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Stress echocardiography is superior to exercise ECG in the risk stratification of patients presenting with acute chest pain with negative Troponin

Paramjit Jeetley, Leah Burden, Roxy Senior
DOI: http://dx.doi.org/10.1016/j.euje.2005.05.002 155-164 First published online: 1 March 2006


Objective To compare exercise electrocardiography (ExECG) and stress echocardiography (SE) in the risk stratification of patients presenting to hospital with cardiac-sounding chest pain, non-diagnostic ECGs and negative cardiac Troponin.

Methods Patients presenting with acute chest pain were prospectively randomised to early ExECG or SE. A post-test likelihood of CAD was determined by the pre-test likelihood and the result of the stress test. Patients with a low post-test likelihood of CAD were discharged; those with a high post-test probability were considered for coronary angiography. All others were managed according to standard hospital protocols.

Results A total of 302 patients underwent either ExECG or SE. SE identified significantly more patients with a low post-test probability of CAD (80% vs 31%, p<0.0001) and significantly fewer patients with an intermediate post-test likelihood of CAD compared to ExECG (3% vs 47%; p<0.0001). Significantly fewer patients undergoing SE were referred for further tests to exclude or refute the diagnosis of CAD (16% vs 52%; p<0.0001). In total, 36 (12%) had flow limiting CAD demonstrated by coronary angiography. Significant CAD was seen in fewer patients with a positive ExECG than with a positive SE (56% vs 84% (p=0.12)). Event rates were low for both modalities in patients with low post-test probability (3.5% for SE vs 5.1% for ExECG; p=ns) though the number of patients identified as low risk was higher if SE was performed.

Conclusion Despite negative cardiac Troponin, 12% of patients with acute chest pain had significant CAD. SE is superior to ExECG in discriminating between those patients with a low and intermediate risk of CAD and correctly identified patients with significant CAD, as well as conferring an excellent prognosis in those considered low risk. SE significantly reduces the requirement for further tests to diagnose CAD compared to ExECG.

  • Stress echocardiography
  • Exercise echocardiography
  • Coronary artery disease
  • Prognosis


The evaluation of patients presenting to hospital with acute chest pain suggestive of myocardial ischaemia remains a challenge.1 Patients with acute chest pain account for 20–30% of emergency medical admissions.2,3 Only a proportion of these patients have a diagnosis of acute myocardial infarction or unstable angina and they can be easily be identified based on history, clinical examination, ECG, and the use of serum markers.4 The greatest problem arises in patients with chest pain of recent onset, which may not be typical in nature, and is associated with non-diagnostic or even normal presenting ECGs. A variety of triage algorithms have been suggested for risk stratification and to identify those patients with significant underlying coronary disease.5–8 The use of highly sensitive serum markers (cardiac Troponin T and I) have helped identify those patients at high risk4,9 but such markers are indicators of myocardial necrosis and their absence does not exclude the presence of significant coronary artery disease (CAD) as the cause of presenting symptoms.8

Current ESC guidelines10 recommend pre-discharge exercise tests for this cohort of patients to provide additional prognostic information reflecting the extent and severity of underlying CAD. The most common method of stress testing in the UK is the exercise ECG (ExECG). It is relatively inexpensive, widely available and has the benefit of extensive clinical experience, but has poor specificity and sensitivity compared to other stress testing techniques.11,12 Confounding variables such as left ventricular hypertrophy (LVH), resting ST-depression and digoxin effects13 reduce its specificity and exercise testing in women is even less accurate.14

Stress echocardiography (SE) is an accepted test for the detection of CAD and can be performed easily using either treadmill exercise15 or pharmacological stress agents, such as dobutamine,16,17 in patients unable to exercise.

We therefore hypothesised that SE was superior to ExECG in risk stratifying patients presenting to hospital with acute chest pain and a negative cardiac Troponin but with coronary risk factors.


We conducted a prospective, randomised study on patients presenting to hospital with acute cardiac-sounding chest pain. Written, informed consent was obtained from all patients and the study was approved by the local ethics committee.

Patient selection

Patients presenting to hospital with a history of acute chest pain, a normal or non-diagnostic ECG, and two or more risk factors for CAD were eligible for inclusion into the study. Risk factors for CAD were defined as: men aged >45 yrs old, women aged >55 yrs old, diabetes mellitus, current or ex-smoker, hyperlipidaemia, hypertension, previous history of ischaemic heart disease (documented angina, previous myocardial infarction, previous percutaneous coronary intervention or coronary artery bypass grafting), a family history of ischaemic heart disease. Patients were excluded from the study if any of the following conditions were present: ST-segment elevation >1mm in 2 leads or significant planer ST-segment depression (>1mm in 2 leads) suggestive of acute infarction or ischaemia on the presenting ECG; any significant rise in cardiac Troponin (Troponin I >0.03 or Troponin T >0.1); patients with known coronary artery disease awaiting revascularisation; patients in whom history and clinical examination suggested a non-cardiac source of chest pain; patients with absolute contra-indications for exercise testing (acute intercurrent illness, serious arrhythmia, known significant obstructive hypertrophic cardiomyopathy, severe LV dysfunction and uncontrolled hypertension).

Standard hospital protocols were followed in the acute management of patients. Evaluation included careful history taking, physical examination, serial 12-lead ECGs and serum cardiac Troponin measurements. Serial ECGs were recorded on presentation and during any new episode of chest pain during the observation period. Cardiac Troponin measurements were taken at a minimum of 12h after the onset of pain using either a bed-side kit in the case of Troponin T (TnT) or laboratory assay for Troponin I (TnI). Patient management e.g. the decision to order additional tests, admission to hospital and further therapy was at the discretion of the attending physician.

TIMI Risk Score was used as a guide to a pre-test probability of coronary disease18–20 (Table 1). Patients were categorised as having a low, intermediate or high pre-test likelihood of CAD; a score of 0 or 1 was considered low risk; 2–4 intermediate risk and 5 or more, high risk of significant CAD.

View this table:
Table 1

Pre-test probability determined by TIMI Risk Score

Age≥65 yrs1
≥3 Risk factors for CADa1
Known CADb1
Aspirin use within the last 7 days1
Recent (≤24h) severe angina1
ST-segment (≥0.5mm) deviation1
Elevated serum cardiac markersc1
Risk Score=total points(0–7)
  • a Risk factors included family history of CAD, hypertension, hyperlipidaemia, diabetes mellitus, or being a current smoker.

  • b Included prior myocardial infarction, prior revascularisation procedure or documented CAD on angiography with stenosis≥50%.

  • c Cardiac Troponin.

Patients were then randomised to undergo either standard exercise ECG testing or stress echocardiography within 24h of admission to hospital. Testing was carried out during the patients hospital stay and a post-test likelihood of CAD was determined on the basis of the pre-test probability of CAD and the result of the test. Patients with a low post-test likelihood of CAD were given a diagnosis of non-anginal chest pain and were discharged. Any further investigations were made at the discretion of the attending physician. Patients with a high post-test probability of CAD were counselled, advised on risk factor management and started on appropriate therapy e.g. Aspirin, β-blockers, statins. They were also considered for coronary angiography and subsequent revascularisation.

Patients with an intermediate post-test probability of CAD were considered for further investigation at the discretion of the attending physician. Such tests included further non-invasive imaging where appropriate or coronary angiography.

Exercise ECG testing

Patients randomised to exercise ECG underwent symptom limited Bruce (or modified Bruce) protocol exercise testing performed using a treadmill with continuous monitoring of a 12-lead ECG and regular blood pressure measurements. Standard end-points were used: fatigue, severe ischaemia (severe angina, >2mm ST-segment depression), hypertension (systolic BP >220mmHg), hypotension, pre-syncope or arrhythmia. Details regarding anginal symptoms, ST-segment deviation and haemodynamic response to exercise and exercise capacity were documented.

Patients able to perform to a workload of ≥9 METS21 without haemodynamic compromise or ECG changes were considered to have a low probability of significant CAD. Patients who developed significant hypotension, arrhythmia or ≥1mm planar or downsloping ST depression during exercise or in recovery were considered to have a high probability of CAD. All other patients were considered to have an intermediate risk of CAD.

Stress echocardiography

Patients randomised to stress echocardiography underwent either exercise or pharmacological testing at the discretion of the attending cardiologist. A 2-D echocardiogram was performed in the left lateral decubitus position using harmonic imaging (HDI 5000, Philips Medical Systems, Eindhoven, Netherlands). Digitized images of the left ventricle were obtained in the parasternal long-axis, short-axis and apical 4-, 2-, and 3-chamber views.

In the case of exercise stress echocardiography, standard symptom limited treadmill exercise testing was performed. Further images were acquired immediately (usually 60s) after peak exercise. Post-exercise images with the best endocardial definition were selected and displayed in a quad screen format side by side with the corresponding baseline images.

In patients who were considered unsuitable for exercise testing, dobutamine was infused peripherally in 3min dose increments, starting from 10μg/kg/min and increased to 20, 30 and 40μg/kg/min. If no end-point was reached, atropine was added to the continuing 40μg/kg/min dobutamine infusion in 4 divided doses of 0.3mg up to a maximum of 1.2mg.

End-points were the achievement of 85% of age predicted target heart rate; development of severe ischaemia (severe angina, extensive wall motion abnormality); achievement of peak dose (40μg/kg/min of dobutamine IV+1.2mg atropine IV) or the occurrence of intolerable side effects. The stress images were then acquired and assessed in the same way as in the exercise stress protocol.

In technically difficult patients, intravenous contrast (Optison, Amersham Health, UK) was used to enhance endocardial definition. Bolus injections of 0.3ml were administered via a peripheral cannula followed by a flush with 0.9% NaCl solution. Imaging with a low mechanical index was then performed.

Image analysis

On-line digital images in a multi-screen format were interpreted qualitatively for the presence, extent and location of segmental wall motion abnormality. Images were analysed by an experienced observer (RS) for systolic wall thickening and endocardial wall motion according to a 4 point score (1=normal; 2=reduced; 3=akinetic and 4=dyskinetic motion) using a 17-segment left ventricular model.22 Results were considered normal if all the segments that were normal at baseline showed a normal hyperdynamic response with increased systolic wall thickening after stress.

Inducible ischaemia was defined as the development of new or worsening regional synergy during stress; no change in basal asynergy was considered secondary to myocardial infarction.

Patients with evidence of inducible ischaemia at stress, or a resting wall motion abnormality in at least one segment (except isolated basal inferior or basal inferior septal segment) without prior history of myocardial infarction were considered to have a high probability of significant CAD. Patients who achieved a workload of >7 METS23 and achieved target heart rate and/or achieved maximum dose of dobutamine with no evidence of inducible ischaemia were considered to have a low risk of CAD. All other patients were considered to have an intermediate risk of CAD.

Coronary angiography

Coronary angiography was performed in patients in whom there was a high post-test likelihood of CAD, and in those patients who had an intermediate post-test likelihood but were considered to be high risk of having underlying CAD. It was performed in multiple projections using standard techniques. The images were analysed by the clinician managing the patient using a visual quantitative scoring system as is routine practice in our institution. CAD was defined as a >50% luminal diameter narrowing in 1 or more epicardial arteries or their major branches with the most severe stenosis used. In patients who had undergone previous coronary artery bypass surgery, a stenosis of >50% was taken to demonstrate CAD within the graft.


Patients were followed-up from the date of testing. A combined end-point of all-cause mortality, myocardial infarction and revascularisation was used. Data were collected prospectively by questionnaires sent at 3 monthly intervals to record patient events. Telephone follow-up, as well as a review of hospital and computer records were used where appropriate.

Statistical analysis

Continuous variables are shown as mean (standard deviation) except for those that are not normally distributed, which are presented as medians with 95% confidence intervals (CI). All categorical variables are shown as proportions. Comparison of continuous data was made by one-way ANOVA or student's t-test, whichever was appropriate. For categorical variables, Chi-squared analysis was used. Sensitivity was defined as true-positive×100 divided by the sum of true-positive and false negative tests. Specificity was defined as the number of true-negatives×100 divided by the sum of the true-negative and false positive tests. A p value of <0.05 was considered significant. Statistical analyses were performed using Analyse-it version 1.62 (Leeds, UK).


Patient characteristics

A total of 302 patients were enrolled into the study; 154 patients underwent exercise ECG, 148 underwent stress echocardiography at a mean of 1.7 (1.7) days after admission to hospital. A total of 190 patients (63%) were tested within 1 day of admission. Baseline characteristics of the study population (Table 2) demonstrated a high proportion of patients of South Asian origin (132 patients – 43%) reflecting the ethnic diversity of our local community. At randomisation, over 75% of patients were taking Aspirin, over half on statins and over 40% on β-blockers (Table 3).

View this table:
Table 2

Baseline characteristics

ExECGStress echop Value
Patient demography
Age (yrs)60 (12.5)61 (12.8)0.42
Male56% (87)57% (84)0.94
BMI27 (5)27 (7)0.98
-Caucasian45% (69)51% (75)0.37
-South Asian47% (72)41% (60)0.33
Cardiac risk factors
Family history of CAD47% (73)48% (71)0.99
Hypertension62% (95)70% (103)0.18
Hyperlipidaemia65% (100)55% (81)0.09
Smoking history
-Previous34% (53)23% (34)0.03
-Current15% (23)15% (22)0.89
Diabetes mellitus25% (39)23% (34)0.73
Previous Hx IHD31% (48)23% (34)0.14
MI18% (27)12% (18)0.25
PCI19% (29)9% (13)0.02
CABG13% (20)9% (13)0.32
Presentation ECG
Normal58% (88)59% (89)0.86
Non-diagnostic ST depression19% (29)14% (20)0.27
Non-specific T wave inversion29% (45)24% (36)0.41
View this table:
Table 3

Medication at randomisation

ExECGStress echop Value
Aspirin87% (134)76% (112)0.02
Clopidogrel43% (66)40% (59)0.68
Beta-blocker40% (62)42% (62)0.86
Calcium antagonist23% (36)22% (33)0.93
Statin53% (81)51% (76)0.92
ACE inhibitor/ARB36% (56)28% (42)0.17

Exercise ECG

Of the 154 patients randomised to exercise ECG, 6 patients did not undergo dynamic testing. New ECG changes suggestive of ischaemia were seen in 2 patients and 1 patient had an episode of ventricular tachycardia immediately prior to testing. These patients were considered to have a high probability of significant CAD and were referred for coronary angiography. Significant hypertension prevented dynamic testing in 1 patient who subsequently self-discharged; the other 2 patients were unable to perform treadmill testing due to poor mobility. These patients were considered to have an intermediate post-test probability of significant CAD.

Of the remaining 148 patients, 122 (82%) underwent treadmill testing using the standard Bruce protocol; 26 (17%) used the modified Bruce protocol. Table 4 provides relationship between positive, negative, inconclusive ExECG and patients who did not perform ExECG and coronary arteriographic data.

View this table:
Table 4

Relationship between stress testing results and coronary arteriography

nNumber of patients undergoing coronary angiographyNumber of patients with significant CAD on angiography
Stress echo148
Not performed311
Exercise ECG154
Not performed632

Stress echocardiography

A total of 148 patients were randomised to stress echocardiography of which 3 patients were found to have new resting wall motion abnormalities without prior history of myocardial infarction. These were therefore considered positive scans giving a high probability of underlying CAD and the patients were referred for coronary angiography.

The remaining 145 patients underwent stress echocardiography using either treadmill exercise or pharmacological stress (60% and 40%, respectively), of which 6 (4%) patients required the use of intravenous contrast in order to improve endocardial definition. Table 5 provides the relationship between positive, negative, inconclusive SE and those who did not perform SE and coronary arteriographic data.

View this table:
Table 5

Relationship between stress testing results and end-points

nNumber available for follow-upDeathMIRevascularisationDeath/MIDeath/MI/revascularisation
ExECG154151 (98%)1222325
Not performed6600303
SE148142 (96%)1116218
Not performed3300101

Risk stratification

The proportion of patients having a low, intermediate and high pre-test probability of CAD was comparable for both ExECG and SE (21% vs 20%; 65% vs 72%; 14% vs 9%, respectively; p=ns). A post-test probability of CAD was determined on the basis of the pre-test likelihood and the result of stress testing in both groups (Fig. 1). Compared to ExECG, significantly more patients undergoing SE had a low post-test probability of CAD (80% vs 31%; p<0.0001). Significantly fewer patients undergoing SE had an intermediate risk post-test probability of CAD (3% vs 47%; p<0.0001). There was no difference in the number of patients with a high post-test probability of CAD in each group (23% vs 17%; p=ns).

Figure 1

Risk stratification by exercise ECG and stress echocardiography.

Of the patients undergoing ExECG, 88 (58%) had normal baseline ECGs. When analysed separately, only 36% of this group had a low post-test of significant CAD. Of the remainder, 38% still had an intermediate post-test probability of significant CAD despite a normal baseline ECG.

Significantly fewer patients undergoing SE were referred for further testing to exclude or refute the diagnosis of CAD compared to those who underwent exercise ECG testing (16% vs 52%; p<0.0001).

Patients with low post-test probability of CAD

Exercise ECG

Of the 154 patients in the exercise ECG arm of the study, 47 patients had a low post-test probability of significant CAD. The mean exercise time in this group was 9.3 (2.1) min with a mean workload of 10.5 (2.3) METS. A workload of 9 METS or more was achieved in 42 (89%) of patients and 40 patients (85%) achieved 85% or more of their target heart rate. A normal baseline ECG was seen in 32 (68%) patients. Only 7 patients (14%) had a low likelihood of significant CAD prior to exercise ECG testing; 34 patients (72%) had an intermediate pre-test likelihood of CAD.

Stress echocardiography

Stress echocardiography was found to be normal in 119 (80%) patients; 70 having undergone treadmill testing, 49 had pharmacological stress. A low pre-test probability of CAD was seen in 15 patients (13%) whereas 88 patients (74%) had an intermediate pre-test probability.

In patients undergoing exercise stress echo, mean exercise time was 8.0 (2.3) min with a mean workload of 9.1 (2.6) METS. A workload of 7 METS or more was achieved by 91% (64) of patients. The number of patients achieving ≥85% and ≥80% of target heart rate was 56 (80%) and 62 (89%), respectively.

Of the patients undergoing pharmacological stress echo, 33 (67%) achieved 85% or more of target heart rate; 11 of the remaining 16 patients received atropine in addition to the maximum dose of dobutamine; 3 achieved >80% of target heart rate. An infusion of dobutamine at a peak rate of 30μg/kg/min or higher was used in 90% (44) of patients.

Coronary angiography

In our study population, 57 coronary angiograms were performed, of which 36 (63%) patients had flow limiting disease; 13 patients with single vessel disease, 12 patients with 2 vessel disease and 11 patients with 3 vessel disease. Thus 12% of this population demonstrated significant CAD. Revascularisation was performed on 31 patients (86%); 22 underwent PTCA, the remainder CABG, including 1 patient who also underwent aortic valve replacement. Of the patients demonstrating significant CAD by coronary angiography, 60% (21/36) had a normal ECG on presentation and only 40% (14/36) had a high pre-test probability of significant CAD. A TIMI score of 4 or more was seen in 40% (14/36) and a score of 5 or more was seen in only 8% (3/36) patients with significant CAD.

Of the total population who underwent stress testing, 50 patients were found to have a positive result by either methods of testing (Table 4). Of these, 36 underwent coronary angiography. Significant CAD was detected in 83% (15/18) of patients with a positive SE compared to 56% (10/18) in those with a positive ECG (p=ns). Only 8/26 (31%) had a high pre-test likelihood of significant CAD in this group; only 31% had a TIMI score of 4 or more. Patients with a positive ExECG and a normal baseline ECG had a positive predictive value of CAD by angiography of only 46%. Of the remaining 21 patients undergoing angiography, 3 did not undergo ExECG testing but were considered high risk for CAD due to the presence of new ECG changes immediately prior to testing and 15 had inconclusive exercise ECG tests; 1 patient had a new resting wall motion abnormality and was therefore considered high risk for stress testing and 2 had inconclusive SEs. At angiography, the rate of significant CAD in these 4 groups was 67%, 53%, 100% and 0%, respectively. The presence of CAD by angiography was not predicted by any of the baseline patient characteristics including TIMI Risk Score. Due to the study design only patients with positive stress test underwent coronary arteriography. Consequently only positive predictive values were obtained and they were 85% for SE and 56% for ExECG.


Follow-up data were available for 293 (97%) of the study cohort at a mean time of 8.5±4.9 months after testing (Table 5). The total pre-determined events were 43 (15%) out of 293 patients. Of those available for follow-up, the event rate for those patients with a low pre-test probability of CAD was comparable for the two modalities (3.5% for SE vs 5.1% for ExECG at mean follow-up 9.7±4.7 months and 8.7±3.8 months, respectively). It is important to note, however, that significantly fewer patients were classified as having normal tests in the ExECG arm compared to SE. The accuracy of a positive and negative SE and ExECG for predicting cardiac events is shown in Table 6. The accuracy of SE was significantly superior to ExECG.

View this table:
Table 6

Accuracy of SE and ExECG for predicting cardiac events

Sensitivity (%)Specificity (%)Positive predictive value (%)Negative predictive value (%)Accuracy
p value1.0<


Our finding that a proportion of patients presenting to hospital with acute chest pain and negative serum markers but with at least 2 coronary risk factors have significant event rate (15%) is in keeping with previous studies.8 The 30-day mortality rates in patients with negative Troponin measures can be as high as 5–10% in some series24,25 and therefore represent a significant population at risk. It is for this reason that the recent AHA/ACC guidelines specifically state that “…troponins should not be relied upon as the sole marker for risk…”.26 It remains the case, however, that some patients with negative serum markers are discharged from hospital either with no further follow-up, or for out-patient investigation. This leads to delays in diagnosis and subsequent treatment for patients with disease and inappropriate treatment and the mis-diagnosis of CAD in patients without disease. Identification of patients who are at high risk of CAD appears problematic in this population. Of all the baseline characteristics measured, none were able to predict which patients had CAD by coronary angiography. Over half the patients in our study with angiographically proven CAD had a normal presenting ECG. Equally less than half the patients with CAD had a TIMI score of 4 or more. As a result, ESC guidelines have recommended stress testing for further risk stratification.10 Exercise ECG is widely used in this scenario despite sub-optimal risk stratification with this technique.

SE is well established as a tool for the diagnosis and risk stratification of patients with CAD. Its high sensitivity and specificity27 as well as its ability to use both exercise and pharmacological stress modalities make it ideally suited for use in risk management after significant myocardial necrosis has been excluded. Indeed, the more widespread use of harmonic imaging and intravenous contrast for left ventricular opacification now makes it possible for adequate images to be obtained in all patients.28 Our study showed that SE was more accurate than ExECG in correctly classifying patients with an intermediate pre-test probability of CAD into high and low risk groups. This resulted in 80% of the patients to be discharged compared to only 31% in the ExECG group. The cardiac event rates were similarly low in these 2 groups of low risk patients. Significantly more patients after ExECG continued to be classified as intermediate risk (47%) compared to only 3% after SE. This resulted in more patients being admitted and investigated further after ExECG (52%) compared to SE (16%). SE was also more accurate in correctly identifying high risk population compared to ExECG resulting in less unnecessary coronary arteriography procedure being performed compared to the ExECG arm. Cardiac event rates were higher in patients with a positive SE (59%) compared to ExECG (33%).

There have been a number of studies that have previously demonstrated the feasibility of performing stress echocardiography in the emergency room soon after presentation to hospital.32–34 Geleijnse et al. performed dobutamine stress echocardiography within the emergency department in 89 patients presenting with acute chest pain with a non-diagnostic ECG and normal creatinine kinase levels at 6 and 12h.32 At 6 month follow-up, they demonstrated a 14% event rate (death, non-fatal MI or revascularisation) at 6 months, with 10% of patients having uninterpretable or inconclusive studies. Their event rate for a negative study was 5%. Trippi et al. demonstrated the use of remote interpretation of echocardiographic images at rest and following dobutamine stress in 163 patients presenting acutely, demonstrating a sensitivity of nearly 90% in the detection of CAD.33 Buchsbaum et al. assessed 145 low risk patients and demonstrated an event rate for normal dobutamine stress echocardiography of 1% at 6 months.34

Though these previous studies have demonstrated that stress echocardiography can allow rapid assessment of this population of patients, we are the first to study and demonstrate its superiority over exercise ECG prospectively. We have also demonstrated that with either modality, it is possible to quickly assess patients with a mean time to testing of 1.7 days and a median time of only 1 day. This shows that rapid stress testing is possible in the district general hospital setting. Orlandini et al. similarly showed the value of having a chest pain protocol in place which included stress testing facilities. In their study, they were able to discharge a significant number of patients after stress testing with excellent outcome.29 In this study SE also correctly identified a significant percentage of patients with high risk. Conti et al. also showed similar efficiency in managing patients with indeterminate ECG and normal cardiac enzyme when a chest pain assessment protocol with stress testing facilities were in place.30 The use of SE dramatically enhanced the ability to risk stratify patients which enables rapid discharge from hospital in patients without CAD and the appropriate prioritisation of patients with positive tests to coronary angiography with a view to intervention if necessary.31

Limitations of the study

The major limitation of the study is the relatively small number of patients undergoing coronary arteriography. This precluded the calculations of comparative diagnostic values of each test. However, the main aim of the study was to assess risk stratification of patients by ExECG and SE rather than diagnostic accuracy of each test. Another limitation of the study is to exclude patients with only diabetes mellitus with no other coronary risk factors. The protocol was set up before the concept that late-onset diabetes mellitus is equivalent to having cardiovascular disease. Finally, despite recommendation by ACC/AHA that all patients with baseline ECG changes should undergo imaging test, we included these patients in the study. This is because in the UK, due to limited access to cardiac imaging, these patients continue to undergo ExECG. However, interestingly, we found that even when patients with baseline ECG changes, were excluded (41%), a significant proportion of these patients (38%) showed indeterminate ExECG results compared to only 3% with SE. Furthermore, the positive predictive value of ExECG of patients with normal baseline ECG was only 46% for predicting CAD, which was not significantly different from the overall ExECG result.


Despite negative serum markers, 15% of patients presenting to hospital with acute chest pain and normal or non-diagnostic ECGs have cardiac events. SE is superior to ExECG in the risk stratification of patients with acute chest pain into high and low risk groups with a significant reduction in the number of further tests required to confirm or refute the diagnosis of CAD. A normal SE was also associated with an excellent prognosis with low event rates conversely an abnormal SE predicted a high risk group. When compared to coronary angiography, the number of patients with significant CAD correctly identified by SE was greater than that of exercise ECG.


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