急性心力衰竭與心肌肌鈣蛋白指數(shù)的關(guān)系與臨床結(jié)果分析ppt課件

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.,andAlan H.B. Wu, for the ADHERE InvestigatorsUniversity of California at San Francisco, San Francisco;N Engl J Med 2021;358:2117-26.Cardiac Troponin and Outcomein

2、Acute Heart FailureBackgroundCardiac 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

3、 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 observat

4、ional 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 c

5、ardiac 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 tr

6、oponin 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 t

7、roponin 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 th

8、e 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

9、 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

10、 with the use of SAS software, version 8.2 (SAS Institute).Results 急性急性G-CSFG-CSF干涉下，模擬缺血條件下心室肌細(xì)胞干涉下，模擬缺血條件下心室肌細(xì)胞ICa.LICa.L的的I-VI-V曲線發(fā)生了改動(dòng)，呈劑量依賴性添加；失活曲線未曲線發(fā)生了改動(dòng)，呈劑量依賴性添加；失活曲線未發(fā)生變化，激活曲線在發(fā)生變化，激活曲線在300g/kg300g/kg的時(shí)候向右偏移，闡明的時(shí)候向右偏移，闡明離子通道更容易激活；離子通道更容易激活；300g/kg G-CSF300g/kg G-CSF同同100g/kg G-100g/kg G-CSF

11、CSF相比，電流密度無明顯統(tǒng)計(jì)學(xué)差別。相比，電流密度無明顯統(tǒng)計(jì)學(xué)差別。 給予最大劑量給予最大劑量 300g/kg300g/kgG-CSFG-CSF對缺氧條件下心室肌對缺氧條件下心室肌細(xì)胞急性干涉，細(xì)胞急性干涉，INaINa的的 I-V I-V曲線、激活曲線、失活曲線和曲線、激活曲線、失活曲線和靜態(tài)失活曲線均無明顯變化。靜態(tài)失活曲線均無明顯變化。第二部分 心臟整體電生理研討ResultsTroponin was measured at the time of admission in 84,872 of 105,388 patients(80.5%) who were hospitalized

12、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 pos

13、itive 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).In our data set, which included

14、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. patien

15、ts 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 de

16、ath, 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.DiscussionOur find

17、ings 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

18、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 cardiac troponin and brain natriu

19、retic 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 the measurement of troponin

20、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. Ho

21、wever, 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

22、 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 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