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 ≥ 0.014 ng/mL).
Results
More than half (61.2%) of the 103 included patients had an hs-TnT concentration ≥ 0.014 ng/mL. hs-TnT concentrations were significantly higher in those who died compared with survivors (0.292 ± 0.516 vs. 0.069 ± 0.154 ng/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 ≥ 0.042 ng/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.
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 ± 154 ng/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 ≥ 0,042 ng/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.
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 . Diagnosing AAD can be difficult, and assessing the prognosis of AAD patients is also challenging. Concentrations of D-dimer (a biomarker for fibrin degradation) , C-reactive protein (CRP) and matrix metalloproteinases 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 . The relationship between increased cardiac troponin concentration and the prognosis of AAD patients is not clear .
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 . These studies have also suggested that hs-TnT is a novel biomarker for occult heart diseases . 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 ; a time interval between symptom onset and hospital admission of ≤ 3 hours; 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 (≥ 0.2 mV) or ST-segment depressions (≥ 0.2 mV) 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 0.003 ng/mL and 0.005 ng/mL, respectively. An imprecision corresponding to a coefficient of variation of 10% was reported at 0.013 ng/mL, and that of the 99th percentile of a healthy reference population at 0.014 ng/mL .
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 χ 2 test. According to the admission concentration of hs-TnT, patients were assigned to an hs-TnT(–) group (< 0.014 ng/mL) or an hs-TnT(+) group (≥ 0.014 ng/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 , 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 < 0.014 ng/mL, while 63 had an hs-TnT concentration ≥ 0.014 ng/mL. The mean hs-TnT concentration for all patients was 0.173 ± 0.385 ng/mL. The mean values of hs-TnT in the hs-TnT(–) and hs-TnT(+) groups were 0.011 ± 0.010 ng/mL and 0.276 ± 0.464 ng/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 ± 0.154 ng/mL; P = 0.003) ( Fig. 1 ).
| Clinical variables | hs-TnT < 0.014 ng/mL ( n = 40; 38.8%) | hs-TnT ≥ 0.014 ng/mL ( n = 63; 61.2%) | P value |
|---|---|---|---|
| Age (years) | 56.5 ± 13.8 | 53.3 ± 13.2 | 0.240 |
| Men | 28 (70) | 43 (68.3) | 0.852 |
| Hospitalization time (days) | 9.6 ± 7.7 | 10.5 ± 11.1 | 0.622 |
| Death | 9 (22.5) | 27 (42.8) | 0.035 |
| Smoking | 23 (57.5) | 38 (60.3) | 0.777 |
| History of hypertension | 31 (77.5) | 50 (79.4) | 0.811 |
| History of diabetes mellitus | 13 (32.5) | 18 (28.6) | 0.667 |
| Medications before admission | |||
| Aspirin | 17 (42.5) | 31 (49.2) | 0.548 |
| Clopidogrel | 7 (17.5) | 13 (20.6) | 0.801 |
| Statin | 15 (37.5) | 20 (31.7) | 0.670 |
| Time to surgical or interventional treatment (hours) | 8.6 ± 4.4 | 9.2 ± 5.2 | 0.327 |
| Abnormal ECG | 17 (42.5) | 28 (44.4) | 0.846 |
| Surgical or interventional treatment | 28 (70) | 42 (66.7) | 0.724 |
| Maximal aortic diameter (mm) | 44.8 ± 5.4 | 47.9 ± 7.5 | 0.026 |
| Admission SBP (mmHg) | 168.5 ± 37.0 | 177.8 ± 39.1 | 0.264 |
| Admission DBP (mmHg) | 106.3 ± 24.2 | 110.4 ± 21.3 | 0.412 |
| Heart rate (bpm) | 84.3 ± 17.1 | 78.5 ± 19.8 | 0.132 |
| Platelet count (×10 9 /L) | 192.1 ± 70.3 | 156.3 ± 89.7 | 0.042 |
| Prothrombin time (s) | 11.9 ± 1.6 | 13.0 ± 3.2 | 0.074 |
| Fibrinogen (g/L) | 5.5 ± 3.0 | 4.3 ± 2.0 | 0.018 |
| hs-CRP (mg/L) | 9.8 ± 7.8 | 14.3 ± 10.1 | 0.025 |
| Uric acid (μmol/L) | 296.8 ± 105.6 | 331.9 ± 88.0 | 0.087 |
| Creatinine (μmol/L) | 105.6 ± 44.9 | 120.5 ± 61.6 | 0.193 |
| Blood urea nitrogen (mmol/L) | 7.6 ± 3.8 | 7.8 ± 4.1 | 0.674 |
| Body mass index (kg/m 2 ) | 23.5 ± 2.4 | 24.3 ± 2.7 | 0.452 |
| D-dimer (μg/L) | 711.5 ± 697.2 | 1348.1 ± 1332.5 | 0.011 |
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