| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Guest Access | Sign In via User Name/Password
|
|
|
|||||||
Guest Access | Sign In via User Name/Password |
|||||||||
University Hospital Groningen, Groningen, the Netherlands
Correspondence to: Esther A. P. van Bockel, MD, Intensive & Respiratory Care Unit (ICB), Department of Internal Medicine, University Hospital Groningen, PO Box 30001, NL-9700 RB Groningen, the Netherlands; e-mail: e.a.p.van.bockel{at}anest.azg.nl
To the Editor:
With great interest, we read the recent review by Roongsritong et al1 (May 2004) on the causes of elevations in troponin level in patients who had not experienced myocardial infarction, particularly the section about troponin levels in septic and critically ill patients. As the authors state, the exact mechanism of increased cardiac troponin levels in patients with sepsis remains unknown.
The authors suggest several mechanisms for troponin release in septic patients. One of their suggestions is that cytokines or endotoxin might cause myocardial injury. Circulating mediators such as tumor necrosis factor (TNF)-
and interleukin-1ß have indeed been shown to cause myocardial depression in patients with sepsis.2 Cytokines might increase the permeability of the myocyte membrane with the leakage of free cardiac troponin I (cTnI) from the cytoplasm while the myocyte-contraction complex remains intact. We could not confirm this using a human endotoxin model.3 Our volunteers showed a septic profile after being injected with endotoxin. Troponin levels were not measurable, although TNF- levels where high enough to cause myocardial depression. In these volunteers, we also measured increased levels of death hormones, TNF, and tumor necrosis factor-related apoptosis-inducing ligand treatment, suggesting active apoptosis.4 Therefore, we think that it is unlikely that cTnI levels are elevated due to the leakage of free cytoplasmic cTnI induced by cytokines or apoptosis during the early phase of sepsis. Another proposed mechanism of troponin release is the dysfunction of microcirculation. However, it is questionable whether dysfunctional microcirculation during sepsis also occurs in the heart.5
Finally, Roongsritong et al1 conclude that troponin measurements in critically ill septic patients provide valuable prognostic information. We would like to point out that, although several studies678 have shown that troponin could be used as a prognostic marker in critically ill patients, Kollef et al9 have shown with a multivariate analysis that left ventricular function, not troponin level, was a predictor for mortality.
We conclude that the mechanism and meaning of the elevation of troponin levels in patients with sepsis still has to be elucidated, but that the confusion exists only with marginally elevated troponin levels. Higher levels of troponin (ie, > 10 ng/mL), especially when used in the context of the clinical suspicion of myocardial ischemia, and negative troponin results are still valuable in excluding myocardial damage.
References
and interleukin 1ß are responsible for in vitro myocardial cell depression induced by human septic shock serum. J Exp Med 1996;183,949-958Texas Tech University Health Sciences Center, Lubbock, TX
Correspondence to: Chanwit Roongsritong, MD, Texas Tech University Health Sciences Center, School of Medicine, Department of Internal Medicine, 3601 4th St STOP 8410, Lubbock, TX 79430-9410
To the Editor:
We appreciate the interest in and comments on our recent article in CHEST (May 2004)1 by van Bockel et al. Unfortunately, the reports that they cited23 had not yet been published at the time of our review and thus were not included. However, Ammann et al4 recently reported higher levels of tumor necrosis factor-, its soluble receptor, and interleukin-6 in troponin-positive critically ill patients compared to those who were negative for troponin. Therefore, we believe that controversy still exists, at the present time, regarding the role of cytokines in troponin release in this subset of patients.
We also maintain our opinion on the prognostic value of elevated troponin levels in sepsis and/or critically ill patients. In addition to the several reports cited in our review, two recent studies by Ammann et al4 and Wu et al5 found troponin to be an important risk factor for mortality in these patients. As stated by Dr. van Bockel and colleagues, a study by Kollef et al6 found clinically recognized cardiac dysfunction but not elevation of troponin levels to be an independent predictor of mortality in their patients. However, Kollef et al6 defined clinically recognized cardiac dysfunction as the presence of cardiac arrest, congestive heart failure, unstable angina, or myocardial infarction. We believe that their study design may have underestimated the prognostic value of troponin levels.
Finally, we agree that further studies are needed, and we laud van Bockel and colleagues for their effort at elucidating the mechanism and importance of the elevation of troponin levels in septic and critically ill patients.
References
This article has been cited by other articles:
|
|
 |
|
  J.-P. Quenot, G. Le Teuff, C. Quantin, J.-M. Doise, M. Abrahamowicz, D. Masson, and B. Blettery Myocardial Injury in Critically Ill Patients: Relation to Increased Cardiac Troponin I and Hospital Mortality Chest, October 1, 2005; 128(4): 2758 - 2764. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
