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We aimed to determine the prognostic value of troponin T (TNT) for in-hospital and 1-yr mortality in a large sample of patients with pulmonary embolism (PE). Patients presenting at the emergency department of a tertiary care centre from January 1998 to December 2006 with PE were included. A blood sample was taken at the time of presentation. To det...
Contexts in source publication
Context 1
... major cause of death in the first year was PE in TNT- positive patients and in patients without TNT measurement, while in TNT-negative patients the cause of death was cancer (table 2). Of the 48 patients who died from PE, 45 died in hospital. ...
Context 2
... PE was the most frequent cause of in-hospital and 1-yr mortality in the overall study population, followed by cancer. Clearly, this was not true for TNT-negative patients, in whom cancer was the primary cause of 1-yr mortality (table 2). Therefore, the reasons for long-term mortality differed in TNT-positive and TNT-negative patients. ...
Citations
... Troponin elevation is the most sensitive and specific biochemical indicator of ischemic myocardial injury. However, non-ischemic myocardial injury-related pathological conditions such as sepsis, pulmonary embolism, viral myocarditis, and renal failure are also likely to occur, and as one of the critical factors influencing longterm prognosis [47]. The autonomic nervous system dysfunction causes overactivation of the sympathetic nerve and an increase in catecholamine effect in cardiomyocytes. ...
Background
For patients with acute exacerbation of COPD (AECOPD), type 2 diabetes mellitus (T2DM) as comorbidity have poor outcomes. However, data on the impact of previously diagnosed and new- diagnosed T2DM in such a patient population is lacking.
Methods
Inpatients diagnosed with AECOPD in the department of Pulmonary and Critical Care Medicine of The First Hospital of China Medical University during 2011–2017 were enrolled. Data on demography, prevalence of type 2 DM, other comorbidities, hospital stays and laboratory tests (including arterial partial pressure of oxygen [PaO2]) results were recorded. Results were compared with AECOPD patients having previously diagnosed and new-diagnosed type 2 diabetes. Markers associated with development of type 2 DM and the prognosis of AECOPD patients were identified.
Results
Of the 196 patients enrolled in this study, the overall prevalence of T2DM was 26%. The PaO2 in the newly diagnosed T2DM group was considerably lower versus non-diabetic group. The T2DM group had a longer hospital stay and higher troponin level versus the non-diabetic group. AECOPD patients with T2DM were found to be correlated with hypertension. Age, need for assisted ventilation, increased troponin, and elevated fasting blood glucose on admission were risk factors for death in hospitalized AECOPD patients.
Conclusions
AECOPD patients had a higher prevalence of T2DM than the general population; T2DM comorbidity caused lower PaO2, longer hospital stays, and increased troponin. Poor blood glucose control may increase the risk of death in AECOPD patients.
... All adult patients admitted for the management of acute PE at Hamad General Hospital and had at least one blood collection for cTn measurement during initial 24 h as well as RV assessment by CTPA were included in the study. The diagnosis of PE was made by CT scan examination in addition to clinical, laboratory and echocardiographic findings (10)(11)(12)(13)(14). ...
... Austria reported an association between advanced age, higher comorbidities, presentation with severe clinical manifestations of PE and elevated cTn (11). The possible explanation for the release of cTn is attributed to acute RV strain, decreased coronary blood flow, and hypoxemia secondary to PE (18). ...
... The RV is integral to normal cardiac function; however, the crescent-shaped geometry of the RV makes the chamber poorly tolerant of acute elevations in pulmonary circulation which can cause acute RV dilation, damaging the contractile sarcomere apparatus (19) with resultant RV dysfunction and troponin and BNP release. cTn has a prognostic relevance for risk stratification and outcome of PE due to its high negative predictive value (11,12). Moreover, in patients with acute PE, increased levels of cTn indicate a significant RV strain which might be related to the higher risk of severe PE as well as a higher overall mortality (6,20,21). ...
Background:
To evaluate the implications of elevated cardiac troponin (cTn) in patients presenting with pulmonary embolism (PE).
Methods:
We conducted a retrospective analysis for patients with PE between 2011 and 2015 with an average of 3 years follow-up. Patients were categorized into two groups based on the cTn status on admission (negative vs. positive) and RV/LV ratio (≤1.2 vs. >1.2). PE diagnosis was made by computed tomography pulmonary angiography (CTPA) examinations.
Results:
Among 220 patients with PE, 52.7% had positive cTn and 31.7% had RV dysfunction. Protein S and C deficiency were significantly higher in patients with negative cTn. Patients with positive cTn were more likely to have high-risk simplified pulmonary embolism severity index (sPESI), RV dilation, RV/LV ratio >1.2, severe inferior vena cava reflux and high Qanadli score (QS >18 points). Thrombolytic therapy was used in 15 patients; 9 (60%) of them had elevated troponin. Combined cTn and sPESI had higher sensitivity, negative predictive value and negative likelihood ratio to predict in-hospital mortality. Overall 30-day and 3 years morality were 10.0% and 22.3%; that were significantly higher in patients with positive troponin. Cox regression analysis showed that mortality increased 2.5 times with positive cTn after adjusting for age, sex, and RV dysfunction (adjusted HR 2.5; 95% CI: 1.25-5.01), P=0.009.
Conclusions:
Elevated cTn is independent predictor of short and long-term mortality. The predictive power of cTn increases when combined with the clinical probability score. Further, larger prospective studies are needed to confirm the findings of the present study.
... The in-hospital or short-term mortality after an episode of acute PE ranges from 3% to 65%, influenced largely by hemodynamic instability and evidence of right ventricular (RV) dysfunction upon initial presentation. [1][2][3][4][5][6][7][8][9][10][11][12][13] The mortality risk in patients with acute PE remains significantly elevated after hospital discharge, with 1-year mortality rates reaching 25%. 1,2,6,[8][9][10][11]14 Long-term mortality after acute PE seems to be influenced by comorbidities, especially malignancy and cardiovascular conditions. ...
... 1,2,6,[8][9][10][11]14 Long-term mortality after acute PE seems to be influenced by comorbidities, especially malignancy and cardiovascular conditions. 1,[4][5][6]8,10,14 Several clinical risk stratification models, biomarkers, and imaging tools have shown value in identifying acute PE patients at increased mortality risk. Among the clinical risk models, the Pulmonary Embolism Severity Index (PESI) is the most widely validated, demonstrating a high negative predictive value (NPV), thus accurately identifying patients at low risk for short-term mortality. ...
... 7 In addition, an elevated cardiac troponin level, being a marker of RV injury and dysfunction, has been shown to serve as an independent prognostic marker with a high NPV for in-hospital adverse events and mortality. 5,9,11,18,19 Therefore, cardiac troponin can aid in identifying low-risk patients who may be suitable for outpatient treatment. 11,20 Furthermore, 2 studies have demonstrated the prognostic utility of cardiac troponin T (cTnT) for long-term mortality after hospital discharge; however, they proposed disparate cTnT thresholds for predicting risk, which limits their clinical applicability. ...
Background:
In patients with acute pulmonary embolism (PE), detectable levels of cardiac troponin I (cTnI) using a highly sensitive assay have been associated with increased in-hospital mortality. We sought to investigate the impact of detectable cTnI on long-term survival following acute PE.
Hypothesis:
Detectable cTnI levels in patients presenting with acute PE predict increased long-term mortality following hospital discharge.
Methods:
In a retrospective cohort study, we analyzed consecutive patients with confirmed acute PE and cTnI assay available from the index hospitalization. The detectable cTnI level was ≥0.012 ng/mL. Patients were classified into low and high clinical risk groups according to the Pulmonary Embolism Severity Index (PESI) at presentation. Subjects were followed for all-cause mortality subsequent to hospital discharge using chart review and Social Security Death Index.
Results:
A cohort of 289 acute PE patients (mean age 56 years, 51% men), of whom 152 (53%) had a detectable cTnI, was followed for a mean of 3.1 ± 1.8 years after hospital discharge. A total of 71 deaths were observed; 44 (29%) and 27 (20%) in the detectable and undetectable cTnI groups, respectively (P = 0.05). Detectable cTnI was predictive of long-term survival among low-risk (P = 0.009) but not high-risk patients (P = 0.78) who had high mortality rates irrespective of cTnI status.
Conclusions:
In patients with acute PE, detectable cTnI is predictive of long-term mortality, particularly among patients who were identified as low risk according to PESI score.
... Two studies evaluated the role of troponin T in predicting the long-term mortality rate after an episode of acute PE. 45,46 In the first study, troponin T was determined in 563 patients with objectively diagnosed PE presenting at the emergency department of a tertiary care center. 45 Troponin T was positive in 27% of this population. ...
... Two studies evaluated the role of troponin T in predicting the long-term mortality rate after an episode of acute PE. 45,46 In the first study, troponin T was determined in 563 patients with objectively diagnosed PE presenting at the emergency department of a tertiary care center. 45 Troponin T was positive in 27% of this population. One-year survival was significantly lower in patients with positive troponin T (71% vs 90%; P months (AUROC, 0.77; 95% CI, 0.73-0.81 ...
Pulmonary embolism (PE) is a common disease with a considerable short- and long-term risk of death. An adequate evaluation of the prognosis in patients with PE may guide decision making in terms of the intensity of the initial treatment during the acute phase, duration of treatment, and intensity of follow-up control visits in the long term. Patients with shock or persistent hypotension are at high risk of early mortality and may benefit from immediate reperfusion. Several tools are available to define the short-term prognosis of hemodynamically stable patients. The Pulmonary Embolism Severity Index (PESI) score, simplified PESI score, and N-terminal pro-B-type natriuretic peptide levels are particularly useful for identifying patients at low risk of early complications who might be safely treated at home. However, the identification of patients who are hemodynamically stable at diagnosis but are at a high risk of early complications is more challenging. The current guidelines recommended a multiparametric prognostic algorithm based on the clinical status and comorbidities. Unfortunately, only a few studies have evaluated the role of risk factors potentially affecting the long-term prognosis of these patients. The available studies suggest a potential role of the PESI score and troponin levels evaluated at the time of an index event. However, further studies are warranted to confirm these preliminary findings and to identify other long-term prognostic factors in this setting.
... 7 Deep vein thrombosis, elevated serum troponin, and RV thrombosis are related to increasing mortality. 8,9 elevated serum lactase dehydrogenase or aspartate aminotransferase serum glutamic oxalocetic transaminase with a normal serum bilirubin. ...
Pulmonary thrombus emboli (PTE) have a wide clinical spectrum, from asymptomatic small PTE to life-threatening one, which may cause cardiogenic shock. It is classified as acute/chronic and massive/sub massive. PTE risk factors and relative causes to elevate its mortality are present in this review article. At last, we have a brief recommendation for treatment. There are several diagnosing test such as D-dimer, echocardiography, electrocardiography, brain natriuretic peptide, laboratory tests, chest X-ray, ultrasound, and pulmonary angiography which are different in specificity and sensitivity. Finally, in the diagnostic approach, we explain relative studies to Wells rule, Geneva rule, pulmonary embolism (PE) severity index, and PE rule out criteria.
... Recently, new generations of high-sensitivity troponin assays have been developed for measuring troponin levels that would register as 'zero' or considered to be in the 'normal' range with conventional assays (3,4). Numerous studies have demonstrated that elevated cardiac troponin levels are associated with a high risk of short-term adverse outcome in patients presenting with acute PE (5)(6)(7). It has been shown that a high-sensitivity troponin (hs-cTn) T assay cannot be used alone to diagnose PE (3). ...
... The reason for the release of troponins in a subset of patients with acute PE remains unclear (7). However, explanations include hypoxemia due to perfusion-ventilation mismatch, hypoperfusion as a consequence of low output and reduced coronary blood flow, as well as cell injury caused by acute dilation of the right ventricle, or a combination of these factors (7,23). ...
... The reason for the release of troponins in a subset of patients with acute PE remains unclear (7). However, explanations include hypoxemia due to perfusion-ventilation mismatch, hypoperfusion as a consequence of low output and reduced coronary blood flow, as well as cell injury caused by acute dilation of the right ventricle, or a combination of these factors (7,23). To date, it is still unclear if positive troponin values in hemodynamically stable patients identify those who would benefit from thrombolysis (7,23). ...
High-sensitivity troponin (hs-cTn) assays enable the troponin cutoff value to be lowered, resulting in an increase of sensitivity at the cost of specificity. In the present study, the risk of a short-term adverse outcome was assessed in patients with acute pulmonary embolism (PE) using high-sensitivity troponin I (hs-cTnI). We used a cutoff value of 0.1 ng/ml in accordance with current guidelines for unstable angina (UA)/non-ST-segment elevation myocardial infarction (NSTEMI), although the detection limit of the troponin assay is lower. In addition, the risk of an adverse outcome in patients with acute PE was investigated with respect to initial D-dimer serum concentrations. In 65 patients with confirmed acute PE, hs-cTnI and D-dimer values were measured. Adverse clinical outcome was defined as cardiogenic shock, cardiopulmonary resuscitation, mechanical ventilation, vasopressor therapy, thrombolysis, catheter intervention or mortality within 60 days of PE. Patients with acute PE and serum hs-cTnI values >0.1 ng/ml showed significantly higher D-dimer concentrations (P= 0.0467) and a 5-fold increased risk of an adverse clinical outcome [odds ratio (OR), 4.9; 95% confidence interval (CI), 1.28-18.66; P=0.0235] compared with patients with acute PE and hs-cTnI values <0.1 ng/ml. In patients with acute PE suffering from adverse clinical outcome, D-dimer concentrations were significantly elevated compared with those in patients with acute PE without adverse clinical outcome (P=0.02). In patients with acute PE, a hs-cTnI cutoff value of 0.1 ng/ml, which is identical to the recommended cutoff value of NSTEMI, may identify patients with a 5-fold increased risk of a short-term adverse outcome. D-dimer values are significantly higher in PE patients with elevated hs-cTnI values as well as in patients with an adverse outcome.
... In recent years, it has been recognised that elevated cardiac troponins may be detected in other conditions, including stable coronary artery disease [6], left ventricular failure [7], chronic kidney disease [8], sepsis [9] and mixed critical care populations [10]. Elevated cardiac troponins have also been noted in situations of right ventricular overload, both acute, as in acute pulmonary embolism [11], and chronic, as in pulmonary hypertension [12,13]. Mechanisms other that myocardial necrosis may be responsible for this ''troponin leak'' in these clinical scenarios, even though detectable cardiac troponin is specific for ongoing myocardial damage and generally associated with worse prognosis. ...
Circulating cardiac troponins are markers of myocardial injury. We sought to determine whether cardiac troponin I (cTnI), measured by a sensitive assay, is associated with disease severity and prognosis in pulmonary arterial hypertension (PAH). cTnI was measured in 68 patients with PAH diagnostic category 1 in a research-based sensitive immunoanalyser with a lower limit of detection of 0.008 ng · mL(-1). The associations between cTnI and PAH severity and clinical outcomes were assessed using Chi-squared and Wilcoxon rank sum tests, Kaplan-Meier analysis and Cox regression models. cTnI was detected in 25% of patients. Patients with detectable cTnI had more advanced functional class symptoms, a shorter 6-min walk distance, more pericardial effusions, larger right atrial area, and higher B-type natriuretic peptide and C-reactive protein levels. 36-month transplant-free survival was 44% in patients with detectable cTnI versus 85% in those with undetectable cTnI. cTnI was associated with a 4.7-fold increased risk of death related to right ventricular failure or transplant (hazard ratio 4.74, 95% CI 1.89-11.89; p<0.001), even when adjusted individually for known parameters of PAH severity. Elevated plasma cTnI, even at subclinically detectable levels, is associated with more severe disease and worse outcomes in patients with PAH.
... The association between elevations in TNI, a reduced LVEF, and clinical outcomes has been well documented in many settings; both cardiac diseases and noncardiac causes of TNI elevation have been studied, many of which are common in patients with cancer, such as respiratory disease, pulmonary embolism, sepsis, renal impairment, and critical illness. [3][4][5][6][7] Half of the patients who were enrolled onto the study had metastatic breast cancer, and 62 patients died during the study. The authors do not report whether other causes for a raised TNI were sought or accounted for in such patients. ...
... In massive pulmonary embolism, anatomical obstruction is the most important cause of compromised physiology [1]. As right ventricular afterload increases, tension in the right ventricular wall rises and may lead to dilatation, dysfunction and ischemia of the right ventricle with release of cardiac troponins [2]. Death often results from right ventricular failure [1]. ...
A consumptive coagulopathy resembling disseminated intravascular coagulation (DIC) has been seen in patients with massive pulmonary embolism (PE). We hypothesized that a DIC-like condition is relevant in patients whose pulmonary embolism leads to cardiopulmonary arrest and cardiopulmonary resuscitation (CPR).
This hypothesis was tested by the use of a database consisting of all cases of PE diagnosed at the Department of Emergency Medicine from June 1993 to October 2007. Out of 1018 cases with PE, 113 patients underwent CPR. In this cohort study, the resuscitated patients were compared with those with PE but without CPR.
Patients with PE and CPR had 3-fold higher D-dimer, prolonged prothrombin time (PT), reduced platelet counts and lower fibrinogen and antithrombin (AT) levels compared with PE patients without cardiac arrest (P < 0.001 for all). Among patients with PE and CPR, D-dimer was abnormal in 100%, PT in 44%, AT in 53%, fibrinogen in 19% and platelets in 25%. In comparison, PE without CPR was associated with abnormal D-dimer in 99%, abnormal PT in 15%, low AT in 6%, low fibrinogen in 1% and low platelets in 2%. Nine per cent of the resuscitated patients had a DIC score >or= 5, indicating overt DIC. The DIC score highly correlated with 1-year and in-hospital mortality.
Massive PE leading to CPR is associated with consumptive coagulopathy and overt DIC. In resuscitated patients, DIC markers may indicate pulmonary embolism as the underlying cause of arrest.
