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Sökning: WFRF:(Simoons Maarten L.) > A rapid troponin I ...

  • James, Stefan K.Uppsala universitet,Institutionen för medicinska vetenskaper,Kardiologgruppen, L Wallentin (författare)

A rapid troponin I assay is not optimal for determination of troponin status and prediction of subsequent cardiac events at suspicion of unstable coronary syndromes.

  • Artikel/kapitelEngelska2004

Förlag, utgivningsår, omfång ...

  • 2004
  • printrdacarrier

Nummerbeteckningar

  • LIBRIS-ID:oai:DiVA.org:uu-73031
  • https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-73031URI
  • https://doi.org/10.1016/S0167-5273(03)00157-8DOI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:ref swepub-contenttype
  • Ämneskategori:art swepub-publicationtype

Anmärkningar

  • BACKGROUND: Troponin is a specific marker of myocardial damage. For early prediction of coronary events in patients with suspicion of acute coronary syndromes the assay also needs to be highly sensitive. METHODS AND RESULTS: A rapid troponin I assay was performed prior to inclusion in 4447 acute coronary syndrome patients in the GUSTO-IV trial. A quantitative troponin T analysis was later performed on blood samples obtained at randomization by a central laboratory. There was an agreement between the rapid troponin I assay and troponin T (< or =/>0.1 microg/l) in 3596 (80.9%) patients. A positive rapid troponin I was identifying any elevation of troponin T (>0.01 microg/l) in 1990 patients (90.4%) whereas a negative rapid troponin I was corresponding to negative troponin T (< or =0.01 microg/l) in only 1217 patients (54.2%). Patients with a positive versus negative rapid troponin I had an increased risk of death or myocardial infarction at 30 days (9.3 vs. 5.9%; odds ratio, O.R. 1.64; 95% confidence interval, 1.31-2.06). Troponin T elevation (>0.1 microg/l) provided a better (10.5 v. 4.9%, O.R. 2.26; C.I. 1.79-2.85) risk stratification. Regardless of a positive or a negative rapid troponin I, the troponin T result (>0.1 vs. < or =0.1 microg/l) stratified the patients into high and low risk of events at 30 days, (10.3 vs. 5.7%, P=0.002) and (11.5 vs. 4.8%, P<0.001), respectively. CONCLUSION: In a population with non-ST elevation acute coronary syndrome a positive rapid troponin I assay is a specific indicator of troponin elevation and a predictor of early outcome. However, a negative rapid troponin I is not a reliable indicator of the absence of myocardial damage and does not indicate a low risk of subsequent cardiac events. A rapid troponin I assay was performed prior to inclusion in 4447 acute coronary syndrome patients in the GUSTO-IV trial and related to a centrally analyzed quantitative troponin T test. A positive rapid troponin I was well corresponding to any elevation of troponin T (>0.01 microg/l) and predicted an unfavorable outcome at 30 days. However, a negative rapid troponin I was corresponding to troponin T < or =0.01 microg/l in only half of the patients. Troponin T >0.1 microg/l vs. < or =0.1 microg/l provided a better risk stratification than the rapid troponin I result. For patients with troponin T elevation (>0.1 microg/l) the 30 day event rate was high regardless of the rapid troponin I result.

Ämnesord och genrebeteckningar

  • Acute Disease
  • Aged
  • Antibodies; Monoclonal/therapeutic use
  • Anticoagulants/therapeutic use
  • Comparative Study
  • Coronary Disease/blood/*diagnosis
  • Double-Blind Method
  • Female
  • Follow-Up Studies
  • Humans
  • Immunoglobulins; Fab/therapeutic use
  • Male
  • Middle Aged
  • Platelet Glycoprotein GPIIb-IIIa Complex/antagonists & inhibitors
  • Predictive Value of Tests
  • Research Support; Non-U.S. Gov't
  • Risk Assessment
  • Sensitivity and Specificity
  • Troponin I/*blood
  • Troponin T/blood
  • MEDICINE
  • MEDICIN

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Lindahl, BertilUppsala universitet,Institutionen för medicinska vetenskaper,Kardiologgruppen, L Wallentin(Swepub:uu)belin227 (författare)
  • Armstrong, Paul (författare)
  • Califf, Robert (författare)
  • Simoons, Maarten L. (författare)
  • Venge, PerUppsala universitet,Institutionen för medicinska vetenskaper,Inflammation(Swepub:uu)pervenge (författare)
  • Wallentin, LarsUppsala universitet,Institutionen för medicinska vetenskaper,Kardiologgruppen, L Wallentin(Swepub:uu)larswall (författare)
  • Uppsala universitetInstitutionen för medicinska vetenskaper (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:International Journal of Cardiology93:2-3, s. 113-1200167-52731874-1754

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