Can ED Physicians Assess for AMI With Clinical Judgment?
Can ED Physicians Assess for AMI With Clinical Judgment?
We undertook a prospective diagnostic cohort study at Stockport NHS Foundation Trust, a District General Hospital in Greater Manchester, UK. Ethical approval was obtained from the Research Ethics Committee (reference 09/H1014/74), and all participants provided written informed consent. From this cohort, we have recently reported external validation of the Manchester Acute Coronary Syndromes (MACS) decision rule. We included consecutive adult patients presenting to the ED with suspected cardiac chest pain occurring in the previous 24 h, excluding those with another medical condition necessitating hospital admission; those with renal failure requiring dialysis; patients with chest trauma and suspected myocardial contusion; those who did not speak English; prisoners and patients for whom all means of follow-up would be impossible.
Clinical features were recorded by the treating physician using a custom-designed case report form. The treating physician was asked to record their unstructured 'gestalt' or clinical judgement about the probability of an ACS using a five-point Likert scale as follows: 'definitely not', 'probably not', 'not sure', 'probably' and 'definitely'. As these data were recorded at the time of initial presentation and before the results of investigations were available, the treating clinicians were blinded to the final outcome of the patient. As we recorded clinician gestalt following a genuine consultation with the patient, clinicians were not blinded to the ECG or other clinical information. However, we took a number of measures to ensure that treating clinicians were blinded to the initial troponin level. First, clinical protocols in place at the time of this study did not include troponin testing at the time of presentation unless >12 h had already elapsed since peak symptoms. Second, when troponin levels had been evaluated, research staff would verify that clinicians remained unaware of the initial troponin results before collecting case report forms. All patients were followed up by telephone, home visit or in clinic after 30 days.
Patients underwent venepuncture at the time of presentation in the ED and at least 12 h after symptom onset. All 12 h samples were immediately tested for cardiac troponin T (Roche Diagnostics Elecsys, 4th generation, 99th centile 10 ng/L, coefficient of variation <10% at 35 ng/L). At the time of this study, samples drawn at the time of arrival were not routinely tested for cardiac troponin T except in the case of patients who presented >12 h after their peak symptoms. Serum samples drawn at the time of presentation and 12 h after symptom onset were therefore stored at −70°C and later tested for cardiac troponin T (if not already) and also for high-sensitivity troponin T (hs-cTnT, Roche Diagnostics 5th generation Elecsys, 99th centile 14 ng/L, coefficient of variation <10% at 13 ng/L). After our initial analyses, we became aware that the batch of reagent supplied by the manufacturer for hs-cTnT testing had been affected by a calibration shift. Aliquots of all samples were therefore retested using an unaffected batch of reagent and statistical analyses were repeated.
The primary outcome was a diagnosis of AMI. This was defined in accordance with the Third Universal Definition of Myocardial Infarction as a rise and/or fall of cardiac troponin with at least one level above the 99th centile for a healthy reference population. Based on the analytical characteristics of the troponin assay, a change of 20 ng/L on serial sampling was considered to represent a rise and/or fall. The diagnosis of AMI was adjudicated by two independent investigators blinded to clinician gestalt.
We also analysed data for the secondary outcome of major adverse cardiac events (MACE) within 30 days. This was defined as death (all cause), prevalent or incident AMI or the need for coronary revascularisation within 30 days. New angiographic stenoses >50% the diameter of a major epicardial vessel (as reported by the responsible cardiologist) were also prospectively considered to constitute MACE.
We calculated sensitivity, specificity, positive and negative predictive values using MedCalc V.12.4.0.0 (Mariakerke, Belgium). The area under the receiver operating characteristic (ROC) curve was calculated in IBM SPSS Statistics V.20.0.0. We also evaluated whether gestalt gave independent predictive value once initial troponin level and the presence or absence of ECG ischaemia had been taken into account by entering these data into a logistic regression analysis using IBM SPSS Statistics V.20.0.0
Sample size for this study was determined by calculating the required number of patients to ensure that, for a diagnostic strategy with 100% sensitivity, the lower bound of the 95% CI was no lower than 95%. Assuming a 20% incidence of the primary outcome, this would require a minimum sample size of 450 patients.
Methods
We undertook a prospective diagnostic cohort study at Stockport NHS Foundation Trust, a District General Hospital in Greater Manchester, UK. Ethical approval was obtained from the Research Ethics Committee (reference 09/H1014/74), and all participants provided written informed consent. From this cohort, we have recently reported external validation of the Manchester Acute Coronary Syndromes (MACS) decision rule. We included consecutive adult patients presenting to the ED with suspected cardiac chest pain occurring in the previous 24 h, excluding those with another medical condition necessitating hospital admission; those with renal failure requiring dialysis; patients with chest trauma and suspected myocardial contusion; those who did not speak English; prisoners and patients for whom all means of follow-up would be impossible.
Clinical features were recorded by the treating physician using a custom-designed case report form. The treating physician was asked to record their unstructured 'gestalt' or clinical judgement about the probability of an ACS using a five-point Likert scale as follows: 'definitely not', 'probably not', 'not sure', 'probably' and 'definitely'. As these data were recorded at the time of initial presentation and before the results of investigations were available, the treating clinicians were blinded to the final outcome of the patient. As we recorded clinician gestalt following a genuine consultation with the patient, clinicians were not blinded to the ECG or other clinical information. However, we took a number of measures to ensure that treating clinicians were blinded to the initial troponin level. First, clinical protocols in place at the time of this study did not include troponin testing at the time of presentation unless >12 h had already elapsed since peak symptoms. Second, when troponin levels had been evaluated, research staff would verify that clinicians remained unaware of the initial troponin results before collecting case report forms. All patients were followed up by telephone, home visit or in clinic after 30 days.
Laboratory Analyses
Patients underwent venepuncture at the time of presentation in the ED and at least 12 h after symptom onset. All 12 h samples were immediately tested for cardiac troponin T (Roche Diagnostics Elecsys, 4th generation, 99th centile 10 ng/L, coefficient of variation <10% at 35 ng/L). At the time of this study, samples drawn at the time of arrival were not routinely tested for cardiac troponin T except in the case of patients who presented >12 h after their peak symptoms. Serum samples drawn at the time of presentation and 12 h after symptom onset were therefore stored at −70°C and later tested for cardiac troponin T (if not already) and also for high-sensitivity troponin T (hs-cTnT, Roche Diagnostics 5th generation Elecsys, 99th centile 14 ng/L, coefficient of variation <10% at 13 ng/L). After our initial analyses, we became aware that the batch of reagent supplied by the manufacturer for hs-cTnT testing had been affected by a calibration shift. Aliquots of all samples were therefore retested using an unaffected batch of reagent and statistical analyses were repeated.
Outcomes
The primary outcome was a diagnosis of AMI. This was defined in accordance with the Third Universal Definition of Myocardial Infarction as a rise and/or fall of cardiac troponin with at least one level above the 99th centile for a healthy reference population. Based on the analytical characteristics of the troponin assay, a change of 20 ng/L on serial sampling was considered to represent a rise and/or fall. The diagnosis of AMI was adjudicated by two independent investigators blinded to clinician gestalt.
We also analysed data for the secondary outcome of major adverse cardiac events (MACE) within 30 days. This was defined as death (all cause), prevalent or incident AMI or the need for coronary revascularisation within 30 days. New angiographic stenoses >50% the diameter of a major epicardial vessel (as reported by the responsible cardiologist) were also prospectively considered to constitute MACE.
Statistical Analyses
We calculated sensitivity, specificity, positive and negative predictive values using MedCalc V.12.4.0.0 (Mariakerke, Belgium). The area under the receiver operating characteristic (ROC) curve was calculated in IBM SPSS Statistics V.20.0.0. We also evaluated whether gestalt gave independent predictive value once initial troponin level and the presence or absence of ECG ischaemia had been taken into account by entering these data into a logistic regression analysis using IBM SPSS Statistics V.20.0.0
Sample Size
Sample size for this study was determined by calculating the required number of patients to ensure that, for a diagnostic strategy with 100% sensitivity, the lower bound of the 95% CI was no lower than 95%. Assuming a 20% incidence of the primary outcome, this would require a minimum sample size of 450 patients.
