Elevated serum cardiac troponin I in rhabdomyolysis

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Abstract

Objective: To examine the etiology and clinical significance of elevated serum cardiac troponin I (cTnI) in patients with rhabdomyolysis. Methods: Data on 91 (63 men) consecutive patients with rhabdomyolysis were examined. Results: The mean age was 57.8±19.6 years (range 24–97 years). Patients were divided into two groups: cTnI-positive with serum cTnI >0.6 ng/ml (n=19) and cTnI-negative with serum cTnI <0.6 ng/ml (n=72). Prevalence of cardiovascular risk factors was equal in both groups. Illicit substance use was more common in the cTnI-positive group (31% vs. 14%, P=0.04). Peak creatine kinase (CK) was higher in cTnI-positive group (34,811±38,309 vs. 15,070±21,655 U/l, P=0.04) but there was no difference in the MB isoenzyme (CK-MB) (118±132 vs. 89±451 ng/ml, P=0.63). In cTnI-positive group, there was a strong correlation between peak CK and CK-MB (r2=0.606, P=0.00008) but not between peak cTnI and peak CK (r2=0.164 and P=0.08) or CK-MB (r2=0.134 and P=0.12) levels. Serum creatinine was higher in cTnI-positive group (3.58±2.73 vs. 1.83±2.01 mg/dl, P=0.02) but there was no correlation between serum creatinine and cTnI (r2=0.121, P=0.158). None of the cTnI-positive patient had segmental wall motion abnormalities. Seventeen (89%) patients in cTnI-positive and 19 (26%) in cTnI-negative group required admission to intensive care unit (P=0.0001). Hypotension (37% vs. 6%, P=0.0002) and sepsis (47% vs. 11%, P=0.0003) were more common in cTnI-positive group. Duration of hospitalization was longer in cTnI-positive group (17.7±11.7 vs. 8.9±13 days, P=0.007) but there was no significant difference in mortality. Conclusion: In rhabdomyolysis, serum cTnI may be elevated unrelated to the degree of muscle damage, renal failure and cardiovascular risk factors, and is likely related to the etiology of rhabdomyolysis, as is evidenced by significantly higher serum cTnI with illicit substance use, hypotension, and sepsis. Elevated serum cTnI is associated with a higher morbidity.

Introduction

Troponin I exists in three isoforms: slow skeletal, fast skeletal, and cardiac muscle specific isoforms. The cardiac muscle isoform is a 24 kDa protein uniquely expressed in the adult human heart [1]. Cardiac troponin I (cTnI) is a structural protein located in the myofibril with a small free pool existing in the cytosol. It is the most specific structural protein released to circulation in cases of myocardial damage. Furthermore, the skeletal muscle does not express cTnI throughout ontogeny, or during regenerating muscle disease, or in response to pathological stimuli, conferring high specificity of cardiac isoform for the myocardium [2], [3]. An increased level of cTnI in serum indicates myocyte injury and necrosis, and once outside the myocyte, these macromolecules are cleared from the interstitium by cardiac lymphatics. Eventually when the capacity of the lymphatics to clear the macromolecules is exceeded, the markers become detectable in the peripheral circulation and are released with a stoichiometric relationship proportional to the amount of myocardial injury [4]. So the detectable increases in the biomarkers of cardiac injury are indicative of injury to the myocardium, but elevations are not synonymous with an ischemic mechanism of injury. With a better understanding of the cTnI physiology, and the increasing recognition that cardiac troponins may be elevated in patients with non-ischemic myocardial disease and non-cardiac disease, careful interpretation for a cause and effect relationship is necessary [5], [6], [7], [8], [9], [10], [11]. The purpose of this study was to examine the etiology and clinical significance of increased cTnI levels in the patients with rhabdomyolysis in the absence of acute coronary syndrome and cardiac trauma.

Section snippets

Study population

After institutional approval, all adult patients admitted to our hospital, both to intensive care unit (ICU) and to the floors between January 1997 and January 2002 with the diagnosis of rhabdomyolysis were identified in the hospital information system computer database. Rhabdomyolysis was defined as serum creatine kinase (CK) level >1000 U/l, which is four times the upper limit of normal (250 U/l, Oliver–Rosalki method). The exclusion criteria included patients diagnosed to have acute coronary

Baseline characteristics

From January 1997 to January 2002, there were 96 patients identified with the discharge diagnosis of rhabdomyolysis. Of the 96 patients, 24 (25%) had serum cTnI levels of >0.6 ng/ml, and 72 (75%) had <0.6 ng/ml. Of the 24 patients with positive cTnI, five patients had evidence of acute coronary syndrome and were excluded from the study. Of the 91 patients included in the study, 63 were men and 28 were women. The mean age was 57.8±19.6 years (range 24–97 years). The baseline characteristics of

Findings of the present study

This study shows that elevation in serum cTnI during rhabdomyolysis is not uncommon. There is no relationship between the severity of rhabdomyolysis and the degree of serum cTnI elevation as shown by the absence of a correlation between the peak CK activity and cTnI levels. Similarly, the degree of renal impairment in presence of significant skeletal muscle damage did not correlate with the cTnI elevation. The clinical course of the patients with elevated cTnI tends to be more severe as

Conclusion

In patients with rhabdomyolysis, cTnI may be elevated unrelated to the degree of muscle damage, renal failure, and cardiovascular risk factors, as no relation existed between serum cTnI and serum CK, CK-MB, or creatinine levels. It is likely related to the etiology of rhabdomyolysis as is evidenced by significantly elevated levels of cTnI in patients with illicit substance use, hypotension, and sepsis. Elevated serum cTnI is associated with a higher morbidity.

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      Cardiac troponin I (TnI) elevation is common among patients with rhabdomyolysis,11 but the underlying mechanism of its elevation is unclear. The possible reasons for micro injury to the myocardium as a cause of elevated TnI concentration in cases with rhabdomyolysis include the presence of free radicals or circulating cytokines, cardiotoxicity due to ion fluxes, high acidemia, hypotension and hypoperfusion, and myocardial stretch due to aggressive fluid resuscitation.12 However, the possibility of direct myocardial damage caused by a mycotoxin cannot be completely ruled out, and further study is required.

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