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ACUTE CORONARY
SYNDROM
& Thrombolytic therapy
Dr Aizuddin Bin Misro
DEFINITION
CPG – Management of acute STEMI 2014 – 3rd
edtion (page 2)
ACUTE CORONARY SYNDROME
ACS is a clinical spectrum of ischaemic heart disease
ranging from unstable angina, non-ST segment
elevation myocardial infarction (NSTEMI) to STEMI
depending upon the degree and acuteness ofcoronary
occlusion. In unstable angina, myocardial injuryis
absent and cardiac biomarkers are normal. In
myocardial infarction (MI) [both NSTEMI and STEMI]
cardiac biomarkers are raised.
http://emeddoc.org/?p=383
Myocardial infarction
 Clinical diagnosis based on the presence of myocardial injury or necrosis as
indicated by a rise and fall of serum cardiac biomarkers. There should be at
least one of the following:
i. Clinical history consistent with chest pain of ischaemic origin
ii. ECG changes of ST segment elevation or presumed new LBBB
iii. Imaging evidence of new loss of viable myocardium/new regional wall
motion abnormality
iv. Identification of an intracoronary (IC) thrombus by angiography or autopsy
CPG – Management of acute STEMI 2014 – 3rd
edtion (page 2)
PATHOPHYSIOLOGY
 Reduce of O2 supply
 Increase myocardial 02
demand
stable
unstable
DIAGNOSIS
CHEST PAIN
Begins abruptly and lasts for more than 30min
Located in centre of chest. May radiate to jaw / left arm
May occur at rest / with activity
Usually describe as a pressure / sqeuazzing or severe
crushing pain with a sense of impending doom. Sometimes
the pain may be just a tightness or heaviness
a/w sweating, nausea, vomiting, sob
In elderly, females and diabetic pt, the index of suspicion
has to be high because they may present with atypical sx
eg unexplained fatigue, sob, dizziness, lightheadedness, or
syncope
 Other important points to note in the history are the
presence of:
• Previous history of ischaemic heart disease, PCI or
CABG.
• Risk factors for atherosclerosis.
• Symptoms suggestive of previous transient ischaemic
attack (TIA) or other forms of vascular disease.
Pain differentiation
SYSTEM SYNDROME Clinical
description
Presenting
features
CARDIOVASCULAR Stable angina Retrosternal
pressure,
heaviness, burning;
may radiate to
arms, neck, jaw
Provoked by
physical
/emotional stress
Unstable angina Same as stable but
usually more
severe and
prolonged
Occur at rest or
with minimal
exertion
Acute MI Same as angina but
usually more
severe
Usually > 30min,
a/w dyspnea,
diaphoresis
Pericarditis Pleuritic pain,
worse in supine
position
Fever, pericardial
friction rub
GASTROINTESTINAL Peptic ulcer Burning
retrosternal &
Relieved by antacid
or food
ECG
 12-lead ECG should be performed and interpreted
immediately within 10 minutes of first medical contact
 The presence of ST elevation in two contiguous leads
 The cut-off points for new or presumed new ST segment
elevation (in the absence of LVH and LBBB) is the
presence of ≥ 0.1 mV ST segment elevation in all leads
except leads V2-V3. In leads V2-V3, a cut-off point of ≥
0.25 mV (in males < 40 years), ≥ 0.2 mV (in males ≥ 40
years) and ≥0.15 mV in females is used.
 The presence of a new onset or presumed new LBBB
 Early stage of MI – hyperacute T wave. ECG should be
repeated at 15min intervals
 Patients with inferior STEMI should have an ECG
recording of the right praecordial lead (V4R) to identify
concomitant right ventricular (RV) involvement.
 In those with ST segment depression in leads V1-V3, it
is advisable to have an ECG recording of the posterior
chest wall (V7-V9) to identify a true infero-basal
(formerly known as infero-posterior)STEMI. The cut-off
point for ST segment elevation in the posteriorleads is ≥
0.05 mV (≥ 0.1 mV in men < 40 years).
2) ECG
UA/NSTEMI
 Features suggestive of UA/NSTEMI are:
 Dynamic ST/T changes
 ST depression > 0.5 mm in 2 or more contiguous leads
 T-wave inversion – deep symmetrical T-wave inversion
 Other ECG changes include new or presumed new onset
bundle branch block (BBB)* and cardiac arrhythmias,
especially sustained ventricular tachycardia. Evidence
of previous infarctions such as Q waves may be present.
 However, a completely normal ECG does not exclude
the diagnosisof UA/NSTEMI. Serial ECGs should be done
as the ST changes may evolve.
3) Cardiac
biomarker
CPG – Management of acute STEMI 2014 – 3rd
edtion
MANAGEMENT
Early management of STEMI is directed at:
Pain relief
Establishing early reperfusion
Treatment of complications
TIME LOST is
equivalent to
MYOCARDIUM LOST
A)
CPG – Management of acute STEMI 2014 – 3rd
edtion
DBT – 90MIN
DNT – 30MIN
B) Contraindications to
fibrinolytic therapy
Absolute contraindications
Risk of intracranial haemorrhage
- History of intracranial bleed
- History of ischaemic stroke within 3 months
- Known structural cerebral vascular lesion (e.g AVM)
- Known intracranial neoplasm.
Risk of bleeding
- Active bleeding or bleeding diathesis (excluding menses)
- Significant head trauma within 3 months
- Suspected aortic dissection
CPG – Management of acute STEMI 2014 – 3rd
edtion
B) Contraindications to
fibrinolytic therapy
Relative contraindications
Risk of intracranial haemorrhage
- Severe uncontrolled hypertension on presentation (BP > 180/110 mmH
- Ischaemic stroke more than 3 months
- History of chronic, severe uncontrolled hypertension
Risk of bleeding
- Current use of anticoagulation in therapeutic doses (INR > 2)
- Recent major surgery < 3 weeks
- Traumatic or prolonged CPR > 10 minutes
- Recent internal bleeding within 4 weeks
- Non-compressible vascular puncture
- Active peptic ulcer CPG – Management of acute STEMI 2014 – 3rd
edtion
C) High-risk patients
 Large infarcts
 Anterior infarcts
 Hypotension and cardiogenic shock
 Significant arrhythmias
 Elderly patients
 Post-revascularisation (post-CABG and post-PCI)
 Post-infarct angina
CPG – Management of acute STEMI 2014 – 3rd
edtion
FIBRINOLYTIC AGENT
1) Streptokinase is antigenic and promotes the production of
antibodies. Thus the utilisation of this agent for reinfarction is less
effective if given between 3 days and 1 or even 4 years after the first
administration. PCI or fibrin specific agents should then be considered.
Regimen:
-1.5 mega units in 100 ml normal saline or 5% dextrose over 1 hour
2) Tenecteplase (TNK-tPA) causes more rapid reperfusion of the
occluded artery than streptokinase and is given as a single bolus dose
Regimen: single IV bolus 30 mg if < 60 kg
35 mg if 60 to < 70 kg
40 mg if 70 to < 80 kg
45 mg if 80 to < 90 kg
50 mg if > 90 kg
Indication of Tenecteplase
(TNK-tPA)
 To reduce mortality associated with AMI
 Patient < 50 years old
 Patient have an anterior MI
 Chest pain < 12 hours
Indicators of successful
reperfusion
 Resolution of chest pain (may be confounded
by the use of narcotic analgesics)
 Early return of ST segment elevation to
isoelectric line or a decrease in the height of
the ST elevation by 50% (in the lead that
records the highest ST elevation) within 60-90
minutes of initiation of fibrinolytic therapy
 Early peaking of CK and CK-MB levels
 Restoration and/or maintenance of
haemodynamic and/or electrical stability
Concomitant therapy
A) Oxygen - indicated in the presence of hypoxaemia
(SpO2 < 95%)
B) Antiplatelet agents – Aspirin, Clopidogrel
C) Antithrombotic therapy
Concomitant therapy
D) B-blocker
Contraindications to B-blockers:
1) Bradycardia < 60/minute
2) SBP < 100 mmHg
3) Pulmonary congestion with crepitations beyond the lung bases
4) Signs of peripheral hypoperfusion
5) Second or third degree atrio-ventricular (AV) block
6) Asthma or chronic obstructive airway disease
7) Severe peripheral vascular disease
Concomitant therapy
E) ACE-Is and ARBs
The benefits of ACE-Is are greatest in patients with: HF, Anterior infarcts,
Asymptomatic LV dysfunction [LV ejection fraction (LVEF)] < 40% on
echocardiography)
Contraindications to ACE-I and ARB therapy:
SBP < 100 mmHg
Established contraindications e.g. bilateral renal artery stenosis
Concomitant therapy
F) Statin – Early and intensive high dose statin in ACS have been
proven to produce superior benefits in reduction of major cardiac
events.
G) Calcium channel blocker
H) Nitrates
Complications of stemi
Arrhythmias
LV dysfunction and shock
Mechanical complications
RV infarction
Others e.g. pericarditis
Take home message…..
REFERANCE
 CPG Management of Acute ST Segment Elevation
Myocardial Infarction (STEMI) (3rd Edition) 2014
 CPG UA-NSTEMI 2011
 ECG : http://lifeinthefastlane.com/ecg-library

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Acute coronary syndrome

  • 1. ACUTE CORONARY SYNDROM & Thrombolytic therapy Dr Aizuddin Bin Misro
  • 2. DEFINITION CPG – Management of acute STEMI 2014 – 3rd edtion (page 2)
  • 3. ACUTE CORONARY SYNDROME ACS is a clinical spectrum of ischaemic heart disease ranging from unstable angina, non-ST segment elevation myocardial infarction (NSTEMI) to STEMI depending upon the degree and acuteness ofcoronary occlusion. In unstable angina, myocardial injuryis absent and cardiac biomarkers are normal. In myocardial infarction (MI) [both NSTEMI and STEMI] cardiac biomarkers are raised. http://emeddoc.org/?p=383
  • 4. Myocardial infarction  Clinical diagnosis based on the presence of myocardial injury or necrosis as indicated by a rise and fall of serum cardiac biomarkers. There should be at least one of the following: i. Clinical history consistent with chest pain of ischaemic origin ii. ECG changes of ST segment elevation or presumed new LBBB iii. Imaging evidence of new loss of viable myocardium/new regional wall motion abnormality iv. Identification of an intracoronary (IC) thrombus by angiography or autopsy CPG – Management of acute STEMI 2014 – 3rd edtion (page 2)
  • 5. PATHOPHYSIOLOGY  Reduce of O2 supply  Increase myocardial 02 demand stable unstable
  • 6. DIAGNOSIS CHEST PAIN Begins abruptly and lasts for more than 30min Located in centre of chest. May radiate to jaw / left arm May occur at rest / with activity Usually describe as a pressure / sqeuazzing or severe crushing pain with a sense of impending doom. Sometimes the pain may be just a tightness or heaviness a/w sweating, nausea, vomiting, sob In elderly, females and diabetic pt, the index of suspicion has to be high because they may present with atypical sx eg unexplained fatigue, sob, dizziness, lightheadedness, or syncope
  • 7.  Other important points to note in the history are the presence of: • Previous history of ischaemic heart disease, PCI or CABG. • Risk factors for atherosclerosis. • Symptoms suggestive of previous transient ischaemic attack (TIA) or other forms of vascular disease.
  • 8. Pain differentiation SYSTEM SYNDROME Clinical description Presenting features CARDIOVASCULAR Stable angina Retrosternal pressure, heaviness, burning; may radiate to arms, neck, jaw Provoked by physical /emotional stress Unstable angina Same as stable but usually more severe and prolonged Occur at rest or with minimal exertion Acute MI Same as angina but usually more severe Usually > 30min, a/w dyspnea, diaphoresis Pericarditis Pleuritic pain, worse in supine position Fever, pericardial friction rub GASTROINTESTINAL Peptic ulcer Burning retrosternal & Relieved by antacid or food
  • 9. ECG  12-lead ECG should be performed and interpreted immediately within 10 minutes of first medical contact  The presence of ST elevation in two contiguous leads  The cut-off points for new or presumed new ST segment elevation (in the absence of LVH and LBBB) is the presence of ≥ 0.1 mV ST segment elevation in all leads except leads V2-V3. In leads V2-V3, a cut-off point of ≥ 0.25 mV (in males < 40 years), ≥ 0.2 mV (in males ≥ 40 years) and ≥0.15 mV in females is used.  The presence of a new onset or presumed new LBBB  Early stage of MI – hyperacute T wave. ECG should be repeated at 15min intervals
  • 10.  Patients with inferior STEMI should have an ECG recording of the right praecordial lead (V4R) to identify concomitant right ventricular (RV) involvement.  In those with ST segment depression in leads V1-V3, it is advisable to have an ECG recording of the posterior chest wall (V7-V9) to identify a true infero-basal (formerly known as infero-posterior)STEMI. The cut-off point for ST segment elevation in the posteriorleads is ≥ 0.05 mV (≥ 0.1 mV in men < 40 years).
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  • 19. UA/NSTEMI  Features suggestive of UA/NSTEMI are:  Dynamic ST/T changes  ST depression > 0.5 mm in 2 or more contiguous leads  T-wave inversion – deep symmetrical T-wave inversion  Other ECG changes include new or presumed new onset bundle branch block (BBB)* and cardiac arrhythmias, especially sustained ventricular tachycardia. Evidence of previous infarctions such as Q waves may be present.  However, a completely normal ECG does not exclude the diagnosisof UA/NSTEMI. Serial ECGs should be done as the ST changes may evolve.
  • 20. 3) Cardiac biomarker CPG – Management of acute STEMI 2014 – 3rd edtion
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  • 24. MANAGEMENT Early management of STEMI is directed at: Pain relief Establishing early reperfusion Treatment of complications
  • 25. TIME LOST is equivalent to MYOCARDIUM LOST A) CPG – Management of acute STEMI 2014 – 3rd edtion DBT – 90MIN DNT – 30MIN
  • 26. B) Contraindications to fibrinolytic therapy Absolute contraindications Risk of intracranial haemorrhage - History of intracranial bleed - History of ischaemic stroke within 3 months - Known structural cerebral vascular lesion (e.g AVM) - Known intracranial neoplasm. Risk of bleeding - Active bleeding or bleeding diathesis (excluding menses) - Significant head trauma within 3 months - Suspected aortic dissection CPG – Management of acute STEMI 2014 – 3rd edtion
  • 27. B) Contraindications to fibrinolytic therapy Relative contraindications Risk of intracranial haemorrhage - Severe uncontrolled hypertension on presentation (BP > 180/110 mmH - Ischaemic stroke more than 3 months - History of chronic, severe uncontrolled hypertension Risk of bleeding - Current use of anticoagulation in therapeutic doses (INR > 2) - Recent major surgery < 3 weeks - Traumatic or prolonged CPR > 10 minutes - Recent internal bleeding within 4 weeks - Non-compressible vascular puncture - Active peptic ulcer CPG – Management of acute STEMI 2014 – 3rd edtion
  • 28. C) High-risk patients  Large infarcts  Anterior infarcts  Hypotension and cardiogenic shock  Significant arrhythmias  Elderly patients  Post-revascularisation (post-CABG and post-PCI)  Post-infarct angina CPG – Management of acute STEMI 2014 – 3rd edtion
  • 29. FIBRINOLYTIC AGENT 1) Streptokinase is antigenic and promotes the production of antibodies. Thus the utilisation of this agent for reinfarction is less effective if given between 3 days and 1 or even 4 years after the first administration. PCI or fibrin specific agents should then be considered. Regimen: -1.5 mega units in 100 ml normal saline or 5% dextrose over 1 hour 2) Tenecteplase (TNK-tPA) causes more rapid reperfusion of the occluded artery than streptokinase and is given as a single bolus dose Regimen: single IV bolus 30 mg if < 60 kg 35 mg if 60 to < 70 kg 40 mg if 70 to < 80 kg 45 mg if 80 to < 90 kg 50 mg if > 90 kg
  • 30. Indication of Tenecteplase (TNK-tPA)  To reduce mortality associated with AMI  Patient < 50 years old  Patient have an anterior MI  Chest pain < 12 hours
  • 31. Indicators of successful reperfusion  Resolution of chest pain (may be confounded by the use of narcotic analgesics)  Early return of ST segment elevation to isoelectric line or a decrease in the height of the ST elevation by 50% (in the lead that records the highest ST elevation) within 60-90 minutes of initiation of fibrinolytic therapy  Early peaking of CK and CK-MB levels  Restoration and/or maintenance of haemodynamic and/or electrical stability
  • 32. Concomitant therapy A) Oxygen - indicated in the presence of hypoxaemia (SpO2 < 95%) B) Antiplatelet agents – Aspirin, Clopidogrel C) Antithrombotic therapy
  • 33. Concomitant therapy D) B-blocker Contraindications to B-blockers: 1) Bradycardia < 60/minute 2) SBP < 100 mmHg 3) Pulmonary congestion with crepitations beyond the lung bases 4) Signs of peripheral hypoperfusion 5) Second or third degree atrio-ventricular (AV) block 6) Asthma or chronic obstructive airway disease 7) Severe peripheral vascular disease
  • 34. Concomitant therapy E) ACE-Is and ARBs The benefits of ACE-Is are greatest in patients with: HF, Anterior infarcts, Asymptomatic LV dysfunction [LV ejection fraction (LVEF)] < 40% on echocardiography) Contraindications to ACE-I and ARB therapy: SBP < 100 mmHg Established contraindications e.g. bilateral renal artery stenosis
  • 35. Concomitant therapy F) Statin – Early and intensive high dose statin in ACS have been proven to produce superior benefits in reduction of major cardiac events. G) Calcium channel blocker H) Nitrates
  • 36. Complications of stemi Arrhythmias LV dysfunction and shock Mechanical complications RV infarction Others e.g. pericarditis
  • 38. REFERANCE  CPG Management of Acute ST Segment Elevation Myocardial Infarction (STEMI) (3rd Edition) 2014  CPG UA-NSTEMI 2011  ECG : http://lifeinthefastlane.com/ecg-library

Editor's Notes

  1. ACS is a clinical spectrum of ischaemic heart disease ranging from unstable angina, non-ST segment elevation myocardial infarction (NSTEMI) to STEMI depending upon the degree and acuteness of coronary occlusion (See Figure 1). In unstable angina, myocardial injury is absent and cardiac biomarkers are normal. In myocardial infarction (MI) [both NSTEMI and STEMI] cardiac biomarkers are raised. MI is a clinical diagnosis based on the presence of myocardial injury or necrosis as indicated by a rise and fall of serum cardiac biomarkers. In addition, there should be at least one of the following:4 i. Clinical history consistent with chest pain of ischaemic origin. ii. ECG changes of ST segment elevation or presumed new LBBB. iii. Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality. iv. Identification of an intracoronary (IC) thrombus by angiography or autopsy. This new comprehensive definition of MI which utilises newer cardiac biomarkers and imaging techniques is more sensitive in diagnosing MI.5 ‘Reinfarction’ is used for MI that occurs within 28 days of the incident event while recurrent MI occurs after 28 days.4
  2. Post lead V7 – Left posterior axillary line, in the same horizontal plane as V6. V8 – Tip of the left scapula, in the same horizontal plane as V6. V9 – Left paraspinal region, in the same horizontal plane as V6.
  3. Anterolateral mi ST elevation is present in the anterior (V2-4) and lateral leads (I, aVL, V5-6). Q waves are present in both the anterior and lateral leads, most prominently in V2-4.
  4. [above] Hyperacute anterolateral MI hyperacute t wave v2 –v4, st-elevation v1,
  5.  Inferoposterolateral STEMI: ST elevation is present in the inferior (II, III and aVF) and lateral leads (I, V5-6). ST depression in V1-3 with tall, broad R waves and upright T waves and a R/S ratio &amp;gt; 1 in V2 indicate concomitant posterior infarction (this patient also had ST elevation in the posterior leads V7-9).
  6. Posterior ecg
  7. ST depression I, II and V5-6 subtle ST elevation in V1-2 and aVR
  8. TWI V1-V4
  9. The benefits of early treatment – opening the blocked coronary artery as soon as possible so as to limit myocardial damage to the minimum and preserve heart function. “TIME IS MYOCARDIUM.” Pain relief - s/l GTN , IV morphine 2-5mg Non entereric coated aspirin 300mg Clopidogrel 300mg
  10. Transfer pt to hosp with PCI facility – 2hr DNT