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dc.contributor.authorSanfilippo, F.
dc.contributor.authorHobbs, M.
dc.contributor.authorKnuiman, M.
dc.contributor.authorRidout, S.
dc.contributor.authorBradshaw, P.
dc.contributor.authorFinn, Judith
dc.contributor.authorRankin, J.
dc.contributor.authorSpivulis, P.
dc.contributor.authorHung, J.
dc.date.accessioned2017-01-30T10:37:25Z
dc.date.available2017-01-30T10:37:25Z
dc.date.created2014-11-19T01:13:19Z
dc.date.issued2011
dc.identifier.citationSanfilippo, F. and Hobbs, M. and Knuiman, M. and Ridout, S. and Bradshaw, P. and Finn, J. and Rankin, J. et al. 2011. Can we monitor heart attack in the troponin era: Evidence from a population-based cohort study. BMC Cardiovascular Disorders. 11: 35.
dc.identifier.urihttp://hdl.handle.net/20.500.11937/4225
dc.identifier.doi10.1186/1471-2261-11-35
dc.description.abstract

Background: 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. Methods: 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). Results: 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 MIAHAck declined by 18%. Conclusions: 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 longstanding trends in MI in Western Australia, suggesting that neither MI-HMDC nor MI-AHA reflect the true underlying population trends in MI.

dc.publisherBiomed Central
dc.titleCan we monitor heart attack in the troponin era: Evidence from a population-based cohort study
dc.typeJournal Article
dcterms.source.volume11
dcterms.source.issn1471-2261
dcterms.source.titleBMC Cardiovascular Disorders
curtin.note

This article is published under the Open Access publishing model and distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/2.0/ Please refer to the licence to obtain terms for any further reuse or distribution of this work.

curtin.accessStatusOpen access


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