Objective To assess the incidence of prognostically important myocardial damage in patients with chest pain discharged from the emergency department.
Design Prospective observational study.
Setting District general hospital emergency department.
Participants 110 patients presenting with chest pain of unknown cause who were subsequently discharged home after cardiac causes of chest pain were ruled out by clinical and electrocardiographic investigation.
Interventions Patients were reviewed 12-48 hours after presentation by repeat electrocardiography and measurement of cardiac troponin T.
Main outcome measures Incidence of missed myocardial damage.
Results Eight (7%) patients had detectable cardiac troponin T on review and seven had concentrations [is greater than or equal to] 0.1 [micro]g/1. The repeat electrocardiogram showed no abnormality in any patient.
Conclusion 6% of the patients discharged from the emergency department had missed prognostically important myocardial damage. Follow up measurement of cardiac troponin T allows convenient audit of clinical performance in the emergency department.
Patients presenting to the emergency department with chest pain of unknown cause are a management challenge. Clinical history and examination are imperfect tools for diagnosis. Electrocardiography is the first test, but rigorous comparison based on postmortem diagnosis shows that its diagnostic sensitivity is only 41-61%.[1 2] The admission electrocardiogram, although excellent for selecting patients for thrombolysis, has a diagnostic sensitivity for acute myocardial infarction of 55-75%.[4 5]
Measurement of cardiac troponin T and cardiac troponin I concentrations has greatly improved diagnosis of patients presenting with suspected acute coronary syndromes. The diagnostic time window of these markers is wide, being up to 72 hours; the markers have 100% sensitivity for diagnosing acute myocardial infarction 12 hours after presentation to hospital, and concentrations remain raised for as long as 10 days. Raised concentrations of cardiac troponin T and cardiac troponin I are completely cardiac specific, unlike increases in concentrations of creatine kinase or its MB isoenzyme, which can be due to noncardiac sources. Detection is diagnostic of myocardial damage in patients admitted with suspected acute coronary syndromes and …