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| Journal of the New Zealand Medical Association,
29-June-2012, Vol 125 No 1357
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The use of troponin in general
practice
Sally Aldous, Peter Gent, Graham McGeoch, Denise
Nicholson
International guidelines recommend serial cardiac troponin
(cTn) measurement in patients presenting with symptoms suggestive of acute
coronary syndrome (ACS).1,2 Cardiac troponin is
the gold standard biochemical criterion for the diagnosis of acute myocardial
infarction (AMI)1 and investigations and
treatments guided by cTn results have been shown to influence
outcomes.2–6 As such, cTn is not only a
diagnostic tool but is also highly effective in risk stratification.
The primary care physician or general practitioner (GP)
faces the challenge of identifying patients with ACS and therefore those at risk
of adverse cardiac events such as death, AMI and heart failure. It is often the
task of the GP to initiate further diagnostic procedures in a timely manner in
those with suspected ACS. However, although symptoms such as chest pain are
common in general practice, they are due to acute coronary artery disease in
only a minority of cases. It is therefore also the role of the GP to protect
patients from over-diagnosis and inappropriate treatment, and prevent
overcrowding of specialist and emergency
services.7–10
Cardiac troponin tests are available in the community and
GPs are making increasing use of these tests to help triage such
patients.7
Concerns with the use of cTn in the community are:
MethodsA retrospective audit was performed of all cTn requests
referred to Canterbury Health Laboratories from General Practice in
Christchurch, New Zealand, in 2010. Canterbury Health Laboratories is one of
three laboratory groups in the region that received cTn requests during this
time period.
Patient data was collected by means of a regional and
then national health events search (which identifies any hospital attendance
using an alpha numeric identifier unique to that patient). Admissions to
hospitals outside of New Zealand were not sought. Data was collected regarding
whether admission occurred after index cTn testing and the subsequent diagnosis
according to the discharge notice from the admitting team.
Patients were followed for 6 months for adverse events
including death, non-fatal AMI, revascularisation (percutaneous coronary
intervention or coronary artery bypass surgery) and admission for heart failure
with diagnoses again according to the discharge diagnosis of the admitting team.
These were analysed in those above and those below 75 years of age as an
arbitrary (but not ideal) marker of comorbidity.
The cTn assay utilised by Canterbury Health
Laboratories is Abbott Architect Troponin I
(99th percentile 0.028 mcg/L, 10% coefficient
of variation 0.032 mcg/L, limit of detection 0.010 µg/L, decision cut-point
as per manufacturer >0.03 µg/L)
ResultsThere were 2662 patient episodes in 2575 patients during
2010 in which ≥1 sample for cTn testing were sent to Canterbury Health
Laboratories. The median age was 63 (interquartile range 51 to 74) and 1186
(44.6%) were male. Other patient characteristics were not available. There were
321 (12.1%) patient episodes in which serial samples were taken.
There were 223 patients episodes (8.4%) in which ≥1
cTn results were elevated above the decision threshold, median age 73
(63–83), 131 (58.7%) male. Twenty-one (9.4%) had serial measurements, of
which 11 were elevated on the second sample only. 184 (82.5%) were admitted to
hospital for further evaluation, median age 71 (62–81), 111 (60.3%) male,
median cTn 0.14 (0.06–0.61) µg/L. The discharge diagnoses of those
who were admitted are shown in Figure 1.
Figure 1. Discharge diagnosis of patients
admitted following elevated troponin in general practice
 STEMI – ST elevation myocardial infarction, NSTE
ACS – non ST elevation acute coronary syndrome. Arrhythmia=atrial
fibrillation, supraventricular tachycardia, complete heart block, Respiratory
disease=chronic obstructive pulmonary disease, pulmonary embolus,
pneumonia.
Those with a diagnosis of myocardial infarction had higher
median cTn levels, 0.27 (0.10–1.65) µg/L than those with other
diagnoses, 0.08 (0.05–0.22) µg/L. Those not admitted had a median cTn
of 0.05 (0.03–0.09) µg/L.
Figure 2. Six month event rates according to
troponin result and whether patient was admitted at index testing
(a) Troponin positive/Admitted
 (b) Troponin positive/Not admitted
 (c) Troponin negative/Admitted
 (d) Troponin negative/Not admitted
 Of the 184 admitted, 5 (2.7%) underwent stress testing, 86
(46.7%) underwent coronary angiography and 49 (26.6%) were revascularised, 4
with coronary artery bypass surgery. Events post discharge are shown in Figure
2. The 6-month event rates of the 39 with elevated cTn who were not admitted,
median age 81 (66–88), 19 (48.7%) male, are also shown in Figure 2. The
median cTn of those with (any) 6-month event was 0.10 (0.05–0.58)
µg/L compared with those without events, 0.12 (0.05–0.41)
µg/L.
Figure 3. Discharge diagnosis of patients
admitted following normal level troponin in general practice
 STEMI – ST elevation myocardial infarction, NSTE
ACS – non ST elevation acute coronary syndrome. Other cardiac
diseases=peri/myo/endocarditis, heart failure, valvular disease,
Arrhythmia=atrial fibrillation, supraventricular tachycardia, complete heart
block, Respiratory disease=chronic obstructive pulmonary disease, asthma,
pulmonary embolus, pneumonia, influenza, malignancy, Gastrointestinal
disease=cholecystitis/cholangitis/pancreatitis, ileo/colitis, appendicitis,
peptic ulcer disease.
There were 2439 patients in whom all cTn measurements were
below the decision cut-point, median age 62 (50–73), 1056 (43.1%) male.
Two hundred and ninety seven (12.2%) of these had serial troponin measurement.
Three hundred and forty four (14.1%) were admitted to hospital for further
evaluation, median age 65 (54–78), 136 (39.5%) male. The discharge
diagnoses of those who were admitted are shown in Figure 3.
Of the 344 admitted, 69 (20.1%) underwent stress testing, 31
(9.0%) underwent coronary angiography and 13 (3.8%) were revascularised, 5 with
coronary artery bypass surgery. Events post discharge are shown in Figure 2. The
6 month event rates of the 2095 with normal level cTn who were not admitted,
median age 62 (50–73), 917 (43.8%) male, are also shown in Figure 2.
DiscussionThis audit investigates the use of cTn testing in an urban
community setting over a 1 year period and shows that such a test is highly
utilised.
The utility of cTn in the community should be to:
Previous studies have shown that if suspicion for
ACS is low, GPs are more likely to either order cTn and wait for the result or
manage medically. If suspicion is intermediate, GPs tend to either refer for
admission without cTn results (especially when patients present early after
symptom onset) or order cTn and wait for the result. In contrast, if the
suspicion is high, patients are referred without cTn
results.11
This study shows that the vast majority of patients with
elevated cTn were admitted. This appears highly appropriate as those with
elevated cTn were much more likely to come to harm in the short term with higher
6 month rates of death (8.5% versus 1.1%), AMI (2.2% versus 1.2%),
revascularisation (1.8% versus 0.7%) and heart failure (3.1% versus 1.0%) than
those with normal cTn levels. Those with and without events had similar median
cTn levels.
Those with elevated cTn who were not admitted had higher
event rates than those who were admitted (12.8% versus 7.6% for death, 7.7%
versus 1.1% for AMI, 2.6% versus 1.6% for revascularisation and 7.7% versus 2.2%
for heart failure). Although not all comorbidities were known, the median age of
these patients was 81, suggesting that admission may not have been appropriate
and that community treatment was possibly medical/palliative. However, 2.6% of
these patients were revascularised within 6 months suggesting that this was not
the case in all patients. Figure 2 shows how those ≥75 (a surrogate but
not ideal marker for comorbidity) were more at risk of events, as expected.
The median cTn levels in these patients showed only
borderline elevations which may also contribute to the decision not to admit,
unfortunately we do not have data regarding the level of probability for AMI
assigned by the General Practitioner.
It is likely that a significant number of patients would
have been referred for admission irrespective of the cTn results, for example
the 13 patients with STEMI and the 14.4% of those with negative cTn results who
were still admitted. If admission is inevitable, it is unlikely that measurement
of cTn in the community is necessary and may have economic
implications.11 It can be seen that a negative
result for cTn in the community indicates low risk of subsequent adverse cardiac
events. As such, it seems reasonable to suggest that current management of these
patients in the community is appropriate.
Only approximately 12% of patients had serial testing.
Current International Guidelines recommend serial cTn measurement at
presentation and again at 8–12h after symptom
onset2 or 6–9h post
presentation.1 Previous audit data at
Christchurch Hospital has shown that the cTn used in this study is reliably
negative by 10 hours post symptom onset.
Unfortunately the time from symptom onset to presentation
was unknown. Although a negative cTn in the community appears to indicate low
risk, serial cTn would still be recommended in those presenting less than 10
hours from symptom onset. It was shown that of the 21 patients with elevated cTn
undergoing serial measurements, only 10 had elevations on the first test.
A previous community audit performed elsewhere in New
Zealand showed that 12% of negative tests were performed in patients presenting
less than 10 hours after the onset of
symptoms.7 It may be therefore, that most of
the early presenters in this study did infact have serial measurements.
The indication for cTn testing in all patients was unknown
as clinical information at the time of the test was not collected. Therefore
this did not allow an assessment of the clinical appropriateness of testing.
However, the discharge diagnosis of the patients admitted, demonstrated a wide
variety of conditions.
Previous audit data in Christchurch Hospital shows that in
patients admitted for rule out of ACS, approximately 20–25% have elevated
cTn and approximately 90–95% of these have a diagnosis of AMI. In
contrast, this audit shows that only 8.3% have elevated cTn in the community and
only just over 50% of these had a diagnosis of AMI.
This illustrates the wide variety of conditions that can
lead to cTn elevation although those without AMI had lower median cTn levels
than those with AMI. It should therefore be emphasised that cTn is to only be
measured in patients with suspected ACS. Previous studies have shown that
patients with symptoms such as chest pain presenting in the community are most
likely to have musculoskeletal conditions and a significant number of patients
have psychogenic disorders, respiratory infections and gastrointestinal
diseases.8,9 Only a minority have
ACS,8,9 1 study had an ACS rate of
3.6%9 compared with our 5.4%. The American
Heart Association guidelines2 have suggested
that symptoms suggestive of ACS include acute chest, epigastric, neck, jaw or
arm pain or discomfort or pressure without apparent non-cardiac source. Symptoms
such as fatigue, shortness of breath, syncope or arrhythmia can in a minority of
patients be secondary to AMI but are not symptoms that automatically indicate
the need to measure cTn if ACS is otherwise not suspected. While it is accepted
that many patients present atypically, this highlights perhaps that cTn testing
in the community may not be measured in the appropriate clinical context in a
significant proportion of patients.
A previous study showed that only 25–40% of GPs could
correctly identify other causes of cTn
elevation.11 Other studies suggest that
community cTn testing is indicated to determine the need for acute referral in
those with intermediate suspicion of ACS and not those with a high likelihood
(who should be referred without cTn testing)7,9
and is also not for reassurance of the patient in whom there is low suspicion of
ACS.7
In conclusion, this study suggests that the use of cTn in
the community appropriately triages patients regarding the need for admission.
However, the indication for testing only in cases of suspected ACS and the use
of serial cTn measurement in early presenters should be emphasised.
A clinical pathway for management of suspected ACS in the
community is currently being developed. Each patient is categorised as to
whether their likelihood of ACS is high, intermediate, low or unlikely using
predefined criteria to help determine the best management. If high risk,
immediate referral of patients without prior cTn testing should occur. Low risk
patients should be managed in the community with cTn testing, including serial
measurements in patients presenting less than 10 hours after onset of symptoms.
If unlikely to be ACS, cTn testing is not advised.
However, there is always a limit to how specific such an
algorithm can be and clinical judgment will always be required, especially in
cases of greater uncertainty. It is our intent to repeat this audit in 1 year
following the instigation of this pathway.
Competing interests: None
declared.
Author information: Sally Aldous,
Cardiologist, Cardiology Department, Christchurch Hospital, Christchurch; Peter
Gent, General Practitioner, Christchurch; Graham McGeoch, General Practitioner,
Christchurch; Denise Nicholson, General Practitioner, Clinical Editor Health
Pathways, Canterbury District Health Board, Christchurch
Acknowledgements: We thank all the staff at
Canterbury Health Laboratories for troponin assays.
Correspondence: Sally Aldous, Cardiology
Department, Christchurch Hospital, Riccarton Ave, Christchurch, New Zealand.
Fax: +64 (0)3 3641415; email: sally.aldous@cdhb.govt.nz
References:
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