AJCC
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

American Journal of Critical Care. 2006;15: 280-288
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Respond to This Article
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Right arrow Take the CE Test
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lim, W.
Right arrow Articles by Devereaux, P. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lim, W.
Right arrow Articles by Devereaux, P. J.

CE Article

Elevated Cardiac Troponin Levels in Critically Ill Patients: Prevalence, Incidence, and Outcomes

By Wendy Lim, MD, Deborah J. Cook, MSc(Epid), MD, Lauren E. Griffith, MSc(Math), Mark A. Crowther, MSc, MD and P. J. Devereaux, MSc, MD. From the Departments of Medicine (WL, DJC, MAC, PJD), Clinical Epidemiology and Biostatistics (DJC, PJD), and Occupational Health and Environmental Medicine (LEG), McMaster University, Hamilton, Ontario.


   Abstract
Top
 Abstract
Methods
 Results
 Discussion
 References
 
• Background Levels of cardiac troponin, a sensitive and specific marker of myocardial injury, are often elevated in critically ill patients.

• Objectives To document elevated levels of cardiac troponin I in patients in a medical-surgical intensive care unit and the relationship between elevated levels and electrocardiographic findings and mortality.

• Methods A total of 198 patients expected to remain in the intensive care unit for at least 72 hours were classified as having myocardial infarction (cardiac troponin I level ≥1.2 µg/L and ischemic electrocardiographic changes), elevated troponin level only (≥1.2 µg/L and no ischemic electrocardiographic changes), or normal troponin levels. Events were classified as prevalent if they occurred within 48 hours after admission and as incident if they occurred 48 hours or later after admission. Factors associated with mortality were examined by using regression analysis.

• Results A total of 171 patients had at least one troponin level measured in the first 48 hours. The prevalence of elevated troponin level was 42.1% (72 patients); 38 patients (22.2%) had myocardial infarction, and 34 (19.9%) had elevated troponin level only. After the first 48 hours, 136 patients had at least 1 troponin measurement. The incidence of elevated troponin level was 11.8% (16 patients); 7 patients (5.1%) met criteria for myocardial infarction, and 2 (1.5%) had elevated troponin level only. Elevated levels of troponin I at any time during admission were associated with mortality in the univariate but not the multivariate analysis.

• Conclusions Elevated levels of cardiac troponin I in critically ill patients do not always indicate myocardial infarction or an adverse prognosis.

Notice to CE enrollees:
A closed-book, multiple-choice examination following this article tests your understanding of the following objectives:
  1. Recognize the prevalence and incidence of elevated troponin levels in critically ill patients.
  2. Describe the population of patients used in this study.
  3. Identify relationships found in this study between elevated troponin levels, myocardial infarction, and mortality.

The introduction of assays for cardiac troponins I and T, which are highly sensitive and specific biomarkers for myocardial cell damage, has resulted in increasing detection and diagnosis of acute coronary syndromes. Elevated serum levels of cardiac troponin indicate myocardial damage but not the underlying mechanism, suggesting that clinical evidence of coronary thrombosis is needed to establish a diagnosis of myocardial infarction.1


Elevated cardiac troponin levels indicate myocardial damage, but not the exact mechanism (eg, thrombosis).

 

Elevated levels of cardiac troponin not due to acute coronary syndromes have been reported in various populations of patients in the intensive care unit (ICU): heterogeneous medical and surgical patients and critically ill patients with systemic hypotension and with conditions such as trauma, sepsis, pulmonary embolism, stroke, renal failure, and chronic obstructive pulmonary disease.2–9 The prevalence of increased levels ranges from 15% to 70%10–12 in the general ICU population, and estimates for the prevalence in critically ill patients with sepsis or septic shock are 31% to 80%.2–5,10,13 Abnormal serum levels of cardiac troponin have been detected in critically ill patients with non-cardiac diagnoses14,15; in the study by Ammann et al,14 more than 70% of ICU patients with elevated cardiac troponin levels did not have flow-limiting coronary artery disease as indicated by stress echocardiography or by findings at autopsy.


As many as 70% of ICU patients with elevated cardiac troponin levels do not have flow-limiting coronary artery disease.

 

Elevated troponin levels are clinically important because they may act as an adverse prognostic marker.16 The prognostic value of elevated serum levels of cardiac troponin is well recognized outside the ICU setting.17,18 However, in critically ill patients, the prognostic value and the relationship between elevated cardiac troponin levels and a diagnosis of myocardial infarction remain uncertain. In the consensus document1 of the Joint European Society of Cardiology/American College of Cardiology (ESC/ACC) Committee, myocardial infarction is defined on the basis of pathological findings or on the basis of a typical rise and fall in biochemical markers of myocardial necrosis and the presence of at least one of the following: ischemic signs and symptoms, electrocardiographic (ECG) signs of ischemia or necrosis, or a coronary artery intervention.1 In the ICU, endotracheal intubation, coma due to underlying illness, and use of sedatives and narcotics all limit the ability of patients to report symptoms associated with ischemia. Therefore, in practice, a combination of elevated levels of cardiac troponin and ECG changes indicating ischemia are frequently used to establish a diagnosis of myocardial infarction in the ICU. Use of coronary angiography, routine echocardiography, and continuous ECG recordings is either not feasible on a routine basis or has not been well studied in critically ill patients. Nevertheless, recognition of myocardial infarction in critically ill patients most likely is important because the development of myocardial infarction may contribute to increased morbidity and mortality.19

Outside the ICU setting, patients with a diagnosis of myocardial infarction benefit from thrombolytic therapy, coronary revascularization, and use of anticoagulants, antiplatelet agents, ß-blockers, statins, and angiotensin-converting enzyme inhibitors. However, myocardial infarction due to nonthrombotic mechanisms may not respond favorably to antithrombotic agents, and the impact of these therapies on outcomes in ICU patients with myocardial infarction is unknown. Furthermore, the risk-benefit ratio of these agents in the ICU may differ considerably from when they are used in patients with myocardial infarction outside the ICU. A fundamental understanding of the prognostic significance of elevated levels of cardiac troponin and their relationship to myocardial infarction in critically ill patients is therefore an important first step toward devising and testing appropriate management strategies.

We designed this study to document the prevalence and incidence of elevated serum levels of cardiac troponin I and myocardial infarction among critically ill patients; compare the morbidity and mortality of patients with myocardial infarction, patients with elevated levels of cardiac troponin I alone, and patients with normal cardiac troponin I levels; and assess whether elevated levels of cardiac troponin I are a predictor of ICU and hospital length of stay and mortality. We did not systematically screen patients by measuring levels of cardiac troponin and obtaining ECGs. Rather, we documented all the available results of tests ordered by the ICU team; hence, we determined the clinically recognized incidence and prevalence rates of elevated levels of cardiac troponin I and myocardial infarction.


   Methods
Top
 Abstract
 Methods
Results
 Discussion
 References
 
Sample
All critically ill adults admitted to the 15-bed medical-surgical ICU at St Joseph’s Hospital, Hamilton, Ontario, between November 17, 2000, and January 17, 2002, who were expected to remain in the ICU for at least 72 hours were included in the study. Exclusion criteria included trauma, neurosurgery and cardiac surgery (due to regionalization in critical care), recent orthopedic surgery, pregnancy, and palliative care.

Data Collection
Patients in this study had been enrolled in a prospective cohort study to evaluate the incidence and prevalence of deep vein thrombosis. Prospectively, we collected demographic data, including patients’ age, sex, admitting diagnosis, and Acute Physiology and Chronic Health Evaluation II score.20 Daily, we collected the multiple organ dysfunction score21 and the need for advanced life support (mechanical ventilation, use of inotropic agents or vasopressors, and dialysis). We recorded duration of mechanical ventilation, length of ICU and hospital stays, and death. Retrospectively, we collected data on risk factors for cardiac disease, results of all assays of cardiac troponin I and ECGs performed during the ICU stay, and use of antithrombotic and cardiac medications. Although the medical center has a cardiac care unit, patients requiring mechanical ventilation are admitted to the ICU. The ICU team dictated the frequency and timing of assays of cardiac troponin I and ECGs, which were ordered as clinically indicated.

Analysis of Cardiac Troponin I Levels
Elevation of cardiac troponin I level was defined as a serum level greater than or equal to 1.2 µg/L. Troponin I was measured by using the Abbott AxSYM system (Abbott Laboratories, Mississauga, Ontario). The measurements have a coefficient of variation of 10%.22 The lower detection limit for the assay is 0.3 µg/L.

ECG Interpretation
12-Lead ECGs were recorded by using Pagewriter ECG machines (Hewlett-Packard, Palo Alto, Calif), which provide a computerized ECG interpretation at the top of each ECG. The ICU team dictated the frequency and timing of ECGs. All ECGs were reviewed by a cardiologist within 24 hours of recording, and modifications to the computerized interpretation were made. These reviewed ECGs with the cardiologists’ interpretations were used to classify the ECG findings into 3 categories: ischemic ECG abnormalities, nonischemic ECG abnormalities, and no ECG changes. New ECG findings indicative of ischemic changes were defined according to the joint ESC/ACC committee ECG criteria and included 1 or more of the following: ST-segment elevation 0.1 mV or greater in 2 or more contiguous leads, ST-segment depression, T-wave abnormality, and development of pathological Q waves. Occurrence of new left bundle branch block was also included in the ischemic ECG criteria, because its presence can obscure ST-segment elevation.1 Nonischemic ECG changes were any ECG abnormalities that did not meet ESC/ACC criteria.

Outcome Definitions
Patients were classified into the following groups on the basis of cardiac troponin I levels and ECG classifications: myocardial infarction, defined as 1 or more assays indicating an elevation in cardiac troponin I and ischemic ECG changes; elevated cardiac troponin I only, defined as 1 or more assays indicating an elevation in cardiac troponin I and nonischemic ECG changes (including patients with no ECG changes); and normal levels of cardiac troponin I. Myocardial infarction was defined according to the ESC/ACC guidelines,1 although symptoms of ischemia were not included in our definition because ICU patients are rarely able to report these symptoms. Patients with myocardial infarction were further classified into those with and without ST-segment elevation. All patients were classified in the category of their highest illness severity. Prevalent events were defined as those that occurred less than 48 hours after ICU admission; incident events, as those that occurred 48 hours or later after ICU admission.

Statistical Analysis
Continuous data were reported by using mean and SDs or by using median and interquartile ranges when data were skewed. Binary data were reported by using proportions and 95% CIs. Univariate and multivariate analyses were used to determine the association between ICU mortality and the following independent variables: Acute Physiology and Chronic Health Evaluation II score, use of mechanical ventilation, use of inotropic agents or vasopressors, dependence on acute or chronic dialysis, and elevated serum level of cardiac troponin I (maximum value). Variables associated with ICU mortality in the univariate analysis (P < .10) were retained in the multivariate analysis. A second logistic regression was completed to determine factors associated with hospital mortality. Regression results were expressed by using odds ratios and 95% CIs. The relationship between the degree of elevation of cardiac troponin I and these outcomes was assessed by using the following categories: less than 0.5 µg/L, 0.5 to 2.0 µg/L, 2.1 to 10.0 µg/L and greater than 10.0 µg/L.23 Statistical analyses were performed by using SAS, version 9.1, software (SAS Institute Inc, Cary, NC).


   Results
Top
 Abstract
 Methods
 Results
Discussion
 References
 
Characteristics of the Sample
In the 14-month study period, 817 patients were admitted to the ICU; of these, 285 (34.9%) were 18 years or older and were expected to be in ICU for 72 hours or more. Of these 285, 22 (7.8%) were excluded for the following reasons: second admission to ICU (16), trauma (1), and withdrawal of life support (5). Of 263 eligible patients, 1 patient had no next of kin, and 1 patient’s family declined to consent to the study. A total of 261 patients were enrolled in the prospective study, and 198 (75.9%) had charts available for review. Among the 261 patients, 10 (5.1%) were in the cardiac care unit immediately before admission to the ICU; data on these patients were included in the primary analysis but were also analyzed separately as a sensitivity analysis. Characteristics of the patients enrolled in the study are listed in Table 1Go.


View this table:
[in this window]
[in a new window]
  		Table 1 Baseline characteristics of the sample (n = 198)

 
Prevalence and Incidence of Elevated Cardiac Troponin I Levels
The classification of patients by outcome is shown in the FigureGo. Table 2Go gives the prevalence (<48 hours of ICU admission) and incidence (developing during ICU stay; ≥48 hours) of myocardial infarction and elevated level of cardiac troponin I only. Overall, 185 (93.4%) of the 198 eligible patients had at least 1 measurement of cardiac troponin I completed either at the time of admission or during their ICU stay. A total of 171 (86.4%) patients had cardiac troponin I measured within 48 hours of ICU admission, and the number of patients in this subset was used as the denominator in the prevalence analysis. A total of 136 (68.7%) patients had cardiac troponin I measured after 48 hours of ICU admission; the number of patients in this subset was used as the denominator in the incidence analysis.


Figure 1
View larger version (18K):
[in this window]
[in a new window]
  		Classification of patients in the sample.

 

View this table:
[in this window]
[in a new window]
  		Table 2 Prevalence and incidence of myocardial infarction and elevated troponin level only

 
The prevalence of elevated cardiac troponin I level at the time of admission to the ICU was 42.1% (72 patients; 95% CI 34.6%–49.9%). Criteria for myocardial infarction were met by 38 of these patients (prevalence 22.2%, 95% CI 16.2%–29.2%); 5 had ST-segment elevation and 33 did not. A total of 34 patients (prevalence 19.9%, 95% CI 14.2%–26.7%) had elevated levels of cardiac troponin I only.


Troponin I levels were elevated at ICU admission in 42% of subjects, but only 53% of these met the criteria for myocardial infarction.

 

The incidence of elevated cardiac troponin I level during the ICU admission was 11.8% (16 patients: 95% CI 6.8%–18.4%). Criteria for myocardial infarction were met by 12 patients (incidence 8.8%, 95% CI 4.6%–14.9%), although 5 of these patients met the criteria for myocardial infarction at the time of ICU admission (indicating that their incident myocardial infarction was a recurrent myocardial infarction); hence 7 patients had new myocardial infarction (incidence 5.1%, 95% CI 2.1%–10.3%), which were all of the non–ST-elevation type. A total of 4 patients had elevated cardiac troponin I only during their ICU stay (incidence 2.9%, 95% CI 0.8%–7.4%); elevations were present in 2 patients at admission and developed in 2 patients during the ICU stay (incidence 1.5%, 95% CI 0.2%–5.2%).


During the ICU stay, 11.8% of subjects had elevated troponin I levels, and 75% of these met the myocardial infarction criteria.

 

Association Between Patients’ Characteristics and Outcomes
The baseline characteristics and associated morbidity and mortality outcomes are shown in Table 3Go, divided as patients with myocardial infarction (n = 45), patients with elevated cardiac troponin level only (n = 36), and patients with normal cardiac troponin levels (n = 104). Patients with myocardial infarction more often were older, were admitted with cardiovascular-related diagnoses, had underlying hypercholesterolemia and previous myocardial infarction, and required inotropic agents at some point during their ICU stay. The mean of the maximum cardiac troponin I level was higher in patients with myocardial infarction than in patients with elevated cardiac troponin I level only. The proportion of patients requiring hemodialysis did not differ significantly among the 3 groups. In addition, length of ICU or hospital stay and ICU or hospital mortality did not differ significantly among the 3 groups.


View this table:
[in this window]
[in a new window]
  		Table 3 Characteristics and outcomes of patients by categories

 
Among patients classified as having myocardial infarction, those who received specific anti-ischemic and antithrombotic treatments (including heparin, ß-blockers, angiotensin-converting enzyme inhibitors, and nitrates) and those who did not had similar ICU and hospital stays and ICU and hospital mortality (data not shown). These outcomes were also similar whether patients did or did not have ST-segment elevation.

Factors Associated With Mortality
The predictors of ICU and hospital mortality are shown in Table 4Go. In the univariate analysis, the presence of an elevated level of cardiac troponin I, the score on the Acute Physiology and Chronic Health Evaluation II, the need for inotropic agents or vasopressors, and the need for acute dialysis were all significantly associated with ICU mortality; the score on the Acute Physiology and Chronic Health Evaluation II, use of inotropic agents or vasopressors, mechanical ventilation, and acute dialysis were associated with hospital mortality. In the multivariate analysis, the need for inotropic agents or vasopressors was the only independent predictor of both ICU and hospital mortality. When levels of cardiac troponin I were divided into categories (<0.5 µg/L, 0.5–2.0 µg/L, 2.1–10.0 µg/L, and >10.0 µg/L), the odds ratios for ICU and hospital mortality increased with increasing levels of cardiac troponin I.


View this table:
[in this window]
[in a new window]
  		Table 4 Predictors of intensive care unit and hospital mortality

 
Proportion of Patients With Myocardial Infarction Receiving Antithrombotic and Cardiac Medications
Table 5Go shows treatments administered for patients with myocardial infarction, divided into patients with and without ST-segment elevation. A total of 82.2% of patients received aspirin, and 48.9% received therapeutic doses of heparin. Unfractionated heparin was used in 73%, and low-molecular-weight heparin in 23%. Aspirin and therapeutic heparin were administered to all 5 patients with ST-segment elevation. Other recommended therapies in patients with coronary disease, including angiotensin-converting enzyme inhibitors, ß-blockers, and statins, were used in 80% or less of the eligible patients with ST-segment elevation, and in 63% or less of the patients without ST-segment elevation.


View this table:
[in this window]
[in a new window]
  		Table 5 Proportion of patients receiving antithrombotic and cardiac medications

 

   Discussion
Top
 Abstract
 Methods
 Results
 Discussion
References
 
In this study of patients admitted to a medical-surgical ICU with an expected length of stay of at least 72 hours, the prevalence of an elevated level of cardiac troponin I was 42.1%. According to the definition of myocardial infarction in the consensus document by the joint ESC/ACC committee,1 22.1% of these patients had myocardial infarction within 48 hours of ICU admission. Patients with myocardial infarction were more often admitted with cardiovascular diagnoses and had higher levels of cardiac troponin I and more cardiac risk factors than did patients without elevated levels of troponin I. However, inferences about comparisons of patients’ characteristics are limited. Patients who are known to have coronary artery disease, or who are admitted with cardiovascular diagnoses, may be more likely to have their cardiac risk factors documented in their medical records. Similarly, these patients may have more frequent measurements of cardiac troponin I, thus increasing the likelihood that an elevated level will be detected.


Elevated cardiac troponin levels are common among the critically ill, and the prevalence of myocardial infarction may be higher than expected.

 

Hospital and ICU lengths of stay did not differ significantly between patients with myocardial infarction, patients with elevated cardiac troponin I levels, and patients with normal cardiac troponin I levels. However, our study did not have sufficient power to detect such differences. According to univariate analysis, an elevated cardiac troponin I level was significantly associated with ICU, but not hospital, mortality. According to multivariate analysis, the need for inotropic agents or vasopressors was the only predictor of overall mortality.

In other prospective studies,10–12 15% to 70% of patients in a general ICU had at least a single measurement indicating an elevation in the serum level of cardiac troponin. The prevalence of elevation in cardiac troponin in specific ICU populations has been studied in patients who had sepsis,2–5,10,13 cardiac surgery,24,25 or noncardiac diagnoses. Prevalence estimates for patients with noncardiac diagnoses ranged from 16% to 55%.14,15 In a study of 34 consecutive patients who were treated with mechanical ventilation or who underwent thoracic or vascular surgery, 11 (32%) had elevated levels of cardiac troponin T, and 4 (36%) of the 11 had ECG changes compatible with myocardial infarction.26 These findings suggest that elevated levels of cardiac troponin are common among critically ill patients and that the prevalence of myocardial infarction among critically ill patients may be higher than is generally appreciated. However, the relevance of increased levels of cardiac troponin in relation to coronary ischemia and ECG changes still remains uncertain among ICU patients. The available studies suggest that cardiac troponin may be an adverse prognostic marker in the ICU; elevations in cardiac troponin I levels are associated with increased mortality in medical-surgical ICU patients,10–12 including patients admitted for reasons other than acute coronary syndromes14,27 and patients admitted with acute exacerbations of chronic obstructive pulmonary disease.28 Elevations in cardiac troponin I levels have also been associated with increased ICU and hospital stays in surgical ICU patients.19 Although supported by fewer studies, elevated levels of cardiac troponin T are similarly a predictor of mortality in ICU patients with early sepsis2 and after cardiac surgery24,25,29 and are associated with prolonged ICU stay after cardiac surgery.25

Our results and the results of these other studies may differ for several possible reasons. First, differences among ICUs, including the case mix of critically ill patients with respect to cardiac risk factors and whether or not patients were systematically screened or had cardiac troponin levels measured as clinically indicated, would lead to different incidence and prevalence rates. Second, the type of assay used to measure cardiac troponin and the different thresholds used to classify levels of cardiac troponin as elevated would also influence the observed rates. Finally, and perhaps most important, the use of univariate analysis (which tends to suggest associations between cardiac troponin I levels and adverse outcomes that are unadjusted for other important covariates) in many studies could also account for the observed differences in results.


Although the relevance of increased cardiac troponin values in relation to coronary ischemia and ECG changes remains uncertain among ICU patients, such increased values may be a marker for adverse events in this setting.

 

Results of randomized trials indicate that antithrombotic therapy improves outcomes in patients with myocardial infarction.30 However, it is unclear if similar treatment of critically ill patients with elevated levels of cardiac troponin (which may be related to nonthrombotic causes) will similarly improve outcomes. Few of the patients with myocardial infarction in our study received all of the recommended antithrombotic and anti-ischemic therapies. Although use of aspirin and heparin was common in patients with myocardial infarction who had ST-segment elevation, cardiac medications were used in 80% or fewer of eligible patients with ST-segment elevation and in less than 63% of patients who met criteria for non–ST-segment elevation myocardial infarction. Inferences about use of medications in the group with ST-segment elevation are limited because of the small number of patients.

Our study has several limitations. First, although many of our data were prospectively collected for the original study,31 we collected data specific to myocardial infarction retrospectively. Because we did not screen all patients by obtaining daily measurements of cardiac troponin level and daily ECGs but recorded all available results of tests ordered by the ICU team, we determined the clinically recognized incidence and prevalence rates of elevated levels of cardiac troponin and myocardial infarction. Systematic screening with measurements of cardiac troponin levels and ECGs might lead to higher prevalence and incidence rates; however, this type of systematic screening is not routinely done in clinical critical care practice. Nonetheless, 86% of the patients had at least a single measurement of cardiac troponin I at the time of admission to the ICU, reflecting local practice patterns that may exist in other ICUs.

Second, the estimate of incidence was based on data for only 136 patients who had cardiac troponin I measured 48 hours or later after ICU admission, which resulted in a less precise estimate than estimates based on data for a larger number of patients would have been. Third, although our study included 198 patients, the number of patients in each group limited the power of our between-group comparisons to detect small differences. Fourth, only 1 reviewer abstracted data, a situation that may have resulted in abstraction errors; however, we minimized this risk by using pretested standardized data abstraction forms and classifying ECG changes according to the interpretation by cardiologists who were blinded to our study objectives. Last, we did not include all consecutive patients admitted to the ICU because our focus was not on patients admitted for overnight mechanical ventilation or postoperative monitoring; inclusion of these patients might have resulted in lower incidence and prevalence rates.

Strengths of our study include enrollment of patients during a period of more than 1 year and complete follow-up on all patients. We identified ECG changes indicative of ischemia by using the ECG criteria of the joint ESC/ACC committee,1 and we classified patients into categories reflecting myocardial ischemia as used in clinical practice, a method that indicated a high degree of illness in this cohort of critically ill patients. We used regression analysis to examine the independent contribution of elevated levels of cardiac troponin to mortality. In terms of generalizability, our ICU admits patients with cardiac conditions who need mechanical ventilation; in some centers, such patients may receive care in the cardiac care unit. Of the 10 patients transferred from the cardiac care unit, 4 met criteria for myocardial infarction (3 admitted with cardiac arrest, 1 with heart failure), 2 had elevated levels of cardiac troponin I only, and 4 had normal levels of cardiac troponin I. However, the overall prevalence of elevated levels of cardiac troponin I in our study cohort was still considerable (38.6%, n = 66) when data on patients transferred from the cardiac care unit (n = 10, of whom 4 had myocardial infarction) and on patients admitted with myocardial infarction with ST-segment elevation (n = 5) were not included in the analysis.

In summary, elevated levels of cardiac troponin reflecting myocardial infarction are common in critically ill medical-surgical patients. The role of elevations in cardiac troponin I as a prognostic marker in the ICU is still uncertain. Establishing the diagnosis of myocardial infarction in critically ill patients is challenging because of limitations in determining whether the patients have typical symptoms of ischemia and because of uncertainty about the interpretation of abnormal levels of cardiac troponin. Additional research is urgently needed on the appropriate diagnostic criteria for myocardial infarction in the ICU setting and the optimal management of critically ill patients who have elevated levels of cardiac troponin.


   ACKNOWLEDGMENTS
 
This study was funded by the Canadian Institutes for Health Research and an unrestricted educational grant from Aventis Pharmaceuticals, Montreal, Canada, which played no role in the design, data collection, analysis, or interpretation of results. Dr. Lim is a clinical scholar with a graduate scholarship from the Canadian Institutes of Health Research, Dr. Cook is a Canada Research Chair, Dr. Crowther holds a Career Investigator Award from the Heart and Stroke Foundation of Canada, and Dr. Devereaux holds a Senior Research Fellowship Award of the Canadian Institutes of Health Research.

We appreciate the assistance of Ellen McDonald, France Clarke, and Neala Hoad in conducting this study.

To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 809-2273 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints{at}aacn.org.


   REFERENCES
Top
 Abstract
 Methods
 Results
 Discussion
 References
 

  1. Alpert JS, Thygesen K, Antman E, Bassand JP. Myocardial infarction redefined: a consensus document of the Joint European Society of Cardiology/American College of Cardiology committee for the redefinition of myocardial infarction [published correction appears in J Am Coll Cardiol. 2001;37:973]. J Am Coll Cardiol. 2000;36:959–969.[Free Full Text]
  2. Spies C, Haude V, Fitzner R, et al. Serum cardiac troponin T as a prognostic marker in early sepsis. Chest. 1998;113:1055–1063.[Abstract/Free Full Text]
  3. Fernandes CJ, Akamine N, Knobel E. Cardiac troponin: a new serum marker of myocardial injury in sepsis. Intensive Care Med. 1999;25:1165–1168.[Medline]
  4. Turner A, Tsamitros M, Bellomo R. Myocardial cell injury in septic shock. Crit Care Med. 1999;27:1775–1780.[Medline]
  5. Arlati S, Brenna S, Prencipe L, et al. Myocardial necrosis in ICU patients with acute non-cardiac disease: a prospective study. Intensive Care Med. 2000;26:31–37.[Medline]
  6. La Vecchia L, Ottani F, Favero L, et al. Increased cardiac troponin I on admission predicts in-hospital mortality in acute pulmonary embolism. Heart. 2004;90:633–637.[Abstract/Free Full Text]
  7. James P, Ellis CJ, Whitlock RM, McNeil AR, Henley J, Anderson N. Relation between troponin T concentration and mortality in patients presenting with acute stroke: observational study. BMJ. 2000;320:1502–1504.[Abstract/Free Full Text]
  8. Diris JH, Hackeng CM, Kooman JP, Pinto YM, Hermens WT, van Dieijen-Visser MP. Impaired renal clearance explains elevated troponin T fragments in hemodialysis patients. Circulation. 2004;109:23–25.[Abstract/Free Full Text]
  9. Edouard AR, Benoist JF, Cosson C, Mimoz O, Legrand A, Samii K. Circulating cardiac troponin I in trauma patients without cardiac contusion. Intensive Care Med. 1998;24:569–573.[Medline]
  10. Guest TM, Ramanathan AV, Tuteur PG, Schechtman KB, Ladenson JH, Jaffe AS. Myocardial injury in critically ill patients: a frequently unrecognized complication. JAMA. 1995;273:1945–1949.[Abstract]
  11. Noble JS, Reid AM, Jordan LVM, Glen AC, Davidson JA. Troponin I and myocardial injury in the ICU. Br J Anaesth. 1999;82:41–46.[Abstract/Free Full Text]
  12. Kollef MH, Ladenson JH, Eisenberg PR. Clinically recognized cardiac dysfunction: an independent determinant of mortality among critically ill patients. Is there a role for serial measurement of cardiac troponin I? Chest. 1997;111:1340–1347.[Abstract/Free Full Text]
  13. ver Elst KM, Spapen HD, Nguyen DN, Garbar C, Huyghens LP, Gorus FK. Cardiac troponins I and T are biological markers of left ventricular dysfunction in septic shock. Clin Chem. 2000;46:650–657.[Abstract/Free Full Text]
  14. Ammann P, Maggiorini M, Bertel O, et al. Troponin as a risk factor for mortality in critically ill patients without acute coronary syndromes. J Am Coll Cardiol. 2003;41:2004–2009.[Abstract/Free Full Text]
  15. Booker KJ, Holm K, Drew BJ, et al. Frequency and outcomes of transient myocardial ischemia in critically ill adults admitted for noncardiac conditions. Am J Crit Care. 2003;12:508–517.[Abstract/Free Full Text]
  16. Heidenreich PA, Alloggiamento T, Melsop K, McDonald KM, Go AS, Hlatky MA. The prognostic value of troponin in patients with non-ST elevation acute coronary syndromes: a meta-analysis. J Am Coll Cardiol. 2001;38:478–485.[Abstract/Free Full Text]
  17. Antman EM, Tanasijevic MJ, Thompson B, et al. Cardiac-specific troponin I levels to predict the risk of mortality in patients with acute coronary syndromes. N Engl J Med. 1996;335:1342–1349.[Abstract/Free Full Text]
  18. Ohman EM, Armstrong PW, Christenson RH, et al. Cardiac troponin T levels for risk stratification in acute myocardial ischemia. GUSTO IIA Investigators. N Engl J Med. 1996;335:1333–1341.[Abstract/Free Full Text]
  19. Relos RP, Hasinoff IK, Beilman GJ. Moderately elevated serum troponin concentrations are associated with increased morbidity and mortality rates in surgical intensive care unit patients. Crit Care Med. 2003;31:2598–2603.[Medline]
  20. Knaus WA, Draper EA, Wagner DP, Zimmerman JE. APACHE II: a severity of disease classification system. Crit Care Med. 1985;13:818–829.[Medline]
  21. Marshall JC, Cook DJ, Christou NV, Bernard GR, Sprung CL, Sibbald WJ. Multiple organ dysfunction score: a reliable descriptor of a complex clinical outcome. Crit Care Med. 1995;23:1638–1652.[Medline]
  22. Panteghini M, Pagani F, Yeo KT, et al. Evaluation of imprecision for cardiac troponin assays at low-range concentrations. Clin Chem. 2004;50:327–332.[Abstract/Free Full Text]
  23. Hill SA, Devereaux PJ, Griffith L, et al. Can troponin I measurement predict short-term serious cardiac outcomes in patients presenting to the emergency department with possible acute coronary syndrome? Can J Emerg Med. 2004;6:22–30.
  24. Lehrke S, Steen H, Sievers HH, et al. Cardiac troponin T for prediction of short- and long-term morbidity and mortality after elective open heart surgery. Clin Chem. 2004;50:1560–1567.[Abstract/Free Full Text]
  25. Baggish AL, MacGillivray TE, Hoffman W, et al. Postoperative troponin-T predicts prolonged intensive care unit length of stay following cardiac surgery. Crit Care Med. 2004;32:1866–1871.[Medline]
  26. Klein Gunnewiek JMT, van de Leur JJJ. Elevated troponin T concentrations in critically ill patients. Intensive Care Med. 2003;29:2317–2322.[Medline]
  27. Wright RS, Williams BA, Cramner H, et al. Elevations of cardiac troponin I are associated with increased short-term mortality in noncardiac critically ll emergency department patients. Am J Cardiol. 2002;90:634–646.[Medline]
  28. Baillard C, Boussarsar M, Fosse JP, et al. Cardiac troponin I in patients with severe exacerbation of chronic obstructive pulmonary disease. Intensive Care Med. 2003;29:584–589.[Medline]
  29. Lyon WJ, Baker RA, Andrew MJ, Tirimacco R, White GH, Knight JL. Relationship between elevated preoperative troponin T and adverse outcomes following cardiac surgery. ANZ J Surg. 2003;73:40–44.[Medline]
  30. Harrington RA, Becker RC, Ezekowitz M, et al. Antithrombotic therapy for coronary artery disease: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004;126(3 suppl):513S–548S.[Abstract/Free Full Text]
  31. Cook DJ, Crowther M, Meade M, et al. Deep venous thrombosis in medical-surgical critically ill patients: prevalence, incidence, and risk factors. Crit Care Med. 2005;33:1565–1571.[Medline]



This article has been cited by other articles:


Home page
 Arch Intern MedHome page
W. Lim, I. Qushmaq, P. J. Devereaux, D. Heels-Ansdell, F. Lauzier, A. S. Ismaila, M. A. Crowther, and D. J. Cook
Elevated Cardiac Troponin Measurements in Critically Ill Patients
Arch Intern Med, December 11, 2006; 166(22): 2446 - 2454.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Respond to This Article
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Right arrow Take the CE Test
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lim, W.
Right arrow Articles by Devereaux, P. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lim, W.
Right arrow Articles by Devereaux, P. J.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS