LECTURE OUTLINE

INTRODUCTION –
EPIDEMIOLOGY/PREVALENCE/DEFINITION

PATHOPHYSIOLOGY OF ACUTE CORONARY

SYNDROMES

APPROACH TO SUSPECTED ACUTE CORONARY

SYNDROME – GUIDELINE UPDATE

TREATMENT/MANAGEMENT UPDATE
DEFINITIONS
CAD is a continuum of disease….

Angina -> unstable angina -> AMI -> sudden cardiac death

Acute coronary syndrome encompasses unstable angina, NSTEMI,

STEMI

Stable angina – transient episodic chest pain d/t myocardial

ischaemia, reproducible, frequency constant over time.usually
relieved with rest/NTG.

Classification of angina – Canadian Cardiovascular Society

classification.
CANADIAN CARDIOVASCULAR ASSOCIATION CLASSIFICATION
OF ANGINA

CLASS 1 NO PAIN WITH ORDINARY PHYSICAL ACTIVITY

CLASS 2 SLIGHT LIMITATION OF PHYSICAL ACTIVITY –

PAIN OCCURS WITH WALKING, CLIMBING
STAIRS,STRESS

CLASS 3 SEVERE LIMITATION OF DAILY ACTIVITY – PAIN

OCCURS ON MINIMAL EXERTION

CLASS 4 UNABLE TO CONDUCT ANY ACTIVITY WITHOUT

PAIN, PAIN AT REST
UNSTABLE ANGINA

Pain occurring at rest – duration > 20min, within one

week of first visit
New onset angina – ~ Class 2 severity, onset with last 2
months
Worsening of chest pain – increase by at least 1 class,
increases in frequency, duration

NB! ECG – normal, ST depression(>0.5mm), T wave

changes
ACUTE MYOCARDIAL INFARCTION

WHO CRITERIA :
 Rise and fall in cardiac enzymes
 Ischaemic type chest pain/symptoms
 ECG changes – ST changes, pathological Q waves

NSTEMI = UNSTABLE ANGINA SYMPTOMS/FINDINGS +

POSITIVE CARDIAC ENZYMES
STEMI = ST ELEVATION ON ECG + SYMPTOMS
ACS PATHOPHYSIOLOGY

Distruption 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
 UNSTABLE
PLAQUUES

STABLE
PLAQUES
APPROACH
1. Identifying those with chest pain suggestive of
IHD/ACS.
2. Thorough history required:
3. Character of pain
4. Onset and duration
5. Location and radiation
6. Aggravating and relieving factors
7. Autonomic symptoms
CHARACTERISTICS OF TYPICAL ANGINAL CHEST
PAIN (ADAPTED FROM ROSEN’S, EMERGENCY
MEDICINE)
CHARACTERISTIC SUGGESTIVE OF ANGINA LESS SUGGESTIVE OF
ANGINA
TYPE OF PAIN DULL SHARP/STABBING
PRESSURE/CRUSHING
PAIN
DURATION 2-5 MIN, <20 MIN SECONDS TO
HOURS/CONTINUOUS
ONSET GRADUAL RAPID

LOCATION/CHEST WALL SUBSTERNAL, NOT LATERAL CHEST

TENDERNESS TENDER TO PALP. WALL/TENDER TO PALP.
REPRODUCIBALITY WITH WITH
EXERTION/ACTIVITY BREATHING/MOVING
AUTONOMIC SYMPTOMS PRESENT USUALLY ABSENT
ATYPICAL PAIN
RISK FACTORS FOR DEVELOPING ATYPICAL PAIN:
Diabetes, females, non white patients, elderly, dementia, no prior
history of MI
ATYPICAL SYMPTOMS:
GIT symptoms
Syncope
SOB
Pleuritic/positional pain
Chest wall tenderness
No chest pain/symptoms
NRMI 2 STUDY – MI without chest pain -> increased risk of death (23% vs 9%)
More complications – hypotension,heart failure, stroke
Delayed ED presentation, delayed intervention
RISK STRATIFICATION IN ACS
Reasons :
Provides prognostic information

Determines treatment and level of intervention -> low

risk patients –early discharge, high risk -> admission
to high care
Risk stratification should be ongoing – at admission, 6-8
hrs, 24hrs, discharge
TOOLS USED IN RISK STRATIFICATION
HISTORY

ECG

BIOCHEMICAL MARKERS
ECG
First point of entry into ACS algorithm

Abnormal or normal

Neither 100% sensitive or 100% specific for AMI

Single ECG for AMI – sensitivity of 60%, specificity 90%

Represents single point in time –needs to be read in

context

Normal ECG does not exclude ACS – 1-6% proven to have

AMI, 4% unstable angina
GUIDELINES
Initial 12 lead ECG – goal door to ECG time 10min, read
by experienced doctor (Class 1 B)
If ECG not diagnostic/high suspicion of ACS – serial
ECGs initially 15 -30 min intervals (Class 1 B)

ECG adjuncts – leads V7 –V9, RV 4 (Class 2a B)

Continuous 12 lead ECG monitoring reasonable

alternative to serial ECGs (Class 2a B)
BIOCHEMICAL MARKERS
IDEAL MARKER:
 High concentration in myocardium
 Myocardium specific
 Released early in injury
 Proportionate to injury
 Non expensive testing

Troponins
CKMB
Myoglobin
Other markers
TROPONINS T/I
Troponin T vs I –
both equivalent in diagnostic and prognostic abilities ( except in renal
failure – Trop T less sensitive)

Elevation ~ 2hrs to 12hrs

~30 – 40% of ACS patients without ST elevation – had normal CKMB

but elevated troponins on presentation

Meta-analysis (Heindereich et al) – odds of death increased 3 to 8 fold

with positive troponin
MYOGLOBIN
Rapid release within 2 hours

Not cardiac specific

Rule out for NSTEMI rather than rule in.

CKMB
Used in conjunction with troponins
Useful in diagnosing re-infarction
2007 ACC/AHA GUIDELINES
Cardiac biomarkers measured in all patients with
suspicion of ACS (Class 1 B)

Troponin preferred marker( Class 1 B)

If troponin negative within 6 hours of onset, repeat 8-

12hours later(Class 1 B)

Remeasuring of positive biomarkers to determine infarct

size/necrosis (Class 2a B)

Patients presenting within 6 hours of symptom onset –

myoglobin in conjunction with troponin measured
(Class 2b B)

2hr delta CKMB/Delta troponin considered in <6hr

presentation (Class 2b B)

Class 3 – AST/LDH/CK without CKMB

RISK STRATIFICATION MODELS
TIMI RISK SCORE –INCREASE IN MORTALITY WITH INCREASING
SCORE ~40% ALL CAUSE MORTALITY AT 14 DAYS FOR PATIENTS
REQUIRING URGENT REVASCULARISATION
MANAGEMENT ALGORITHM
 MANAGEMENT UPDATE
2007ACS/AHA GUIDELINES:
Rapid catergorisation of patient (Class 1 C)

Possible ACS, non diagnostic ECG/biomarkers – observed

in facility with cardiac monitoring (Class 1 C)

Alternative to in patient treatment: for those with 12hr

ECG/markers negative – stress ECG in 72hrs (Class 1C)
INITIAL INVASIVE VS CONSERVATIVE STRATEGY
CLASS 1 RECOMMENDATIONS:
Early invasive strategy for refractory angina, hemodynamic instability
(LOE B)
Early invasive strategy for stabilised patients with elevated risk for clinical
events.
High risk factors include:
 Recurrent angina, ischaemia at rest or minimal activity
 Elevated troponins
 New ST depression
 Signs of heart failure/worsening mitral regurg.
 Ventricular tachycardia
 Prior CABG
 PCI in last 6 months
 High TIMI/GRACE scores
 LVEF < 40%
CLASS 2b
May opt for initial conservative strategy in stabilised high risk
patients – dependent on patient/physician preference (LOE B)

CLASS 3
Invasive strategy -not recommended in patients with multiple co
morbidities, low risk patients, patients not consenting.(LOE C)
UA/NSTEMI –PHARMACOTHERAPY UPDATE
GENERAL:
IV B Blockers downgraded from Class 1 to 2a recommendation.
(COMMIT Trial)

Oral B Blockers in first 24hrs still Class 1 – but not used in signs of
heart failure, cardiogenic shock and reactive airway disease.(LOE
B)

MORPHINE downgraded from Class 1 to 2a – findings from

CRUSADE Registry
NSTEMI- PHARMACOTHERAPY UPDATE
ANTIPLATELET THERAPY:
CLASS 1 RECOMMENDATION
Aspirin to all patients as soon as possible and continued (if no C/I)
(LOE A)
Initial dose 162 -325mg
Maintenance 75 -162mg
No added benefit from higher doses except post stenting

Clopidogrel for those allergic to aspirin or major GI bleeding (LOE A)

For initial invasive strategy – aspirin + clopidogrel or IV glycoprotein

2b/3a therapy (LOE A)
Abciximab if no delay in angiography/PCI, eptifibatide/tirofiban if
delayed angiography(LOE B)
 CLASS 2a
In patients managed conservatively who develop recurrent ischaemia –
on clopidogrel/ASA/Anticoagulant – can add glycoprotein inhibitor.
(LOE C)

Invasive strategy – can use clopidogrel + glycoprotein inhibitors(LOE C)

CLASS 2b
In patients managed conservatively – can add glycoprotein inhibitor
therapy, in addition to aspirin & anticoagulant (LOE B)
 CLASS 3
ABCIXIMAB should not be given if PCI not planned (LOE A)
For initial conservative strategy:
Aspirin + Clopidogrel + anticoagulant – administered for
1 month(LOE A), continued ideally up to 1 year(LOE B)

If initial conservative strategy selected but patient has

recurrent ischaemic symptoms/heart
failure/arrythmias – diagnostic angiography
recommended. Clopidogrel or Glycoprotein 2b/3a
inhibitors should be added before angiography.
ANTICOAGULANT THERAPY
CLASS 1
Anticoagulant therapy should be added as soon as possible
For patients undergoing angiography/PCI – enoxaparin/UFH
(LOE A) of Bivalirudin/ fondaparinux (LOE B)

For conservative strategy: enaxaparin, UFH (LOE A),

fondaparinux

For patients with increased risk of bleeding with conservative

strategy – fondaparinux
 CLASS 2a
Enoxaparin /fondaparinux vs UFH

Enoxaparin/fondaparinux preferred except in those undergoing

CABG within 24hrs (LOE B)
ADDITIONAL MANAGEMENT
STRESS TEST should be performed for those managed
conservatively.
If stress test positive/ high risk – needs diagnostic
angiography(Class 1 LOE A)

If classed as low risk –

need to continue aspirin indefinitely ( LOE A)
Clopidogrel for at least 1 month(LOE A), ideally up to 1
year(LOE B)
STEMI
PHARMACOLOGICAL UPDATE:
ANALGESIA – changes from 2004 guidelines

MORPHINE: still remains Class 1 C for STEMI, titrated doses

NSAIDS/COX 2 INHIBITORS: those on it should have it discontinued (

increased risk of mortality, re infarction, heart failure, myocardial
rupture) Class 1 C

NSAIDS should not be administered in hospital for MI (Class 3)

BETA BLOCKERS
Modified recommendation
Oral Beta Blockers should be initiated in first24rs, if no contra-
indications (heart failure, risk of cardiogenic shock) Class 1 B
Patients with early contraindications -> re- evaluated later for
possible use
Role of IV B blockers – used in hypertensive patients with STEMI
Class 2a B
Class 3 LOE A – IV B blockers should not be administrated to
patients with heart failure, risk of cardiogenic shock
REPERFUSION STRATEGY
ECG SOAL 9