)
3. GPI (if not treated with bivalirudin at time of PCI)
·High-risk features, not adequately pretreated
with clopidogrel (Class I; LOE: A)
·High-risk features adequately pretreated with
clopidogrel (Class IIa; LOE: B)
4. Anticoagulant:
·Enoxaparin (Class I; LOE: A) or
·Bivalirudin (Class I; LOE: B) or
·Fondaparinux† as the sole anticoagulant (Class
III: Harm; LOE: B) or
·UFH (Class I; LOE: B)
CABG
Initiate/continue ASA therapy and
discontinue P2Y12 and/or GPI therapy
1. ASA (Class I; LOE: B)
2. Discontinue clopidogrel/ticagrelor 5 d
before, and prasugrel at least 7 d before
elective CABG
3. Discontinue clopidogrel/ticagrelor up to
24 h before urgent CABG (Class I; LOE: B).
May perform urgent CABG <5 d after
clopidogrel/ticagrelor and <7 d after
prasugrel discontinued
4. Discontinue eptifibatide/tirofiban at
least 2-4 h before, and abciximab ≥12 h
before CABG (Class I; LOE: B)
Late Hospital/Posthospital Care
1. ASA indefinitely (Class I; LOE: A)
2. P2Y12 inhibitor (clopidogrel or
ticagrelor), in addition to ASA, up
to 12 mo if medically treated
(Class I; LOE: B)
3. P2Y12 inhibitor (clopidogrel,
prasugrel, or ticagrelor), in
addition to ASA, at least 12 mo if
treated with coronary stenting
(Class I; LOE: B)
Therapy
Ineffective
Therapy
Effective
†In patients who have been treated with fondaparinux (as upfront therapy) who are undergoing PCI,
an additional anticoagulant with anti-IIa activity should be administered at the time of PCI because
of the risk of catheter thrombosis.

59. STEMI
• PCI is the preferred reperfusion strategy of
STEMI, provided it can be performed with a
D2B time of <90 min by a skilled operator
(performing >75 PCIs per year) at a PCI
capable centre (performing >200 PCIs a year,
of which at least 36 are primary PCI for STEMI)
• D2B-
• D2N-

61. • A number of thrombolytic agents are available. The current
recommended doses of some of the more commonly used
thrombolytic agents are as follows:
(1) Streptokinase 1.5 million units (u) given intravenously over 60
min.
(2) t-PA (alteplase) 15 mg initial IV bolus, followed by 0.75 mg/kg
body weight (maximum 50 mg) over the next 30 min and then 0.5
mg/kg body weight (maximum 35 mg) over the remaining 60 min.
(3) TNK-tPA (tenecteplase) 0.5 mg/kg body weight as a bolus
intravenous dose over 5 seconds (minimum dose 30 mg,
maximum dose 50 mg).
(4) r-PA (reteplase) 2x 10 u each over 2 min and given 30 min apart.

62. Though fibrinolytics are well-proven to improve coronary blood
flow, limit infarct size and improve survival, certain
contraindications exist. The absolute contraindications include :
(a) known intracranial haemorrhage at any time,
(b) ischaemic stroke in the preceding 6 months,
(c) presence of intracranial tumour, arterio-venous malformation or bleeding,
(d) major surgery or major trauma/head injury within the preceding 3 weeks,
(e) presence of active internal bleeding (excepting menstruation),
(f) gastrointestinal bleeding within the past month,
(g) bleeding diathesis,
(h) non-compressible punctures in the past 24 h (e.g. liver biopsy, lumbar
puncture, subclavian puncture),
(i) high suspicion of aortic dissection,
(j) pericarditis,
(k) refractory to resuscitation,
(l) allergy to the intended thrombolytic or previous reaction to these agents,
(m) pregnancy.

63. Relative contraindications include:
(a) high blood pressure with at least two
simultaneous readings>180/110 mmHg,
(b) severe renal or liver disease,
(c) prolonged or traumatic CPR but successful
resuscitation,
(d) patients on chronic anti-coagulant therapy
(e.g.warfarin).

64. Which thrombolytic is the right choice???
40,000 for 50 mg40,000 for 50 mg 33,000 for 10IU3500 for 1.5MU
STREPTOKINASE ACTILYSE RETELEX
METALYSE, ELAXIM,
VELIX
INR

65. Reperfusion Decisions in STEMI
• When fibrinolysis is the planned treatment strategy, we
recommend using prehospital fibrinolysis in
comparison with in-hospital fibrinolysis for STEMI
where transport times are greater than 30 minutes and
prehospital personnel are well trained. (strong
recommendation, moderate-quality evidence).
• Where PCI facilities exist and are available in a
geographic region we suggest that direct triage and
transport for PCI is preferred to prehospital fibrinolysis
for STEMI. (weak recommendation, low-quality
evidence)

66. • We recommend against the routine use of fibrinolytic
administration combined with immediate PCI, compared
with immediate PCI alone in patients with STEMI.(strong
recommendation,moderate-quality evidence).
• We provide recommendations on PCI versus fibrinolysis
based on time from symptom onset and potential delay to
PCI.-
In patients with STEMI presenting less than 2 hours after
symptom onset, when PPCI will result in a delay of greater
than 60 minutes, we suggest fibrinolysis in comparison with
PPCI (weak recommendation, low-quality evidence).

68. • After fibrinolysis of STEMI patients in the ED (when
primary PCI is not available on-site), we suggest
transport for early routine angiography in the first 3 to
6 hours (or up to 24 hours) rather than only transport
for ischemia- guided angiography. (weak
recommendation, moderate-quality evidence).
• For adult patients presenting with STEMI in the ED of a
non–PCI-capable hospital, we recommend emergency
transfer without fibrinolysis to a PCI center as opposed
to immediate in-hospital fibrinolysis and transfer only
for rescue PCI. (strong recommendation, moderate-
quality evidence).