Prognostic Implications of Normal (&lt;0.10 ng/ml) and Borderline (0.10 to 1.49 ng/ml) Troponin Elevation Levels in Critically Ill Patients Without Acute Coronary Syndrome

Stein, Russell; Gupta, Bhanu; Agarwal, Savita; Golub, Jason; Bhutani, Divaya; Rosman, Alan S.; Eng, Calvin

doi:10.1016/j.amjcard.2008.04.026

Cited by 55 publications

(30 citation statements)

References 13 publications

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“…Troponin measured in patients who exhibit cardiac angina, a combination of clinical signs, and known coronary disease risk factors allows practitioners to "rule in" heart attack. Troponin loses specificity when measured in patients without cardiac angina risk stratification (12). Unfortunately, unlike a heart attack, AKI does not carry an easily identifiable physical prodrome like cardiac angina.…”

Section: Discussionmentioning

confidence: 99%

“…Just as in the scenario of a potential heart attack, in which troponin levels are tested in patients with cardiac angina (thereby optimizing its use using clinical context), we propose that in scenarios of potential kidney attacks, AKI biomarkers will have greater utility and predictive value in patients who have renal angina fulfillment. Repeated evidence highlights the erosion of troponin performance when measured in patients without chest pain or at low clinical risk of myocardial infarction from coronary disease (10)(11)(12)(13)(14)(15)(16). In addition, independent of troponin, the absence of cardiac angina carries high negative predictive value for the diagnosis of a heart attack (17,18).…”

Section: Introductionmentioning

confidence: 99%

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Incorporation of Biomarkers with the Renal Angina Index for Prediction of Severe AKI in Critically Ill Children

Basu

Wang

Wong

et al. 2014

Clinical Journal of the American Society of Nephrology

137

113

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Background and objectives Novel AKI biomarkers carry variable performance for prediction of AKI in patients with heterogeneous illness. Until utility is demonstrated in critically ill patients outside of the cardiopulmonary bypass population, AKI biomarkers are unlikely to gain widespread implementation. Operationalization of an AKI risk stratification methodology, termed renal angina, was recently reported to enhance prediction at the time of intensive care unit admission for persistent severe AKI. The renal angina index (RAI) was developed to provide the clinical context to direct AKI biomarker testing. This study tested the hypothesis that incorporation of AKI biomarkers in patients fulfilling renal angina improves the prediction of persistent severe AKI.Design, setting, participants, & measurements In a multicenter study of 214 patients admitted to the pediatric intensive care unit with sepsis, the discrimination of plasma neutrophil gelatinase-associated lipocalin (NGAL), matrix metalloproteinase-8 (MMP-8), and neutrophil elastase-2 (Ela-2) were determined individually and in combination with the RAI for severe AKI. Net reclassification improvement (NRI) and integrated discrimination improvement (IDI) were calculated. Conclusions This study shows that incorporation of AKI biomarkers into the RAI improves discrimination for severe AKI. The RAI optimizes the utility of AKI biomarkers in a heterogeneous, critically ill patient population.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Incorporation of Biomarkers with the Renal Angina Index for Prediction of Severe AKI in Critically Ill Children

Basu

Wang

Wong

et al. 2014

Clinical Journal of the American Society of Nephrology

137

113

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“…In our study, we found 37% increase in the level of cTn-T. However, elevated cTn-T may be associated with sepsis, and chronic renal disease which are common concomitant comorbid conditions in patients with acute PE (23)(24)(25). Therefore, it would be misleading to make a connection between elevated cTn-T and acute PE.…”

Section: Discussionmentioning

confidence: 57%

Relationship between cardiac troponin-T and right ventricular Tei index in patients with hemodynamically stable pulmonary embolism: an observational study

Özsu¹,

Kırış²,

Bülbül³

et al. 2012

Anadolu Kardiyol Derg

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Objective: The role of increased troponin level in risk stratification of acute pulmonary embolism (PE) is well documented. However, relation between right ventricular (RV) myocardial performance (Tei) index and cardiac troponin-T (cTn-T) has not been well investigated. The purpose of this observational prospective study was to assess the relationship between the RV Tei index and cTn-T in patients with acute normotensive PE. Methods: Thirty-eight patients with acute PE diagnosed by computed spiral tomography pulmonary angiography were enrolled to this prospective observational study. All study population underwent a comprehensive echocardiographic study including tissue Doppler imaging within first 12 hours of admission. cTn-T levels were measured on admission. Follow-up echocardiography was performed routinely at the 7 th day of hospitalization. Echocardiographic evaluation was repeated at 90 days in patients with insufficient improvement of RV Tei index. The difference between the baseline and follow-up data was analyzed using the paired sample t-test or Wilcoxon test according to normality of distribution. Results: The mean of the RV Tei index was 0.46±0.14 and the mean systolic pulmonary artery pressure (sPAP) was 40±20 mmHg. Increased cTn-T level was detected in 37% of the patients (normal value 0.01< ng/mL). Significant correlations were observed between RV Tei index and sPAP with cTn-T levels (r=0.467 and r=0.468, p<0.001, respectively). In logistic regression analysis, RV Tei index was associated with positive cTn-T values (OR-136, 95% CI: 1.3-14657, p=0.039). After the anticoagulant treatment, RV Tei index and sPAP were significantly improved. Conclusion: RV Tei index is frequently impaired in patients with acute PE and a significant recovery is seen after the treatment. Therefore, RV Tei index may be used both the diagnosis of RV dysfunction and the assessment of treatment effectiveness. RV Tei index is may predict myocardial injury in PE. Yöntemler: Prospektif gözlemsel bu çalışmaya, bilgisayarlı spiral tomografik pulmoner anjiyografi ile tanısı konulan 38 PE hastası dahil edildi. Tüm çalışma popülâsyonuna, hastaneye kabulün ilk 12 saati içinde, doku Doppler görüntülemeyi içeren kapsamlı bir ekokardiyografik inceleme yapıldı. cTn-T seviyesi hastaneye kabulde ölçüldü. Hastanedeki tedavinin yedinci gününde rutin olarak takip ekokardiyografisi yapıldı. SV Tei indeksinde düzelme olmayan hastaların ekokardiyografisi doksanıncı günde tekrarlandı. Başlangıç ve takip değerleri dağılıma uygun olarak bağımsız örneklem t-testi veya Wilcoxon test ile değerlendirildi. Bulgular: Ortalama SV Tei indeksi 0.46±0.14 ve ortalama sistolik pulmoner arter basıncı (sPAP) 40±20 mmHg idi. Hastaların %37'sinde artmış cTn-T düzeyi saptandı (normal değer 0.01< ng/mL). SV Tei indeksi, sPAP ve cTn-T düzeyi arasında anlamlı korelasyon gözlendi (r=0.467 ve r=0.468, p<0.001,

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“…Previous investigations, [15][16][17][18][19][20][21] mostly retrospective observational studies, have indicated that serum levels of CTnI and/or troponin T subunits are reliable prognostic markers for multiple outcomes, including severity of traumatic brain injury as indicated by scores on the Glasgow Coma Scale, hospital mortality and length of stay, and ICU length of stay, among critically ill patients across different medical specialties, including cardiothoracic surgery, neurology, and general surgery (Table 1). However, Minkin et al 22 and Stein et al 23 found that CTnI levels within 24 hours of ICU admission or peak levels during the ICU stay correlated poorly with hospital length of stay, readmission rates, and mortality at 6 months after discharge. The results of these 2 retrospective studies 22,23 suggest that CTnI level is a poor predictor for such outcomes in non-ACS patients and conflict with the findings of Garrett et al 16 Only 3 studies [18][19][20] were conducted prospectively and outside the United States, and none of the studies [15][16][17][18][19][20][21][22][23] included an evaluation of the prognostic value of CTnI levels in long-term care patients.…”

mentioning

confidence: 99%

Prognostic Value of Initial Elevation in Cardiac Troponin I Level in Critically Ill Patients Without Acute Coronary Syndrome

Liu

Shehu

Herrold

et al. 2015

Critical Care Nurse

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Background Cardiac troponin I levels are often obtained to help rule out acute coronary syndrome. Objective To determine if elevation of troponin level within 24 hours for patients without acute coronary syndrome admitted to the intensive care unit provides important prognostic information. METHODS Patients without acute coronary syndrome admitted to the intensive care unit were prospectively divided into 2 groups according to highest serum level of cardiac troponin I within 24 hours of admission (elevated > 0.049 ng/mL; control ≤ 0.049 ng/mL). Hospital mortality, incidence of intubation, and other parameters were compared between the 2 groups. Results Patients with elevated troponin level (n = 40) had higher mortality than did control patients (n = 50) (35% vs 12%; P = .01). Compared with control patients, patients with elevated levels were more likely to be intubated (41% vs 17%; P = .02). Conclusion Critically ill patients without acute coronary syndrome with elevated levels of cardiac troponin I at admission had higher mortality and more intubations than did control patients.

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Prognostic Implications of Normal (<0.10 ng/ml) and Borderline (0.10 to 1.49 ng/ml) Troponin Elevation Levels in Critically Ill Patients Without Acute Coronary Syndrome

Cited by 55 publications

References 13 publications

Incorporation of Biomarkers with the Renal Angina Index for Prediction of Severe AKI in Critically Ill Children

Incorporation of Biomarkers with the Renal Angina Index for Prediction of Severe AKI in Critically Ill Children

Relationship between cardiac troponin-T and right ventricular Tei index in patients with hemodynamically stable pulmonary embolism: an observational study

Prognostic Value of Initial Elevation in Cardiac Troponin I Level in Critically Ill Patients Without Acute Coronary Syndrome

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