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1、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 Outcom
2、e 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
3、 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 o
4、bservational 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 troponi
5、n 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 pos
6、itive 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.
7、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 optimiz
8、ed 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 ass
9、ociations 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
10、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ICa.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，INa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
11、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
12、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.
13、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 b
14、e 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 thos
15、e 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 o
16、f 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
17、 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.,Di
18、scussion,National guidelines for the evaluation of an acute coronary syndrome recommend that levels of cardiac troponin and brain natriuretic peptide be used for prognosis and risk stratification. Current guidelines for the evaluation of heart failure do not mention troponin and recommend the measur
19、ement 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,Fi
20、rst, 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 wit
21、h 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 s
22、tudy.,Limitations,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 incl
23、uded 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 t
24、o the mortality rate. Finally, ADHERE recorded only in-hospital outcomes, not deaths after discharge. Our 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,