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Letters |
1
Unité de Réanimation Chirurg.,
2
Service de Biochim. Gén., Univ. de Paris-Sud, Centre Hosp. de Bicêtre, 94275 Le Kremlin Bicêtre, France
a author for correspondence.
To the Editor:
Early diagnosis of posttraumatic cardiac injury is important for patient outcome (1) but a concomitant rhabdomyolysis may impede its detection by biochemical means. Cardiac troponin I (cTnI) might be a useful tool to specifically assess myocardial damage in trauma patients. We report here serum cTnI, creatine kinase (CK), and CK isoenzyme MB measurements in multiple injured patients with rhabdomyolysis.
Successive trauma patients with rhabdomyolysis [CK activity >500
U/L] during the first 24 h after admission were studied in
accordance with the Helsinki Declaration. Exclusion criteria were age
>55 years, Injury Severity Score (ISS (2)) <16, and
history of prior cardiac or renal disease. Patients were considered to
have chest trauma when the chest Abbreviated Injury Score
(3) was 
2. Electrocardiography and a transesophageal
echocardiography (HP Sonos 1000 with a biplane 5.5 MHz
transducer; Hewlett-Packard, Courtaboeuf, France) were
performed as soon as possible within 48 h after admission and
repeated if needed. Blood was sampled 12 and 24 h after admission.
Total CK activity was assessed according to IFCC recommendations but at
37 °C. CK-MB mass and cTnI were measured in duplicate (the second
analysis after a freeze–thaw cycle and repeat centrifugation) with
commercially available immunoassays (Stratus CK-MB and Stratus cTnI;
Baxter Dade, Maurepas, France); reference values were <7 µg/L and
<1.6 µg/L, respectively. The CK-MB mass index was calculated as
follows: 100 CK-MB (µg/L)/total CK (U/L); our in-house reference
upper limit was 1.1. Results are given as median (and range of all
data).
We studied 18 patients [age 30 (20–48) years; ISS 31 (16–61)]; 9
had a chest trauma but no segmental wall motion abnormality or Q wave
or ischemic changes. Peak total CK activity was 3448 (540–13 170)
U/L. As shown in Fig. 1
, peak CK-MB was above the discrimination value for myocardial
infarction in 13 patients (6 chest traumas), CK-MB mass index was
abnormal in 4 patients (3 chest traumas), and peak cTnI was above the
reference limit in 6 patients (5 chest traumas). The correlation
between peak CK-MB and peak total CK was strong (r =
0.81, P = 0.0009), but we saw no relation between cTnI
and total CK or CK-MB.
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Thus, as previously described in nontraumatic rhabdomyolysis (4), the significant relation between total CK and its isoenzyme indicates that CK-MB is not a valuable indicator of myocardial injury in the trauma setting. Likewise, increasing specificity by using the CK-MB index was obtained at the expense of sensitivity (5).
cTnI is proposed as a highly sensitive marker of cardiac damage (6), and the absence of this structural protein in fetal and adult skeletal muscle confirms its cardiac specificity (7). Significant cTnI serum concentrations without clear evidence of myocardial injury in medical patients (4) or trauma patients (present report) may signify that the clinical component of the diagnosis is incomplete or less sensitive than the biological one, leading to an overestimation of the incidence of "false-positive" results (5). This high sensitivity was recently illustrated by an increased cTnI concentration in a patient with an isolated posttraumatic pericardial effusion probably related to a limited cardiac contusion despite normal echography (5).
We conclude that cTnI remains a valuable tool for the detection of subclinical myocardial damage in patients with skeletal muscle injury, especially in the presence of chest trauma. Indeed, it is probably more sensitive than the available clinical means. A significant increase in cTnI after trauma therefore justifies reinforced early cardiovascular monitoring and prolonged follow-up care.
Acknowledgments
We gratefully acknowledge M.O. Royoux and G. Galpy, Dade France (Maurepas, France), for kindly supplying reagents used in this study.
References
The following articles in journals at HighWire Press have cited this article:
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  C. Karcher, H.-J. Dieterich, and T. H. Schroeder Rhabdomyolysis in an obese patient after total knee arthroplasty Br. J. Anaesth., December 1, 2006; 97(6): 822 - 824. [Abstract] [Full Text] [PDF]
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 J. A. Simpson, R. Labugger, G. G. Hesketh, C. D'Arsigny, D. O'Donnell, N. Matsumoto, C. P. Collier, S. Iscoe, and J. E. Van Eyk Differential Detection of Skeletal Troponin I Isoforms in Serum of a Patient with Rhabdomyolysis: Markers of Muscle Injury? Clin. Chem., July 1, 2002; 48(7): 1112 - 1114. [Full Text] [PDF]
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E. B. Stelow, V. P. Johari, S. A. Smith, J. T. Crosson, and F. S. Apple Propofol-associated Rhabdomyolysis with Cardiac Involvement in Adults: Chemical and Anatomic Findings Clin. Chem., April 1, 2000; 46(4): 577 - 581. [Abstract] [Full Text] [PDF]
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A. Lavoinne and G. Hue Serum Cardiac Troponins I and T in Early Posttraumatic Rhabdomyolysis Clin. Chem., March 1, 1998; 44(3): 667 - 668. [Full Text] [PDF]
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), patients without chest trauma; (•) patients with chest trauma.
Shaded areas depict the reference ranges.