AustralieFrV1, Main, Exploration, bibRecord, 007071

Quantitative troponin and death, cardiogenic shock, cardiac arrest and new heart failure in patients with non-ST-segment elevation acute coronary syndromes (NSTE ACS): insights from the Global Registry of Acute Coronary Events

Identifieur interne : 007071 ( Main/Exploration ); précédent : 007070; suivant : 007072

Quantitative troponin and death, cardiogenic shock, cardiac arrest and new heart failure in patients with non-ST-segment elevation acute coronary syndromes (NSTE ACS): insights from the Global Registry of Acute Coronary Events

Auteurs : Sanjit S. Jolly [Canada] ; Heather Shenkman [États-Unis] ; David Brieger [Australie] ; Keith A. Fox [Royaume-Uni] ; Andrew T. Yan [Canada] ; Kim A. Eagle [États-Unis] ; P Gabriel Steg [France] ; Ki-Dong Lim [Canada] ; Ann Quill [États-Unis] ; Shaun G. Goodman [Canada]

Source :

Heart [ 1355-6037 ] ; 2011-02-01.

RBID : ISTEX:B538572B667D1479B02E9B2F15FDE80AEFE67666

Descripteurs français

Wicri :
- topic : Hospitalisation, Mortalité.

English descriptors

Abstract

Background The objective of this study was to determine if the extent of quantitative troponin elevation predicted mortality as well as in-hospital complications of cardiac arrest, new heart failure and cardiogenic shock. Design 16 318 patients with non-ST-segment elevation acute coronary syndromes (NSTE ACS) from the Global Registry of Acute Coronary Events (GRACE) were included. The maximum 24 h troponin value as a multiple of the local laboratory upper limit of normal was used. The population was divided into five groups based on the degree of troponin elevation, and outcomes were compared. An adjusted analysis was performed using quantitative troponin as a continuous variable with adjustment for known prognostic variables. Results For each approximate 10-fold increase in the troponin ratio, there was an associated increase in cardiac arrest, sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) (1.0, 2.4, 3.4, 5.9 and 13.4%; p<0.001 for linear trend), cardiogenic shock (0.5, 1.4, 2.0, 4.4 and 12.7%; p<0.001), new heart failure (2.5, 5.1, 7.4, 11.6 and 15.8%; p<0.001) and mortality (0.8, 2.2, 3.0, 5.3 and 14.0%; p<0.001). These findings were replicated using the troponin ratio as a continuous variable and adjusting for covariates (cardiac arrest, sustained VT or VF, OR 1.56, 95% CI 1.39 to 1.74; cardiogenic shock, OR 1.87, 95% CI 1.61 to 2.18; and new heart failure, OR 1.57, 95% CI 1.45 to 1.71). The degree of troponin elevation was predictive of early mortality (HR 1.61, 95% CI 1.44 to 1.81; p<0.001 for days 0–14) and longer term mortality (HR 1.18, 95% CI 1.07 to 1.30, p=0.001 for days 15–180). Conclusion The extent of troponin elevation is an independent predictor of morbidity and mortality.

Url:

https://api.istex.fr/document/B538572B667D1479B02E9B2F15FDE80AEFE67666/fulltext/pdf

DOI: 10.1136/hrt.2010.195511

Affiliations:

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Le document en format XML

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<term>Cardiogenic</term>
<term>Cardiogenic shock</term>
<term>Congestive</term>
<term>Congestive heart failure</term>
<term>Coronary syndromes</term>
<term>Elevation</term>
<term>Global registry</term>
<term>Grace risk score variables</term>
<term>Heart failure</term>
<term>Highest troponin group</term>
<term>Hospitalisation</term>
<term>Infarction</term>
<term>Initial hospitalisation</term>
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<term>Previous studies</term>
<term>Previous value</term>
<term>Sensitivity analysis</term>
<term>Syndrome</term>
<term>Systolic blood pressure</term>
<term>Troponin</term>
<term>Troponin elevation</term>
<term>Troponin groups</term>
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<term>Ventricular</term>
<term>Ventricular arrhythmias</term>
<term>Ventricular tachycardia</term>
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<keywords scheme="Teeft" xml:lang="en"><term>Baseline characteristics</term>
<term>Cardiac</term>
<term>Cardiac arrest</term>
<term>Cardiogenic</term>
<term>Cardiogenic shock</term>
<term>Congestive</term>
<term>Congestive heart failure</term>
<term>Coronary syndromes</term>
<term>Elevation</term>
<term>Global registry</term>
<term>Grace risk score variables</term>
<term>Heart failure</term>
<term>Highest troponin group</term>
<term>Hospitalisation</term>
<term>Infarction</term>
<term>Initial hospitalisation</term>
<term>Killip class</term>
<term>Late mortality</term>
<term>Linear trend</term>
<term>Local laboratory</term>
<term>Mortality</term>
<term>Myocardial infarction</term>
<term>Nste</term>
<term>Predictor</term>
<term>Previous studies</term>
<term>Previous value</term>
<term>Sensitivity analysis</term>
<term>Syndrome</term>
<term>Systolic blood pressure</term>
<term>Troponin</term>
<term>Troponin elevation</term>
<term>Troponin groups</term>
<term>Troponin ratio</term>
<term>Troponin ratios</term>
<term>Ventricular</term>
<term>Ventricular arrhythmias</term>
<term>Ventricular tachycardia</term>
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<keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Hospitalisation</term>
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<front><div type="abstract">Background The objective of this study was to determine if the extent of quantitative troponin elevation predicted mortality as well as in-hospital complications of cardiac arrest, new heart failure and cardiogenic shock. Design 16 318 patients with non-ST-segment elevation acute coronary syndromes (NSTE ACS) from the Global Registry of Acute Coronary Events (GRACE) were included. The maximum 24 h troponin value as a multiple of the local laboratory upper limit of normal was used. The population was divided into five groups based on the degree of troponin elevation, and outcomes were compared. An adjusted analysis was performed using quantitative troponin as a continuous variable with adjustment for known prognostic variables. Results For each approximate 10-fold increase in the troponin ratio, there was an associated increase in cardiac arrest, sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) (1.0, 2.4, 3.4, 5.9 and 13.4%; p<0.001 for linear trend), cardiogenic shock (0.5, 1.4, 2.0, 4.4 and 12.7%; p<0.001), new heart failure (2.5, 5.1, 7.4, 11.6 and 15.8%; p<0.001) and mortality (0.8, 2.2, 3.0, 5.3 and 14.0%; p<0.001). These findings were replicated using the troponin ratio as a continuous variable and adjusting for covariates (cardiac arrest, sustained VT or VF, OR 1.56, 95% CI 1.39 to 1.74; cardiogenic shock, OR 1.87, 95% CI 1.61 to 2.18; and new heart failure, OR 1.57, 95% CI 1.45 to 1.71). The degree of troponin elevation was predictive of early mortality (HR 1.61, 95% CI 1.44 to 1.81; p<0.001 for days 0–14) and longer term mortality (HR 1.18, 95% CI 1.07 to 1.30, p=0.001 for days 15–180). Conclusion The extent of troponin elevation is an independent predictor of morbidity and mortality.</div>
</front>
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<name sortKey="Yan, Andrew T" sort="Yan, Andrew T" uniqKey="Yan A" first="Andrew T" last="Yan">Andrew T. Yan</name>
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<name sortKey="Quill, Ann" sort="Quill, Ann" uniqKey="Quill A" first="Ann" last="Quill">Ann Quill</name>
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<country name="Australie"><region name="Nouvelle-Galles du Sud"><name sortKey="Brieger, David" sort="Brieger, David" uniqKey="Brieger D" first="David" last="Brieger">David Brieger</name>
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Quantitative troponin and death, cardiogenic shock, cardiac arrest and new heart failure in patients with non-ST-segment elevation acute coronary syndromes (NSTE ACS): insights from the Global Registry of Acute Coronary Events

Quantitative troponin and death, cardiogenic shock, cardiac arrest and new heart failure in patients with non-ST-segment elevation acute coronary syndromes (NSTE ACS): insights from the Global Registry of Acute Coronary Events

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Abstract

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