Download Acute Coronary Syndrome

Spencer Toombes FRACP
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Challenges of assessing patients with chest pain...
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Terminology & Pathophysiology
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ECG interpretation
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Use of Troponin
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Risk Assessment
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Inpatient management
- how and when to transfer
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Post-discharge management
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For each of the following scenarios...
What is the most likely diagnosis?
What is this patient’s risk of having an
Acute Coronary Syndrome?
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Complaining of intermittent central chest
pain.
Previous ischaemic heart disease:
Coronary angiogram 2 years ago showed
40% LAD and 30% RCA stenosis.
Managed medically.
Has noticed over the past 2 months that he
needs to use his GTN spray whenever he
exerts himself.
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What if he had received a stent 5 months
ago?
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Recent sharp, stabbing pain adjacent to her
left sternum.
There doesn’t seem to be a clear precipitant.
She feels a bit washed out, but otherwise
reasonably well.
…but she is a Type II diabetic.
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10 minutes of central chest heaviness after he
finished mowing the lawn
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Associated with pallor and breathlessness
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His wife thought he looked ill and talked him
into coming up to your practice.
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Positive family history, heavy smoker.
(Includes biliary)
Cardiac
Oesophageal
28%
14%
60%
37%
10%
100%
100%
49%
35%
23%
5%
18%
12%
33%
Back 12%
Back 33%
Bennett et al. Lancet. 1966
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Intensity of Pain - no indication of severity.
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Nature of Pain - no indication of diagnosis:
• 5-19% acute coronary syndromes ‘sharp’ or pleuritic.
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Physical Signs - no indication of diagnosis:
• 15% AMI patients have chest wall tenderness.
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‘Atypical’ Presentations:
• Up to 25% patients with ACS do not present with
“classical” chest pain.
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Acute Coronary Syndrome (ACS)
Stable angina
Unstable angina
Myocardial ischaemia
Q wave infarction
Non-Q wave infarction
STEMI... STEACS
Non-STEMI... Non-STEACS
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little cholesterol content
thick fibrous cap
low risk of rupture
The proportion of the lumen occluded
determines the degree of exercise related
ischaemia, and the severity of symptoms.
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Lots of Low Density Lipoprotein Cholesterol
Thin fibrous cap
Lots of inflammation:
 Activated T cells, Macrophages, Foam Cells
 Mediators: Cytokines and C reactive protein
HIGH RISK OF RUPTURE
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Dynamic Partial Occlusion: No damage
 Worsened Angina pain, possible ECG change
 No cardiac enzyme rise
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Dynamic Partial Occlusion: Some damage
 Worsened Angina pain, probable ECG change
 Rise in cardiac troponin, +/- creatinine kinase
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Complete Occlusion:
 Full thickness myocardial infarction
 ST segment elevation, Q wave formation if not treated
Acute Coronary Syndrome : Terminology
Low-risk
UAP
High-risk
UAP
“minor
myocardial
damage”
Non-ST
Elevation
MI
ST Elevation
MI
Troponin
CK
Serum markers
No detectable
troponin
Normal CK
Detectable
troponin
Normal CK
ECG at evaluation
Normal ECG
ST depression
or transient ST elevation
ECG at discharge
Normal ECG
no Q wave
Detectable
troponin
and elevated CK
ST elevation
Q or no Q wave
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Rapid assessment.
Observed environment.
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Aspirin 300mg.
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ECG within 10 minutes of presentation.
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STEMI: requires immediate reperfusion
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Everything else: still requires risk assessment.
Tnl
TnC
TnT
Ca++
Tropomyosin
Actin
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Exquisitely sensitive marker of myocardial
distress... not necessarily muscle necrosis
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Onset 4-6, peak 24-36 hours, offset 7 days
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Normal initial troponin is NOT reassuring
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Normal 12 hour troponin is quite reassuring
Lindahl NEJM 2000 343:16;1139-47
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Don’t necessarily mean ACS...
 Pulmonary embolus
 Left ventricular failure
 Renal failure
 Sepsis
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True false positives related to assay
 Immune cross reactivity
GENERALLY DO NOT ORDER
IN GENERAL PRACTICE
Presentation of ACS
(clinical presentation, initial ECG)
Working
diagnosis
NSTEACS
STEMI
Time
Evolution of
ECG and
biomarkers
Myonecrosis confirmed
Final
diagnosis
STEMI
NSTEMI
Myonecrosis not confirmed
Unstable angina
ACS = acute coronary syndromes; ECG = electrocardiogram; STEMI = ST-segment-elevation myocardial infarction;
NSTEACS = non-ST-segment elevation acute coronary syndromes; NSTEMI = non-ST-segment elevation
myocardial infarction
Acute Coronary Syndrome Guidelines Working Group. Med J Aust 2006;184(8 Suppl):S9-29.
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Complaining of intermittent central chest
pain.
Previous ischaemic heart disease:
Coronary angiogram 2 years ago showed
40% LAD and 30% RCA stenosis.
Managed medically.
Has noticed over the past 2 months that he
needs to use his GTN spray whenever he
exerts himself.



Recent sharp, stabbing pain adjacent to her
left sternum.
There doesn’t seem to be a clear precipitant.
She feels a bit washed out, but otherwise
reasonably well.
…but she is a Type II diabetic.

10 minutes of central chest heaviness after he
finished mowing the lawn

Associated with pallor and breathlessness

His wife thought he looked ill and talked him
into coming up to your practice.

Positive family history, heavy smoker.
What is their risk of having an
Acute Coronary Syndrome?
These patients can be managed with upgrade to their anti-anginal
medications and outpatient referral for cardiac investigation.
These patients generally require emergency admission to a monitored
environment, and aggressive drug therapy including parenteral anticoagulants.
These patients generally require a period of observation with serial ECG and
biomarker assessment, enabling them to be re-classified as high or low risk...
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Ambulance
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Monitoring
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Oxygen ?
Nitrates ?
Aspirin ?
Pain relief ?
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Intermediate risk: reclassify after 6-12 hours
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Low risk:
Upgrade therapy?
Provocative investigation: EST or MPS
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High risk...
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Aspirin 300mg. stat. then 75 -100mg.
daily.
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Clopidogrel: 300mg. load then 75mg.
daily
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Gp IIbIIIa receptor antagonists:
 Tirofiban (Aggrastat)
 Abciximab (Reopro)
 Eptifibatide (Integrilin)
CLOPIDOGREL
C
ADP
ADP
GPllb/llla
Activation
(Fibrinogen receptor)
Collagen thrombin
2
TXA
COX
ASA
TXA2
COX, cyclooxygenase; ADP, adenosine diphosphate; TxA2, thromboxane A2
Schafer AI Am J Med 1996;101:199–209
Pathways of Blood Coagulation during Hemostasis and Thrombosis
Furie B and Furie B. N Engl J Med 2008;359:938-949
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IV unfractionated heparin infusion
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s/c low molecular weight heparin
(eg. Clexane 1mg./kg. bd.)
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s/c Fondaparinux (Erixtra)
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Beta blockers, IV and/or oral.
Insulin + dextrose infusion for high BSL.
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High dose Statins:
ACE inhibitors
Oxygen
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Morphine & Nitrates for symptom
control
eg. 80mg. Atorvastatin
Evidence supports prompt routine angiography
with a view to angioplasty of the culprit
lesion.
▪ TACTICS TIMI18, FRISC II, RITA 3
▪ ICTUS ???
 Short term death 7% vs. 9%
 STD excld. SHOCK 5% vs. 7%
 Reinfarct rates 3% vs. 7%
 CVA 1% vs. 2%
 Combined endpoint 8% vs. 14%
Cardiologists drive SAABs:
S tatin (high dose atorvastatin)
A nti platelet agents: Aspirin + Clopidogrel
A ce inhibitor
B eta-blocker
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Sexual Relations:
 6-7 METS: Stage II Bruce, 2 flights stairs
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Driving: (private license)
 Angioplasty: 2 days, assuming no MI, no
symptoms and normal ecg.
 Myocardial Infarct: 2 weeks, assuming
uncomplicated
 Cardiac Arrest: 6 months, unless assoc. MI
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Assessing chest pain is notoriously difficult
Early aspirin, Early ECG
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If in doubt, manage as an inpatient
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Risk stratification, with serial data
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Aggressive drug combinations for high risk
patients... Anticoagulants, and Antiplatelets.
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