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W. Frank Peacock IV, M.D., Teresa De Marco, M.D., Gregg C.,Fonarow,M.D., Deborah,Diercks, M.D., Janet Wynne, M.S., Fred S. Apple,Ph.D.,and,Alan H.B. Wu, for the ADHERE Investigators,University of California at San Francisco, San Francisco,;,N,Engl,J Med 2008;358:2117-26.,Cardiac,Troponin,and Outcome,in Acute Heart Failure,Background,Cardiac troponin provides diagnostic and prognostic information in acute coronary syndromes, but its role in acute decompensated heart failure is unclear. The purpose of our study was to describe the association between elevated cardiac troponin levels and adverse events in hospitalized patients with acute decompensated heart failure. With the use of data from the Acute Decompensated Heart Failure National Registry (ADHERE), we analyzed outcomes associated with elevated troponin levels in patients with acute decompensated heart failure.Briefly,ADHERE is an observational registry, involving patients with an ultimate discharge diagnosis of acute decompensated heart failure.,Methods,We examined records from 274 hospitals, from October 2001 through January 2004. Inclusion criteria were hospitalization and documentation of the measurement of cardiac troponin I or cardiac troponin T at the initial evaluation (defined as within 24 hours after admission). Because renal dysfunction may influence cardiac troponin concentrations, patients with a serum creatinine level higher than 2.0 mg per deciliter (176.8 mol per liter) were excluded from the study. A positive troponin test was defined as a cardiac troponin I level of 1.0 g per liter or higher or a cardiac troponinT level of 0.1 g per liter or higher.,Methods,Measurement of cardiac troponin T is performed on a uniform platform in the United States, and the cutoff point of 0.1 g per liter or higher. Because troponin I has different cutoff points that are dependent on the platform used (more than a dozen different assays), a predefined cutoff point was set at 1.0 g per liter or higher. This cutoff point was based on expert consensus, approximating values defined from a ROC curve that was optimized for the detection of myocardial infarction.,Methods,The primary outcome was in-hospital mortality from all causes, and the secondary outcomes included differences in medical management, procedures,and length of stay between the troponin-positive and troponin-negative cohorts.,We also examined associations between therapy and mortality in patients who received inotropes or vasodilators, but not both.,Analysis of variance, Wilcoxon rank-sum tests, or chi-square tests were used for univariate for this analysis.Overall, 1.2% of the records were excluded because of missing values. Analyses were performed with the use of SAS software, version 8.2 (SAS Institute).,results,Results,急性G-CSF干预下，模拟缺血条件下心室肌细胞I,Ca.L,的I-V曲线发生了改变，呈剂量依赖性增加；失活曲线未发生变化，激活曲线在300g/kg的时候向右偏移，表明离子通道更容易激活；300g/kg G-CSF同100g/kg G-CSF相比，电流密度无明显统计学差异。,给予最大剂量 （300g/kg）G-CSF对缺氧条件下心室肌细胞急性干预，I,Na,的 I-V曲线、激活曲线、失活曲线和静态失活曲线均无明显变化。,第二部分 心脏整体电生理研究,Results,Troponin,was measured at the time of admission in 84,872 of 105,388 patients(80.5%) who were hospitalized for acute,decompensated,heart failure. Of these patients,67,924 had a,creatinine,level of less than 2.0 mg per deciliter. Cardiac,troponin,I was measured in 61,379 patients, and cardiac,troponin,T in 7880,patients(both,proteins were measured in 1335 patients). Overall, 4240 patients (6.2%) were,positive for,troponin,. Patients who were positive for,troponin,had lower systolic,blood pressure on admission, a lower ejection fraction, and higher in-hospital mortality(8.0% vs. 2.7%, P0.001) than those who were negative for,troponin,. to 2.89; P0.001 by the,Wald,test).,Discussion,In our data set, which included data from 105,388,patients,troponin,was measured in 80.5% of the,hospitalized patients with acute,decompensated,heart failure. Of,these patients, 6.2% were found to be positive for,troponin, including those with and those without,a history of coronary artery disease or myocardial,infarction.,patients presenting,with acute,decompensated,heart failure and a positive,troponin,status were found to be a high-risk,cohort. Patients in this cohort, as compared with,those who were negative for,troponin, required,more cardiac procedures and longer hospitalization,and had a higher risk of in-hospital death,even after adjustment for other risk factors.,These,results suggest that measurement of,troponin,adds important prognostic information to the initial,evaluation of patients with acute,decompen,-sated heart failure and should be considered as,part of an early assessment of risk.,Discussion,Our findings add to the,existing risk-stratification data for predicting the,short-term risk of death among patients with,acute,decompensated,heart failure.,Patients with,an initial blood urea nitrogen level of more than,43 mg per deciliter (15.4,mmol,per liter), systolic,blood pressure of less than 115 mm Hg, or a,creatinine,level of more than 2.75 mg per deciliter,(243.1,mol,per liter) have high short-term,mortality, exceeding 22% if all three factors are,present.,Discussion,National guidelines for the evaluation of an,acute coronary syndrome recommend that levels,of cardiac,troponin,and brain,natriuretic,peptide,b,e,used for prognosis and risk stratification. Current,guidelines for the evaluation of heart failure do,not mention,troponin,and recommend the measurement,of brain,natriuretic,peptide only in,cases in which the diagnosis is uncertain. Our,data suggest that the measurement of,troponin,levels in patients who present with heart failure,provides independent prognostic information regarding,in-hospital death and other clinical outcomes.,Discussion,First, we used the results,of various cardiac,troponin,I assays for,which we defined cutoff points, rather than core,laboratory results. However, the,generalizability,of our data,allows the findings to be considered in actual,patient-care scenarios.,Second, we were unable to analyze,those patients with heart failure in whom,troponin,was not assessed. Because,troponin,was measured only at the time of admission to,the hospital, we cannot comment on the number,of patients with an acute myocardial infarction,.,Finally, the other,biomarkers,such,as brain,natriuretic,peptide, was not explored,in this study.,L,imitations,Several limitations of the study are a function,of the registry itself.,Inclusion in ADHERE required,a discharge diagnosis of heart,failure,. Because,the diagnosis was not objectively,ascertained,some,patients with both heart failure and,an acute coronary syndrome may have been included,in our analysis. However, when only data,from patients who were categorized as having,nonischemic,heart failure were analyzed,troponin,levels retained their prognostic significance.,In addition, ADHERE did not consistently report,the cause of death, and,noncardiac,events may,have contributed to the mortality rate.,Finally, ADHERE recorded only in-hospital outcomes,not deaths after discharge.,O,ur findings may,underrepresent,adverse,outcomes,since,others have found that mortality at 30 days,may exceed in-hospital mortality.,Discussion,Conclusions,In patients with acute decompensated heart failure, a positive cardiac troponin test is associated with higher in-hospital mortality, independently of other predictive variables.,Thank you,
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