Impact of the recommendations for the redefinition of myocardial infarction on diagnosis and prognosis in an unselected United Kingdom cohort with suspected cardiac chest pain

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Abstract

We prospectively and blindly assessed the diagnostic and prognostic impact of implementation of the European Society of Cardiology/American College of Cardiology recommendations for redefinition of myocardial infarction (MI) in an unselected cohort of patients with suspected cardiac chest pain, with particular attention to prespecified clinical groups. All patients admitted to our institute with suspected cardiac chest pain were enrolled. Physicians provided usual care using serial electrocardiograms/creatine kinase (CK)/aspartate transaminase according to World Health Organization (WHO) criteria for MI, while blinded to additional measurements of cardiac troponin T (cTnT) and CK-MB mass. After discharge, diagnoses based on WHO and new criteria were compared, and major adverse cardiac events monitored for 6 months. Implementation of the new recommendations classified an additional 26.1% of patients as having MI compared with WHO criteria, and produced an overall diagnostic alteration in 11.5%. Two thirds of the additional patients with MI were previously diagnosed with unstable angina, whereas one third had “other cardiac” or “noncardiac” diagnoses. A similar MI cohort to the cTnT diagnosis was identified using a CK-MB mass discriminator value of 5 μg/L, but not 10 μg/L. The 6-month prognosis was similar in patients diagnosed with MI by new (cTnT) and WHO criteria, with the new criteria thus identifying a further high-risk cohort in the WHO negative group. In our cohort, the new Joint European Society of Cardiology/American College of Cardiology recommendations identify one fourth more patients as having MI. The 6-month prognosis of those patients reclassified as having MI was similar to those diagnosed with MI by both criteria.

Section snippets

Patients

Patients aged ≥18 years admitted with suspected cardiac chest pain over a 6-month period were enrolled. Patients with serum creatinine >200 μmol/L were excluded. Management by the admitting medical team was based on WHO criteria using serial electrocardiograms and daily CK/aspartate transaminase. Extra blood samples were drawn 12 hours after symptom onset for the measurement of cTnT and CK-MB mass to ensure optimal timing for diagnostic accuracy. The admitting team was not aware of these

Patients

Four hundred one consecutive patients were enrolled in the study (Table 1). Patients with a WHO diagnosis of MI or UAP were more likely to be men and hypercholesterolemic. The median time for presentation from symptom onset was 193 minutes. CK-MB mass and cTnT samples were obtained at a median time of 750 minutes. A “cTnT diagnosis” of MI was made in 161 patients (40.1%), of whom 74 (46.0%) had a diagnostic electrocardiogram (ST elevation or new Q waves); 71 patients had ST elevation on the

Discussion

In our unselected cohort of patients admitted with suspected cardiac chest pain, adoption of the new criteria for MI produced a significant diagnostic alteration in 11.5% of patients, and reclassified 26.1% of MIs currently not identified by the WHO criteria. The 6-month prognosis of this reclassified MI group, with respect to all major adverse cardiac events, was similar to the prognosis in patients identified as having MI using both the new and WHO criteria.

With use of predefined clinical

Acknowledgements

We gratefully acknowledge Waeng-Ken Lee for help with data collection and database entry, and Mervyn Stokes for sample analysis.

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    As a result, the new definition of myocardial infarction has had a high impact on both laboratory and clinical practice [3–8]. The clinical application of international guidelines [1] generated main social/economical effects, leading to a 25–55% increment of diagnosed AMI [3–5]. Although increased cTnI or cTnT values always indicate myocardial tissue damage, a positive test is unable to identify the mechanism responsible for that cardiac damage (which could be not due to ischemia).

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Dr. Trevelyan was supported by the National Heart Research Fund, Leeds, United Kingdom, and Mr. Needham and Dr. Mattu were supported by the British Heart Foundation, London, United Kingdom.

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