Can we monitor heart attack in the troponin era: evidence from a population-based cohort study
- Equal contributors
1 School of Population Health M431, University of Western Australia, 35 Stirling Highway, Crawley 6009 WA, Australia
2 Discipline of Emergency Medicine M516, School of Primary, Aboriginal & Rural Health Care, University of Western Australia, 35 Stirling Highway, Crawley 6009 WA, Australia
3 Department of Cardiology, Royal Perth Hospital, Wellington Street, Perth 6000 WA, Australia
4 Department of Emergency Medicine, Fremantle Hospital, Alma Street, Fremantle 6160 WA, Australia
5 School of Medicine and Pharmacology M503, University of Western Australia, 35 Stirling Highway, Crawley 6009 WA, Australia
6 Cardiology Department, Sir Charles Gairdner Hospital, Hospital Avenue, Nedlands 6009 WA, Australia
BMC Cardiovascular Disorders 2011, 11:35 doi:10.1186/1471-2261-11-35Published: 24 June 2011
Troponins (highly sensitive biomarkers of myocardial damage) increase counts of myocardial infarction (MI) in clinical practice, but their impact on trends in admission rates for MI in National statistics is uncertain.
Cases coded as MI or other cardiac diagnoses in the Hospital Morbidity Data Collection (MI-HMDC) in Western Australia in 1998 and 2003 were classified using revised criteria for MI developed by an International panel convened by the American Heart Association (AHA criteria) using information on symptoms, ECGs and cardiac biomarkers abstracted from samples of medical notes. Age-sex standardized rates of MI-HMDC were compared with rates of MI based on AHA criteria including troponins (MI-AHA) or traditional biomarkers only (MI-AHAck).
Between 1998 and 2003, rates of MI-HMDC decreased by 3.5% whereas rates of MI-AHA increased by 17%, a difference largely due to increased false-negative cases in the HMDC associated with marked increased use of troponin tests in cardiac admissions generally, and progressively lower test thresholds. In contrast, rates of MI-AHAck declined by 18%.
Increasing misclassification of MI-AHA by the HMDC may be due to reluctance by clinicians to diagnose MI based on relatively small increases in troponin levels. These influences are likely to continue. Monitoring MI using AHA criteria will require calibration of commercially available troponin tests and agreement on lower diagnostic thresholds for epidemiological studies. Declining rates of MI-AHAck are consistent with long-standing trends in MI in Western Australia, suggesting that neither MI-HMDC nor MI-AHA reflect the true underlying population trends in MI.