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1、Cardiac Troponin and Outcomein Acute Heart FailureBackground 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 tr

2、oponin levels and adverse e v e n t s i n h o s p i t a l i z e d p a t i e n t s w i t h a c u t e 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

3、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 Januar y 2004. Inclusion criteria were hospitalization

4、 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 (

5、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 Stat

6、es, 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 exper t consensus, approx

7、imating values defined from a ROC curve that was optimized for the detection of myocardial infarction. Methods The primar y 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-pos

8、itive and troponin-negative cohorts. We also examined associations between therapy and mor tality 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 recor

9、ds were excluded because of missing values. Analyses were performed with the use of SAS software, version 8.2 (SAS Institute).Results 急性急性G-CSF干预下,模拟缺血条件下心室肌细胞干预下,模拟缺血条件下心室肌细胞ICa.L的的I-V曲线发生曲线发生了改变,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;的时候向右偏移,表明离子通道更容易激活;300g

10、/kg G-CSF同同100g/kg G-CSF相比,电流密度无明显统计学差异。相比,电流密度无明显统计学差异。 给予最大剂量给予最大剂量 (300g/kg)G-CSF对缺氧条件下心室肌细胞急性干预,对缺氧条件下心室肌细胞急性干预,INa的的 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。曲线、激活曲线、失活曲线和静态失活曲线均无明显变化。第二部分第二部分 心脏整体电生理研究心脏整体电生理研究ResultsTroponin was measured at the time of admission in 84,872 of 105,388 patients(80.5%) who w

11、ere 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 patient

12、s (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).DiscussionIn ou

13、r 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 my

14、ocardial 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 hi

15、gher 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

16、 of risk.DiscussionOur 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 pr

17、essure 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. DiscussionNational guidelines for the evaluation of an acute coronary syndrome recommend that levels of cardia

18、c 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 measurement of brain natriuretic peptide only in cases in which the diagnosis is uncertain. Our data suggest that t

19、he 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

20、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

21、 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.LimitationsSeveral limitations of the study are a function of the registry itself. Inclusion in ADHERE req

22、uired 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 fail

23、ure 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. Our finding

24、s may underrepresent adverse outcomes,since others have found that mortality at 30 days may exceed in-hospital mortality.DiscussionConclusions In patients with acute decompensated heart failure, a positive cardiac troponin test is associated with higher in-hospital mortality, independently of other

25、predictive variables.Methods We examined records from 274 hospitals, from October 2001 through Januar y 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

26、). 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

27、 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 exper t consensus, approximating values defined from a ROC curve that was optimized for the detection of myocardial infarction. 第二部分第二部分 心脏整体电生理研究心脏整

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