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PAGE 20 diagnosis . The development
of highly sensitive troponin assays has allowed for the assessment of myocardial necrosis with greater precision than CK measurements or earlier standard troponin assays . In patients with an acute infarction , levels of tro-
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Image courtesy Dr J Wong |
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ponin rise rapidly ( within one hour of | ||||
symptom onset ) and typically remain | ||||
elevated for several days . The diagnosis | ||||
of MI requires a rise and / or fall in | ||||
the level of troponin . Troponin levels | ||||
are typically not elevated in patients | ||||
with unstable angina ; however , in the | ||||
minority of patients who do have a | ||||
non-dynamic elevation , outcomes are | ||||
significantly worse in the short and | ||||
long term . 18 | ||||
Serial sampling of cardiac-specific | ||||
troponin levels at hospital presentation | ||||
and at clearly defined periods after | ||||
presentation is a key recommendation | ||||
in the 2016 Australian Clinical Guidelines |
for the Management of Acute Coronary Syndromes . 2 Compared with standard troponin assays , high sensitivity troponin assays have a greater negative predictive value for acute |
Figure 3 . Hyperacute ST elevation in the inferior leads . |
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MI , increase the detection of type 1 MI |
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and can be interpreted as quantitative markers of cardiomyocyte damage . 19
According to the 2018 Fourth Universal Definition of Myocardial Infarction , a key criterion for the diagnosis of MI is one troponin value above the 99th percentile of the upper reference limit ,
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Image courtesy Dr J Wong |
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with acute injury considered when | ||||
there is a rise and / or fall of troponin values . 20 Bear in mind that several conditions , both cardiac and non-cardiac | ||||
in origin , may influence the serum levels | ||||
of troponin ( see box 3 ). | ||||
There are two scenarios where it | ||||
may be reasonable for a GP to utilise a | ||||
troponin test in the community . First , | ||||
when a patient presents having experienced | ||||
symptoms of ACS several days | ||||
earlier and is currently asymptomatic , |
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and second , in a low-risk patient with atypical symptoms where the test can ‘ rule out ’ ACS . 21 Do not perform a troponin level in asymptomatic patients as this can lead to uncertainty and unnecessary investigations .
INVESTIGATIONS
NON-INVASIVE imaging provides cli-
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Figure 4 . ST elevation in leads V1 to V3 and aVL indicating acute anterior ST elevation myocardial infarction . |
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nicians the opportunity to exclude | ||||
the presence of CAD and the opportunity | ||||
for diagnosis and risk stratification | ||||
. Echocardiography ( see figure 6 ) | ||||
can be useful in assessing the patient | ||||
with non-diagnostic ECG changes and | ||||
ongoing chest pain , as it can identify | ||||
wall-motion abnormalities that may | ||||
be attributable to acute myocardial ischaemia . 22 Echocardiography has a high sensitivity ( greater than 90 %) and | ||||
high negative predictive value ( greater | ||||
than 95 %) for patients in this clinical |
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context . 22
Once an ACS has been ruled out in a patient , they may be discharged from the hospital , as their short-term risk of a coronary event is low . Following discharge , clinicians have several diagnostic options available to assess the
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Figure 5 . Posterior wall STEMI and first-degree block , with total occlusion of the distal RCA . |
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presence and extent of CAD .
Coronary CT angiography ( CCTA , see figure 7 ) can be used for patients deemed at intermediate risk to evaluate for the presence of CAD ( see figures 8 and 9 ). 23 CCTA is an anatomic test that has become increasingly available and is a viable alternative to invasive coro-
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modification and aids in the diagnosis of non-coronary causes of chest pain . 23 A higher CAC score in both symptomatic and asymptomatic patients is associated with an increased risk of further cardiovascular events . 24 CCTA also assists in the identification of congeni- |
MANAGEMENT
Pre-hospital
Refer patients who present in general
practice with chest pain and a suspected ACS to ED or a facility capable of definitive risk stratification and diagnosis of ACS . Initiate treatment , where
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five minutes for up to three doses , in the absence of contraindications . 2 Contraindications to use of GTN include hypotension , severe anaemia , hypersensitivity to nitroglycerin , recent PDE-5 inhibitor use , raised intracranial pressure and severe aortic stenosis . 26 |
documented aspirin allergy ( for example , asthma or anaphylaxis ), a known platelet disorder or the presence of active bleeding . 27 Evidence indicates that NSAIDs are linked with increased risk of major adverse cardiovascular events ; avoid their use in patients with |
nary angiography . CCTA may be used in conjunction with functional studies |
tal anomalous coronary arteries . 25 Contraindications to CCTA include a |
this is possible and in the absence of contraindications , with aspirin and |
In the absence of contraindications , give all patients presenting with |
28 , 29 suspected ACS . Do not provide additional antiplate- |
such as a stress ECG / echocardiogram . |
history of anaphylactic reaction to con- |
sublingual nitroglycerin ( GTN ). |
a possible ACS aspirin 300mg ( orally , |
let or anticoagulation therapy or other |
CCTA facilitates the calculation of a coronary artery calcium ( CAC ) score , helps guide the intensity of risk factor |
trast dye , haemodynamic instability , AMI , decompensated heart failure and renal impairment . 23 |
In the presence of ongoing chest pain , administer GTN sublingual tablet ( 0.3-0.6mg ) or spray ( 0.4-0.8mg ) every |