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A sensitive cardiac troponin T assay in stable coronary artery disease.

ABSTRACT: BACKGROUND:In most patients with stable coronary artery disease, plasma cardiac troponin T levels are below the limit of detection for the conventional assay. The distribution and determinants of very low circulating troponin T levels, as well as their association with cardiovascular events, in such patients are unknown. METHODS:We used a new, high-sensitivity assay to determine the concentration of cardiac troponin T in plasma samples from 3679 patients with stable coronary artery disease and preserved left ventricular function. Results of the assay were analyzed in relation to the incidence of cardiovascular events during a median follow-up period of 5.2 years. RESULTS:With the highly sensitive assay, concentrations of cardiac troponin T were at or above the limit of detection (0.001 microg per liter) in 3593 patients (97.7%) and at or above the 99th percentile for apparently healthy subjects (0.0133 microg per liter) in 407 patients (11.1%). After adjustment for other independent prognostic indicators, there was a strong and graded increase in the cumulative incidence of cardiovascular death (adjusted hazard ratio per unit increase in the natural logarithm of the troponin T level, 2.09; 95% confidence interval [CI], 1.60 to 2.74; P<0.001) and of heart failure (adjusted hazard ratio, 2.20; 95% CI, 1.66 to 2.90; P<0.001) in this study group. Increased risk associated with higher levels of troponin T was evident well below the limit of detection of conventional cardiac troponin T assays and below the 99th percentile of values in a healthy population. There was no association between troponin T levels as measured with the highly sensitive assay and the incidence of myocardial infarction (adjusted hazard ratio, 1.16; 95% CI, 0.97 to 1.40; P=0.11). CONCLUSIONS:After adjustment for other independent prognostic indicators, cardiac troponin T concentrations as measured with a highly sensitive assay were significantly associated with the incidence of cardiovascular death and heart failure but not with myocardial infarction in patients with stable coronary artery disease.

SUBMITTER: Omland T

PROVIDER: S-EPMC2997684 | biostudies-literature | 2009 Dec

REPOSITORIES: biostudies-literature

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A sensitive cardiac troponin T assay in stable coronary artery disease.

Omland Torbjørn T de Lemos James A JA Sabatine Marc S MS Christophi Costas A CA Rice Madeline Murguia MM Jablonski Kathleen A KA Tjora Solve S Domanski Michael J MJ Gersh Bernard J BJ Rouleau Jean L JL Pfeffer Marc A MA Braunwald Eugene E

The New England journal of medicine 20091125 26

<h4>Background</h4>In most patients with stable coronary artery disease, plasma cardiac troponin T levels are below the limit of detection for the conventional assay. The distribution and determinants of very low circulating troponin T levels, as well as their association with cardiovascular events, in such patients are unknown.<h4>Methods</h4>We used a new, high-sensitivity assay to determine the concentration of cardiac troponin T in plasma samples from 3679 patients with stable coronary arter ...[more]

PMID: 19940289

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Project description:BackgroundWe determined whether high-sensitivity cardiac troponin I can improve the estimation of the pretest probability for obstructive coronary artery disease (CAD) in patients with suspected stable angina.Methods and resultsIn a prespecified substudy of the SCOT-HEART trial (Scottish Computed Tomography of the Heart), plasma cardiac troponin was measured using a high-sensitivity single-molecule counting assay in 943 adults with suspected stable angina who had undergone coronary computed tomographic angiography. Rates of obstructive CAD were compared with the pretest probability determined by the CAD Consortium risk model with and without cardiac troponin concentrations. External validation was undertaken in an independent study population from Denmark comprising 487 patients with suspected stable angina. Higher cardiac troponin concentrations were associated with obstructive CAD with a 5-fold increase across quintiles (9%-48%; P<0.001) independent of known cardiovascular risk factors (odds ratio, 1.35; 95% confidence interval, 1.25-1.46 per doubling of troponin). Cardiac troponin concentrations improved the discrimination and calibration of the CAD Consortium model for identifying obstructive CAD (C statistic, 0.788-0.800; P=0.004; χ2=16.8 [P=0.032] to 14.3 [P=0.074]). The updated model also improved classification of the American College of Cardiology/American Heart Association pretest probability risk categories (net reclassification improvement, 0.062; 95% confidence interval, 0.035-0.089). The revised model achieved similar improvements in discrimination and calibration when applied in the external validation cohort.ConclusionsHigh-sensitivity cardiac troponin I concentration is an independent predictor of obstructive CAD in patients with suspected stable angina. Use of this test may improve the selection of patients for further investigation and treatment.Clinical trial registrationURL: https://www.clinicaltrials.gov. Unique identifier: NCT01149590.

Project description:IntroductionTroponin elevation is an independent risk factor for mortality, but the prognosis of patients with troponin elevation and non-obstructive coronary artery disease (CAD) is unknown. Recent data have suggested an increased risk of mortality. This study was performed to further investigate the outcomes of troponin-positive patients with obstructive and non-obstructive CAD.MethodsA retrospective cohort analysis was performed of all patients with raised troponin presenting to Kettering General Hospital (January 2010 to December 2011, n = 1,351). The patients who had angiograms were stratified anatomically into obstructive CAD and non-obstructive CAD (?50% stenosis). The obstructive CAD group (O-CAD) was sub-analyzed by management strategy: emergency re-vascularization (<12 h), urgent, delayed, and medically managed. Patients with non-obstructive CAD were grouped by the cause of the raised troponin if this could be identified (NO-CAD-I) or cause remained unidentified (NO-CAD-U). The major adverse cardiac and cerebrovascular event (MACCE) and mortality rates were calculated at 30 days and 1-year follow-up.ResultsThere was a preponderance of hypertension and severe renal impairment in the non-obstructive CAD group. The patients with NO-CAD-U were a low-risk group (MACCE at 1-year follow-up = 0). The remaining NO-CAD-I group had a similar risk to the O-CAD group for MACCE and mortality at 30 days and 1-year follow-up. In fact, at 1-year follow-up, the NO-CAD-I patients when compared with the subgroups of O-CAD, had higher MACCE rates and mortality compared with the emergency re-vascularized group [MACCE: relative risk (RR) (95% CI) = 2.27 (1.29-3.40), P = 0.0047; mortality: RR (95% CI) = 2.08 (1.10-3.93), P = 0.024]. This was driven by higher risk non-cardiac death [RR (95% CI) = 4.10 (1.53-10.99), P = 0.005].ConclusionPatients with identified cause for raised troponin and non-obstructive CAD are at equivalent risk of MACCE and mortality at 30 days and 1-year follow-up compared to those with obstructive CAD.

Project description:BackgroundCardiac troponin concentrations are used to identify patients who would benefit from urgent revascularization for acute coronary syndromes. We hypothesized that they might be used in patients with stable ischemic heart disease to identify those at high risk for cardiovascular events who might also benefit from prompt coronary revascularization.MethodsWe measured the cardiac troponin T concentration at baseline with a high-sensitivity assay in 2285 patients who had both type 2 diabetes and stable ischemic heart disease and were enrolled in the Bypass Angioplasty Revascularization Investigation in Type 2 Diabetes trial. We tested for an association between the troponin T concentration and a composite end point of death from cardiovascular causes, myocardial infarction, or stroke; we then evaluated whether random assignment to prompt revascularization reduced the rate of the composite end point in patients with an abnormal troponin T concentration (≥14 ng per liter) as compared with those with a normal troponin T concentration (<14 ng per liter).ResultsOf the 2285 patients, 2277 (99.6%) had detectable (≥3 ng per liter) troponin T concentrations and 897 (39.3%) had abnormal troponin T concentrations at baseline. The 5-year rate of the composite end point was 27.1% among the patients who had had abnormal troponin T concentrations at baseline, as compared with 12.9% among those who had had normal baseline troponin T concentrations. In models that were adjusted for cardiovascular risk factors, severity of diabetes, electrocardiographic abnormalities, and coronary anatomy, the hazard ratio for the composite end point among patients with abnormal troponin T concentrations was 1.85 (95% confidence interval [CI], 1.48 to 2.32; P<0.001). Among patients with abnormal troponin T concentrations, random assignment to prompt revascularization, as compared with medical therapy alone, did not result in a significant reduction in the rate of the composite end point (hazard ratio, 0.96; 95% CI, 0.74 to 1.25).ConclusionsThe cardiac troponin T concentration was an independent predictor of death from cardiovascular causes, myocardial infarction, or stroke in patients who had both type 2 diabetes and stable ischemic heart disease. An abnormal troponin T value of 14 ng per liter or higher did not identify a subgroup of patients who benefited from random assignment to prompt coronary revascularization. (Funded by the National Institutes of Health and Roche Diagnostics; BARI 2D ClinicalTrials.gov number, NCT00006305.).

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A sensitive cardiac troponin T assay in stable coronary artery disease.

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A sensitive cardiac troponin T assay in stable coronary artery disease.

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