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Archives of cardiovascular diseases
Volume 109, n° 3
pages 163-170 (mars 2016)
Doi : 10.1016/j.acvd.2015.09.007
Received : 24 Mars 2015 ;  accepted : 10 September 2015
High-sensitivity cardiac troponin T: A biomarker for the early risk stratification of type-A acute aortic dissection?
Troponine T cardiaque hypertensive : un biomarqueur pour la stratification précoce du risque dans la dissection aortique de type A
 

Gang Li a, b, Xiao-Wei Wu c, Wei-Hua Lu b, Jian Cheng b, Xin-Ying Wu d, Rong Ai e, Zi-Hua Zhou a, Zhong-Zhi Tang b, Yu-Hua Liao a,
a Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Huazhong University of Science and Technology, 430022 Wuhan, China 
b Emergency Department, Wuhan General Hospital of Guangzhou Military Command, Wuhan, China 
c Department of Thoracic Surgery, TongJi Hospital, TongJi Medical College, Huazhong University of Science and Technology, Wuhan, China 
d Department of Cardiology, Pu’ai Hospital, Huazhong University of Science and Technology, Wuhan, China 
e College of Foreign Language, Huazhong Agriculture University, Wuhan, China 

Corresponding author.
Summary
Background

High-sensitivity cardiac troponin is the most specific and sensitive biomarker of myocardial injury. However, no study has investigated whether the early concentration of high-sensitivity cardiac troponin is increased or is of value in predicting short-term prognosis in patients with type-A acute aortic dissection (AAD) in the emergency department.

Aims

To measure the high-sensitivity cardiac troponin T (hs-TnT) concentration in patients with type-A AAD upon hospital admission, and to assess its value in predicting short-term prognosis.

Methods

We enrolled consecutive patients with type-A AAD. Blood samples were collected on admission; hs-TnT concentrations were measured on the Elecsys 2010 system. High-sensitivity C-reactive protein (hs-CRP), D-dimer and other biochemical indicators were measured. Patients were divided into two groups according to hs-TnT concentration on admission (< or ≥0.014ng/mL).

Results

More than half (61.2%) of the 103 included patients had an hs-TnT concentration ≥0.014ng/mL. hs-TnT concentrations were significantly higher in those who died compared with survivors (0.292±0.516 vs. 0.069±0.154ng/mL; P =0.003). Multivariable Cox regression analysis suggested that hs-TnT is an independent factor for predicting in-hospital mortality risk (odds ratio: 2.202, 95% confidence interval: 1.111–4.367; P =0.024). Kaplan–Meier curves revealed a significant increase in hospital mortality in the hs-TnT(+) group compared with the hs-TnT(–) group (P =0.021). When hs-TnT was ≥0.042ng/mL, the sensitivity and specificity in predicting hospital short-term mortality were 70.8% and 76.4%, respectively.

Conclusions

Our study suggests that hs-TnT concentration could be used as an early biomarker for the risk stratification of patients with type-A AAD in the emergency department; the relationship between hs-TnT concentration and long-term prognosis needs further investigation.

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Résumé
Justification

La troponine cardiaque hypersensible (hs-cTn) est le biomarqueur le plus sensible et le plus spécifique de l’atteinte myocytaire. Cependant, il n’y a pas d’étude évoluant le taux de troponine T ultrasensible dans ce contexte, qu’il s’agisse de son taux ou de sa valeur prédictive du pronostic à court terme dans les départements d’accueil des urgences, lorsque le diagnostic de dissection aortique aiguë est évoqué.

Méthode

Nous avons inclus 103 patients consécutifs ayant une dissection aortique A. Les prélèvements sanguins ont été obtenus à l’admission et les niveaux de troponine hypersensible ont été mesurés à l’aide d’un système Elecsys 2010. Dans le même temps, la CRP hypersensible, le taux de D-dimères et d’autres biomarqueurs ont été mesurés. Les patients ont été séparés en deux groupes en fonction du niveau initial de troponine T ultrasensible à l’admission.

Résultats

Plus de la moitié des patients (61,2 %) avaient à l’admission un taux de troponine T hypersensible élevé, en particulier chez les patients décédés (0,292±0,516 versus 0,069±154ng/mL, p =0,003). L’analyse en régression multivariée selon le modèle de Cox suggère que le taux de troponine T hypersensible est un facteur prédictif indépendant de la mortalité hospitalière (OR : 2,202, IC 95 % : 1,111–4,367, p =0,024). Les courbes de Kaplan-Meyer révèlent une augmentation significative de la mortalité hospitalière dans le groupe troponine T hypersensible élevé, en comparaison au groupe ayant une troponine T cardiaque hypersensible négative (p =0,021). Lorsque le taux de troponine hypersensible à l’admission est ≥0,042ng/mL, la sensibilité et la spécificité pour prédire la mortalité hospitalière est de respectivement, 70,8 et 76,4 %.

Conclusion

Cette étude suggère que le taux de troponine T cardiaque hypersensible pourrait être utilisé comme un biomarqueur utile pour la stratification du risque précoce des patients suspects de dissection aortique aiguë de type A, dans un département d’accueil des urgences. La relation entre le taux de troponine T hypersensible et le pronostic à long terme dans ce contexte nécessite des investigations complémentaires.

The full text of this article is available in PDF format.

Keywords : High-sensitivity cardiac troponin T, Acute aortic dissection, In-hospital mortality, Prognosis

Mots clés : Troponine T cardiaque hypersensible, Dissection aortique aiguë, Mortalité hospitalière, Pronostic

Abbreviations : AAD, CI, hs-CRP, hs-TnT, OR


Background

Acute aortic dissection (AAD) is characterized by separation of the layers of the wall of the aorta. AAD is seen most often in diseases of the aorta, which require emergency surgery. The annual incidence of AAD has been estimated to be 5–30 cases per million individuals, with a peak at 60–70 years of age [1]. Diagnosing AAD can be difficult, and assessing the prognosis of AAD patients is also challenging. Concentrations of D-dimer (a biomarker for fibrin degradation) [2], C-reactive protein (CRP) [3] and matrix metalloproteinases [4] have been associated with the prognosis of AAD.

Cardiac troponin is the most widely used biomarker of myocardial injury. However, certain conditions, such as increased demand for blood flow, myocardial strain due to volume load or pressure load, and damage to the integrity of myocardial cell membranes caused by systemic inflammation or apoptosis, can also increase the cardiac troponin concentration. Historically, AAD was considered to be a haematoma of the aortic medial layer that did not cause an increase in cardiac troponin concentration. However, several studies have shown that such an increase occurs in a significant number of AAD patients [5, 6, 7, 8]. The relationship between increased cardiac troponin concentration and the prognosis of AAD patients is not clear [5, 6].

Improvements in the methods and efficiency of assays have allowed physicians to detect increases in the concentration of high-sensitivity cardiac troponin in patients who do not exhibit the symptoms and signs of coronary artery disease. Several studies have suggested that high-sensitivity cardiac troponin T (hs-TnT) assays can improve early risk stratification and assessment of the prognosis of acute coronary syndromes [9, 10]. These studies have also suggested that hs-TnT is a novel biomarker for occult heart diseases [11]. However, it is not known whether the early concentration of hs-TnT is increased in patients with type-A AAD, and whether the early concentration can predict the prognosis in these patients. Therefore, the aims of the present study were to measure the concentration of hs-TnT in patients with type-A AAD upon hospital admission, and to assess the value of hs-TnT in predicting the short-term prognosis of these patients.

Methods
Ethical approval of the study protocol

The study protocol was approved by the Ethics Committee of Wuhan General Hospital of Guangzhou Military Command, and complied with the Declaration of Helsinki. All participants provided written informed consent to their inclusion in the study.

Study population

In this prospective cohort study, we included all consecutive patients with suspected AAD admitted to the emergency department at four local large-scale hospitals (Wuhan, China) from May 2010 to June 2014. Inclusion criteria were symptoms of chest pain, abdominal pain, back pain, syncope and other symptoms due to hypoperfusion, according to guidelines set by the European Society of Cardiology [12]; a time interval between symptom onset and hospital admission of ≤ 3hours; and type-A AAD verified by aortic computed tomography angiography, transoesophageal echocardiography or transthoracic echocardiography. We classified AAD according to the Stanford classification.

Exclusion criteria were typical electrocardiogram displays of acute myocardial infarction, including ST-segment elevations (≥0.2mV) or ST-segment depressions (≥0.2mV) in two adjacent leads, and pathological Q waves; a history of recent myocardial infarction or undergoing percutaneous coronary intervention; heart failure; severe aortic regurgitation; and severe liver disease or renal insufficiency.

Biochemical measurements

Blood samples were collected in ethylenediaminetetraacetic acid (EDTA)-containing tubes on admission to the emergency department. Creatinine, uric acid and high-sensitivity CRP (hs-CRP) were measured with the automated Cobas® C6000 Chemistry Analyzer (Roche Diagnostics, Basel, Switzerland). D-dimer concentrations were measured with the automated STA®-LIATEST® D-DI, based on latex agglutination (Diagnostica Stago for Roche Diagnostics).hs-TnT concentrations were measured on the Elecsys 2010 system (Roche Diagnostics), and the limit of blank and limit of detection were determined to be 0.003ng/mL and 0.005ng/mL, respectively. An imprecision corresponding to a coefficient of variation of 10% was reported at 0.013ng/mL, and that of the 99th percentile of a healthy reference population at 0.014ng/mL [13, 14].

Statistical analysis

SPSS statistical software, version 18.0 (SPSS Inc., Chicago, IL, USA) was used for statistical analysis. Continuous variables with a normal distribution were compared using Student's t -test and analysis of variance. Categorical variables were analysed using the χ2 test. According to the admission concentration of hs-TnT, patients were assigned to an hs-TnT(–) group (<0.014ng/mL) or an hs-TnT(+) group (≥0.014ng/mL). To assess the value of hs-TnT concentration in predicting the in-hospital mortality of type-A AAD, we used univariate and multivariable Cox regression analysis. Survival curves were estimated according to the Kaplan–Meier method, and compared by the log-rank test. Additionally, receiver operating characteristic analysis was performed to determine the cut-off value for hs-TnT for predicting in-hospital mortality with high-sensitivity and specificity. A P value<0.05 was considered to be statistically significant.

Results
Basic clinical information

During the study period, 686 patients with suspected AAD in the emergency department were eligible for enrolment; of these, 521 (75.9%) were enrolled and 305 (58.5%) finally had AAD diagnosed, including 202 cases of Stanford type-B AAD and 103 cases of Stanford type-A AAD. In accordance with the European Society of Cardiology guidelines [12], type-A AAD was confirmed by transoesophageal echocardiography (n =21), transthoracic echocardiography (n =10) or aortic computed tomography angiography (n =72).

In the Stanford type-B patients, nearly 81.2% of patients underwent interventional therapy for repair of aortic dissection; the remaining type-B patients were treated with drugs. However, only 67.9% of type-A patients underwent surgical treatment. Nearly one-third of type-A patients were treated medically. The reasons for medical treatment were comorbid conditions, old age, refusal by the patient and economic factors. Among the type-A AAD patients, 40 had an hs-TnT concentration<0.014ng/mL, while 63 had an hs-TnT concentration ≥0.014ng/mL. The mean hs-TnT concentration for all patients was 0.173±0.385ng/mL. The mean values of hs-TnT in the hs-TnT(–) and hs-TnT(+) groups were 0.011±0.010ng/mL and 0.276±0.464ng/mL, respectively.

Maximal aortic diameter and concentrations of hs-CRP and D-dimer were significantly higher in the hs-TnT(+) group compared with the hs-TnT(–) group. However, platelet count and fibrinogen concentrations were significantly lower in the hs-TnT(+) group. Of the 103 patients with type-A AAD, 36 died in hospital (34.9%) (Table 1). The common cause of death was rupture, which accounted for more than half (58.3%) of the deaths, followed by pericardial effusion (16.6%), intestinal ischaemia/kidney failure (11.1%), malignant arrhythmia (8.4%) and neurological deficit (5.6%). We found that hs-TnT concentrations were significantly higher in those who died compared with those who survived (0.292±0.516 vs. 0.069±0.154ng/mL; P =0.003) (Figure 1).



Figure 1


Figure 1. 

Analysis of high-sensitivity cardiac troponin T (hs-TnT) in patients who died and survived (0.292±0.516 vs. 0.069±0.154ng/mL, respectively; P =0.003).

Zoom

Univariate and multivariable Cox regression analysis for in-hospital mortality

In the univariate Cox regression model, we analysed the association between clinical variables and the risk of in-hospital mortality. The data indicated that six variables were associated with hospital short-term mortality (including admission systolic blood pressure, surgical or interventional treatment, hs-TnT, hs-CRP, D-dimer and platelet count), with a statistically significant P value in the univariate analysis (Table 2). In the multivariable Cox regression model, we put these variables and other risk factors into the model for analysis. We found that hs-TnT (odds ratio [OR]: 2.202, 95% confidence interval [CI]: 1.111–4.367; P =0.024) and hs-CRP (OR: 1.051, 95% CI: 1.009–1.094; P =0.017) concentrations could independently predict the risk of in-hospital mortality in patients with type-A AAD (Table 3).

The relative risk of different hs-TnT concentrations

In our participants, we found that the in-hospital mortality rate was higher in the hs-TnT(+) group than in the hs-TnT(–) group (27 vs. 9 deaths; 42.8% vs. 22.5%; P =0.035). The Kaplan–Meier curves stratified according to hs-TnT concentration are shown in Figure 2. Log-rank testing revealed a significant increase in hospital mortality in the hs-TnT(+) group (P =0.021).



Figure 2


Figure 2. 

Kaplan–Meier curves stratified according to high-sensitivity cardiac troponin T (hs-TnT) concentration; log-rank testing revealed a significant increase in in-hospital mortality in the hs-TnT(+) group compared with the hs-TnT(–) group (P =0.021).

Zoom

Sensitivity and specificity of hs-TnT in predicting in-hospital mortality

We performed receiver operating characteristic analysis to determine the cut-off value of hs-TnT in evaluating in-hospital mortality in all patients: the cut-off value was 0.042ng/mL (95% CI: 0.016–0.049; sensitivity: 70.8%; specificity: 76.4%; P <0.0001). The areas under the curve were 0.719 (95% CI: 0.621–0.803; P <0.0001), 0.700 (95% CI: 0.599–0.789; P =0.0003) and 0.818 (95% CI: 0.724–0.891; P <0.0001) for hs-TnT, hs-CRP and D-dimer, respectively (Table 4 and Figure 3).



Figure 3


Figure 3. 

Receiver operating characteristic curve analysis showing the prognostic value of high-sensitivity cardiac troponin T (hs-TnT), D-dimer and high-sensitivity C-reactive protein (hs-CRP) concentrations in predicting in-hospital mortality in all patients.

Zoom

Discussion

This is the first study to measure early concentrations of hs-TnT in type-A AAD patients in the emergency department. More than half of the patients (61.2%) showed an above-reference hs-TnT concentration. Concentrations of hs-TnT were elevated significantly in patients who died. Kaplan–Meier curves revealed a significant increase in hospital mortality in the hs-TnT(+) group compared with the hs-TnT(–) group. Multivariable Cox regression analysis suggested that hs-TnT was an independent factor for predicting risk of in-hospital mortality. When hs-TnT was ≥0.042ng/mL, the sensitivity and specificity in predicting in-hospital short-term mortality were 70.8% and 76.4%, respectively.

AAD has been considered to be a haematoma of the aortic medial layer. Former opinion assumed that the concentration of cardiac troponin in AAD patients would not increase because cardiac troponin is expressed specifically in myocardial cells and not in vascular smooth muscle cells. However, several studies have suggested the concentration of TnT is elevated in a significant number of AAD patients [5, 6, 7, 8]. The mechanism of action of such elevation of TnT concentration is not clear; some researchers have suggested that it is a special stress response to severe organ damage [5], but the elevation of TnT concentration has a limited relationship with myocardial damage. It has been reported that some inflammatory biomarkers are associated with the development and prognosis of AAD [15, 16]. Ventricular overload, as well as the stimulation caused by vasoactive substances and inflammatory cytokines, also have synergistic effects, inducing myocardial damage and elevation of TnT concentration.

With improvements in the methods and efficiency of assays, hs-TnT is now used widely for the diagnosis of myocardial injury. Compared with assays for conventional TnT, hs-TnT assays are more sensitive, and can detect elevations of TnT concentration in patients without the symptoms and signs of coronary artery disease. Large-sample studies have suggested that the measurement of hs-TnT concentration could significantly reduce diagnosis time and improve sensitivity in diagnosing acute myocardial infarction [17]. Measurement of hs-TnT concentration is also helpful for early risk stratification and assessment of the prognosis of acute coronary syndrome patients [9, 10]. In patients with stable coronary disease, the concentration of hs-TnT is associated significantly with the incidence of cardiac death and heart failure [17, 18]. In addition, combining the hs-TnT assay with the N-terminal of the prohormone brain natriuretic peptide (NT-proBNP) assay is likely to enable more accurate prediction of the prognosis of patients with heart failure [19, 20]. This evidence highlights the necessity and advantage of hs-TnT assays in patients with heart diseases.

Similar to the results of previous studies [8, 21] that showed that cardiac troponin was increased in patients with AAD, a significant number of patients with type-A AAD in our study had an elevated hs-TnT concentration. However, the proportion of patients with an elevated hs-TnT concentration was higher than in the previous studies. We speculate that this could be attributed to hs-TnT being detected much earlier than conventional cardiac troponin T. This finding suggests that most patients with type-A AAD develop myocardial injury to a certain extent. Concentrations of hs-TnT in patients who died were significantly higher than in surviving patients. In the hs-TnT(+) group, the risk of mortality was increased significantly. Elevated hs-TnT may not only be a maker of myocardial injury, but may also reflect a serious stress state. Another study has reported that elevated hs-TnT is a strong mortality risk marker in hospitalized older patients in general [22].

Our results suggest that elevation of the hs-TnT concentration may reflect the severity of type-A AAD. In our study, multivariable Cox regression analysis suggested that hs-TnT was an independent factor in predicting the risk of in-hospital mortality. Kaplan–Meier curves revealed a significant increase in hospital mortality in the hs-TnT(+) group compared with the hs-TnT(–) group (P =0.021). AAD has a close relationship with systemic inflammation [2, 15], as well as concentrations of D-dimer [2] and inflammatory cytokines [16]. Our findings indicated that significantly increased concentrations of plasma D-dimer and hs-CRP were present in hs-TnT(+) patients. D-dimer is a biomarker indicating activation of the fibrinolytic system, while an increased hs-CRP concentration is a marker of systemic inflammation. These findings further suggest that the elevation of hs-TnT concentration in type-A AAD patients results from the synergistic functions of multiple mechanisms.

AAD is a high-risk disease, and type-A AAD is highly lethal. The untreated mortality rate can approximate 1–2% per hour following symptom onset, with the majority of patients succumbing within 30 days [1, 23, 24]. Surgical repair transforms the high mortality risk to a chance of survival that is>70% in the short-term [25]. In our patients, Kaplan–Meier curves revealed a significant increase in hospital mortality in the hs-TnT(+) group compared with the hs-TnT(–) group. Our findings suggest that we need to proceed with early risk stratification of type-A AAD in the emergency department. Although this is a fatal disease, we hypothesized whether earlier aggressive surgical treatment in patients with elevated hs-TnT might increase the chance of survival in the short-term. However, the times to surgical or interventional treatment in the hs-TnT(+) and hs-TnT(–) groups were not different in our study.

We undertook receiver operating characteristic curve analysis for each patient. We found that the diagnostic value of the hs-TnT concentration in predicting the in-hospital mortality of patients with type-A AAD was similar to that of the D-dimer concentration and superior to that of the hs-CRP concentration. Concentrations of D-dimer and hs-CRP, acting as biomarkers of activation of the fibrinolytic system and systemic inflammation, respectively, are highly valuable for predicting the prognosis of patients with AAD [2, 3]. When hs-TnT was ≥0.042ng/mL, the sensitivity and specificity in predicting hospital short-term mortality were 70.8% and 76.4%, respectively. In our study, the value of hs-TnT (which acts as a biomarker of myocardial injury) in predicting in-hospital mortality of patients with type-A AAD was similar to that of D-dimer and hs-CRP (areas under the curve 0.719 vs. 0.818 vs. 0.700, respectively). hs-TnT has the potential to be a biomarker for the early risk stratification of type-A AAD patients in the future.

Study limitations

Our study had limitations. First, although it was a multicentre study, the number of patients with type-A AAD enrolled was limited compared with large-scale international clinical trials, such as the International Registry of Acute Aortic Dissections (IRAD) study [1]. Second, the follow-up of patients in hospital was limited, and the primary endpoint was in-hospital mortality; the short duration of follow-up and the lack of a secondary endpoint were limitations. Third, blood tests were taken only in emergencies, and changes in hs-TnT concentration and peak hs-TnT concentration were not monitored dynamically; this oversight may have influenced analyses of the results. Finally, we did not exclude patients whose coronary sinus ostium had been involved. However, not all of the patients underwent coronary angiography. It has been reported that some AAD patients develop secondary myocardial infarction [26], and that this phenomenon probably affects the hs-TnT concentration.

Conclusion

This is the first study to detect the early concentration of hs-TnT in patients with type-A AAD in the emergency department. Our results showed that more than half (61.2%) of the patients had an above-reference hs-TnT concentration. We conclude that the concentration of hs-TnT is an independent prognostic factor for in-hospital mortality of patients with type-A AAD, with a cut-off value of 0.042ng/mL. Kaplan–Meier curves revealed a significant increase in hospital mortality in the hs-TnT(+) group compared with the hs-TnT(–) group. When the hs-TnT concentration was ≥0.042ng/mL, the sensitivity and specificity in predicting in-hospital short-term mortality were 70.8% and 76.4%, respectively. Our study suggests that hs-TnT concentration could be used as an early biomarker for the risk stratification of type-A AAD patients in the emergency department. The relationship between hs-TnT concentration and the long-term prognosis of type-A AAD patients needs further investigation.

Disclosure of interest

The authors declare that they have no competing interest.

Sources of funding : This study was supported by the Youth Fund of Wuhan General Hospital of Guangzhou Military Command.


Acknowledgements

All authors read and approved the final manuscript. L. G. participated in the study design, drafted the manuscript and was the main executant of the experiments. W. X.-W., Z. Z.-H. and W. X.-Y. also performed some experiments and contributed to the writing of the manuscript. A. R. and L. W.-H. performed the statistical analysis. C. J. and T. Z.-Z. supervised the study. L. Y.-H. had the original idea for the study.

References

Hagan P.G., Nienaber C.A., Isselbacher E.M., and al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease JAMA 2000 ;  283 : 897-903 [cross-ref]
Wen D., Du X., Dong J.Z., Zhou X.L., Ma C.S. Value of D-dimer and C reactive protein in predicting inhospital death in acute aortic dissection Heart 2013 ;  99 : 1192-1197 [cross-ref]
AlMahameed S.T., Novaro G.M., Asher C.R., and al. Predictive value of high sensitivity C-reactive protein in the diagnosis and outcomes of acute aortic syndromes Heart Asia 2010 ;  2 : 136-139
Song Y., Xie Y., Liu F., and al. Expression of matrix metalloproteinase-12 in aortic dissection BMC Cardiovasc Disord 2013 ;  13 : 34 [cross-ref]
Bonnefoy E., Godon P., Kirkorian G., Chabaud S., Touboul P. Significance of serum troponin I elevation in patients with acute aortic dissection of the ascending aorta Acta Cardiol 2005 ;  60 : 165-170 [cross-ref]
Jerjes-Sanchez C., Garcia N., Diaz de Leon-Gonzalez E., Garcia-Sosa A., Sanchez-Ramirez C.J. Significance of biomarker panel including cardiac troponin I, D-dimer, and B-type natriuretic peptide in acute aortic dissection J Cardiol Therap 2013 ;  1 : 58-63
Kelley W.E., Januzzi J.L., Christenson R.H. Increases of cardiac troponin in conditions other than acute coronary syndrome and heart failure Clin Chem 2009 ;  55 : 2098-2112 [cross-ref]
Rapezzi C., Longhi S., Graziosi M., and al. Risk factors for diagnostic delay in acute aortic dissection Am J Cardiol 2008 ;  102 : 1399-1406 [inter-ref]
Thelin J., Borna C., Erlinge D., Ohlin B. The combination of high sensitivity troponin T and copeptin facilitates early rule-out of ACS: a prospective observational study BMC Cardiovasc Disord 2013 ;  13 : 42 [cross-ref]
Vaidya A., Severens J.L., Bongaerts B.W., and al. High-sensitive troponin T assay for the diagnosis of acute myocardial infarction: an economic evaluation BMC Cardiovasc Disord 2014 ;  14 : 77 [cross-ref]
Diamond G.A., Kaul S. How would the Reverend Bayes interpret high-sensitivity troponin? Circulation 2010 ;  121 : 1172-1175 [cross-ref]
Erbel R., Aboyans V., Boileau C., and al. 2014 ESC Guidelines on the diagnosis and treatment of aortic diseases: Document covering acute and chronic aortic diseases of the thoracic and abdominal aorta of the adult. The Task Force for the Diagnosis and Treatment of Aortic Diseases of the European Society of Cardiology (ESC) Eur Heart J 2014 ;  35 : 2873-2926
Giannitsis E., Kurz K., Hallermayer K., Jarausch J., Jaffe A.S., Katus H.A. Analytical validation of a high-sensitivity cardiac troponin T assay Clin Chem 2010 ;  56 : 254-261 [cross-ref]
Mingels A., Jacobs L., Michielsen E., Swaanenburg J., Wodzig W., van Dieijen-Visser M. Reference population and marathon runner sera assessed by highly sensitive cardiac troponin T and commercial cardiac troponin T and I assays Clin Chem 2009 ;  55 : 101-108
Agg B., Benke K., Szilveszter B., and al. Possible extracardiac predictors of aortic dissection in Marfan syndrome BMC Cardiovasc Disord 2014 ;  14 : 47 [cross-ref]
Wen D., Zhou X.L., Li J.J., and al. Plasma concentrations of interleukin-6, C-reactive protein, tumor necrosis factor-alpha and matrix metalloproteinase-9 in aortic dissection Clin Chim Acta 2012 ;  413 : 198-202 [cross-ref]
Thygesen K., Mair J., Giannitsis E., and al. How to use high-sensitivity cardiac troponins in acute cardiac care Eur Heart J 2012 ;  33 : 2252-2257 [cross-ref]
Schulz O., Reinicke M., Berghoefer G.H., and al. High-sensitive cardiac troponin I (hs-cTnI) values in patients with stable cardiovascular disease: an initial foray Clin Chim Acta 2010 ;  411 : 812-817 [cross-ref]
Apple F.S., Steffen L.M., Pearce L.A., Murakami M.M., Luepker R.V. Increased cardiac troponin I as measured by a high-sensitivity assay is associated with high odds of cardiovascular death: the Minnesota Heart Survey Clin Chem 2012 ;  58 : 930-935 [cross-ref]
Kawahara C., Tsutamoto T., Sakai H., and al. Prognostic value of serial measurements of highly sensitive cardiac troponin I in stable outpatients with nonischemic chronic heart failure Am Heart J 2011 ;  162 : 639-645 [inter-ref]
Hansen M.S., Nogareda G.J., Hutchison S.J. Frequency of and inappropriate treatment of misdiagnosis of acute aortic dissection Am J Cardiol 2007 ;  99 : 852-856 [inter-ref]
Iversen K., Kober L., Gotze J.P., and al. Troponin T is a strong marker of mortality in hospitalized patients Int J Cardiol 2013 ;  168 : 818-824 [cross-ref]
Fann J.I., Smith J.A., Miller D.C., and al. Surgical management of aortic dissection during a 30-year period Circulation 1995 ;  92 : II113-II121 [cross-ref]
Scholl F.G., Coady M.A., Davies R., and al. Interval or permanent nonoperative management of acute type A aortic dissection Arch Surg 1999 ;  134 : 402-405[discussion 5–6].  [cross-ref]
Ranasinghe A.M., Bonser R.S. Biomarkers in acute aortic dissection and other aortic syndromes J Am Coll Cardiol 2010 ;  56 : 1535-1541 [cross-ref]
Luo J.L., Wu C.K., Lin Y.H., and al. Type A aortic dissection manifesting as acute myocardial infarction: still a lesson to learn Acta Cardiol 2009 ;  64 : 499-504



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