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Diagnostic Value of Parameters Related to White Blood Cell Counts for Troponin I Elevation in CO Poisoning

  • J. M. Moon
  • B. J. Chun
  • Y. S. Cho
  • S. M. Lee
Article
  • 13 Downloads

Abstract

To assess myocardial injury related to acute carbon monoxide (CO) poisoning, serial troponin I is measured in patients not presenting with troponin I elevation. This retrospective study investigated whether parameters related to white blood cell (WBC) counts (total and differential WBC counts, neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio) improved predictive accuracy for troponin I elevation (> 0.04 ng/ml) in patients not presenting with evidence of myocardial injury. Serial parameters, troponin I values, and clinical courses were collected in 241 patients. Troponin I was elevated in 33 (13.7%) patients after hospitalization. The median lag times to troponin I elevation in patients with undetectable and detectable troponin I (0.015 ng/ml ≤ troponin I ≤ 0.04 ng/ml) at presentation were 5.9 h and 3.0 h, respectively. Patients with troponin I elevation after presentation had higher total WBC and neutrophil counts and NLRs and a lower lymphocyte count during the first 4 h after presentation than patients without troponin I elevation during hospitalization. Total WBC count, neutrophil count, and log NLR at presentation were selected as independent predictive factors for troponin I elevation after presentation. However, only the neutrophil count and log NLR at presentation improved the predictive accuracy in combination with clinical parameters compared with that achieved with a predictive model including only clinical parameters. The optimal cut-off neutrophil count and NLR were 5.21 × 103 /uL and 4.02, respectively. The total neutrophil count and NLR, which are widely available and inexpensive parameters obtained in the emergency department (ED), are promising screening tools for predicting the risk of troponin I elevation in patients without evidence of myocardial injury-related acute CO poisoning at presentation.

Keywords

Carbon monoxide Lymphocyte Neutrophil Poisoning Troponin I 

Notes

Compliance with Ethical Standards

Conflict of interest

The authors declare that we have no conflict of interest.

Supplementary material

12012_2018_9501_MOESM1_ESM.docx (12 kb)
Supplementary material 1 (DOCX 11 KB)

References

  1. 1.
    Lippi, G., Rastelli, G., Meschi, T., Borghi, L., & Cervellin, G. (2012). Pathophysiology, clinics, diagnosis and treatment of heart involvement in carbon monoxide poisoning. Clinical Biochemistry, 45, 1278–1285.CrossRefGoogle Scholar
  2. 2.
    Satran, D., Henry, C. R., Adkinson, C., Nicholson, C. I., Bracha, Y., & Henry, T. D. (2005). Cardiovascular manifestations of moderate to severe carbon monoxide poisoning. Journal of the American College of Cardiology, 45, 1513–1516.CrossRefGoogle Scholar
  3. 3.
    Cha, Y. S., Cha, K. C., Kim, O. H., Lee, K. H., Hwang, S. O., & Kim, H. (2014). Features and predictors of myocardial injury in carbon monoxide poisoned patients. Emerg Med J, 31, 210–215.CrossRefGoogle Scholar
  4. 4.
    Kao, H. K., Lien, T. C., Kou, Y. R., & Wang, J. H. (2009). Assessment of myocardial injury in the emergency department independently predicts the short-term poor outcome in patients with severe carbon monoxide poisoning receiving mechanical ventilation and hyperbaric oxygen therapy. Pulmonary Pharmacology and Therapeutics, 22, 473–477.CrossRefGoogle Scholar
  5. 5.
    Thygesen, K., Alpert, J. S., Jaffe, A. S., Chaitman, B. R., Bax, J. J., Morrow, D. A., & White, H. D., ESC Scientific Document Group. Fourth universal definition of myocardial infarction (2018). European Heart Journal. 2018;  https://doi.org/10.1093/eurheartj/ehy462.Google Scholar
  6. 6.
    Aslan, S., Uzkeser, M., Seven, B., Gundogdu, F., Acemoglu, H., Aksakal, E., & Varoglu, E. (2006). The evaluation of myocardial damage in 83 young adults with carbon monoxide poisoning in the East Anatolia region in Turkey. Human and Experimental Toxicology, 25, 439–446.CrossRefGoogle Scholar
  7. 7.
    Rose, J. J., Wang, L., Xu, Q., McTiernan, C. F., Shiva, S., Tejero, J., & Gladwin, M. T. (2017). Carbon monoxide poisoning: pathogenesis, management, and future directions of therapy. American Journal of Respiratory and Critical Care Medicine, 195, 596–606.CrossRefGoogle Scholar
  8. 8.
    Mochizuki, K., Miyauchi, R., Misaki, Y., Kasezawa, N., Tohyama, K., & Goda, T. (2012). Associations between leukocyte counts and cardiovascular disease risk factors in apparently healthy Japanese men. Journal of Nutritional Science and Vitaminology, 58, 181–186.CrossRefGoogle Scholar
  9. 9.
    Nordestgaard, B. G., Adourian, A. S., Freiberg, J. J., Guo, Y., Muntendam, P., & Falk, E. (2010). Risk factors for near-term myocardial infarction in apparently healthy men and women. Clinical Chemistry, 56, 559–567.CrossRefGoogle Scholar
  10. 10.
    Sabatine, M. S., Morrow, D. A., Cannon, C. P., Murphy, S. A., Demopoulos, L. A., DiBattiste, P. M., McCabe, C. H., Braunwald, E., & Gibson, C. M. (2002). Relationship between baseline white blood cell count and degree of coronary artery disease and mortality in patients with acute coronary syndromes: a TACTICS-TIMI 18 (treat angina with aggrastat and determine cost of therapy with an invasive or conservative strategy- thrombolysis in myocardial infarction 18 trial) substudy. Journal of the American College of Cardiology, 40(10), 1761–1768.CrossRefGoogle Scholar
  11. 11.
    Azab, B., Chainani, V., Shah, N., & McGinn, J. T. (2013). Neutrophil-lymphocyteratio as a predictor of major adverse cardiac events among diabeticpopulation: a 4-year follow-up study. Angiology, 64, 456–465.CrossRefGoogle Scholar
  12. 12.
    Xiang, F., Chen, R., Cao, X., Shen, B., Liu, Z., Tan, X., Ding, X., & Zou, J. (2018). Monocyte/lymphocyte ratio as a better predictor of cardiovascular and all-cause mortality in hemodialysis patients: a prospective cohort study. Hemodialysis International, 22, 82–92.CrossRefGoogle Scholar
  13. 13.
    Manini, A. F., Nelson, L. S., Skolnick, A. H., Slater, W., & Hoffman, R. S. (2010). Electrocardiographic predictors of adverse cardiovascular events in suspected poisoning. Journal of Medical Toxicology, 6, 106–115.CrossRefGoogle Scholar
  14. 14.
    DeLong, E. R., DeLong, D. M., & Clarke-Pearson, D. L. (1988). Comparing the areas under two or more correlated receiver operating characteristic curves: a nonparametric approach. Biometrics, 44, 837–845.CrossRefGoogle Scholar
  15. 15.
    Thom, S. R., Bhopale, V. M., Han, S. T., Clark, J. M., & Hardy, K. R. (2006). Intravascular neutrophil activation due to carbon monoxide poisoning. American Journal of Respiratory and Critical Care Medicine, 174, 1239–1248.CrossRefGoogle Scholar
  16. 16.
    Schnittger, V., Rosendahl, K., Lind, F., & Palmblad, J. (2004). Effects of carbon monoxide poisoning on neutrophil responses in patients treated with hyperbaric oxygen. Journal of Investigative Medicine, 52, 523–530.Google Scholar
  17. 17.
    Lee, S. S., Choi, I. S., & Song, K. S. (1994). Hematologic changes in acute carbon monoxide intoxication. Yonsei Medical Journal, 35, 245–251.CrossRefGoogle Scholar
  18. 18.
    Dong, C. H., Wang, Z. M., & Chen, S. Y. (2018). Neutrophil to lymphocyte ratio predict mortality and major adverse cardiac events in acute coronary syndrome: a systematic review and meta-analysis. Clinical Biochemistry, 52, 131–136.CrossRefGoogle Scholar
  19. 19.
    Han, Y. Y., Wang, Y., Zhao, G. Q., Yang, J. L., Wang, L., & Wang, W. Z. (2018). Relationship between neutrophil-to-lymphocyte ratio and myocardial injury induced by acute carbon monoxide poisoning. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi, 36, 362–364.Google Scholar
  20. 20.
    Thomson, S. P., McMahon, L. J., & Nugent, C. A. (1980). Endogenous cortisol: a regulator of the number of lymphocytes in peripheral blood. Clinical Immunology and Immunopathology, 17, 506–514.CrossRefGoogle Scholar
  21. 21.
    Ishikawa, T., Quan, L., Michiue, T., Kawamoto, O., Wang, Q., Chen, J. H., Zhu, B. L., & Maeda, H. (2013). Postmortem catecholamine levels in pericardial and cerebrospinal fluids with regard to the cause of death in medicolegal autopsy. Forensic Science International, 228, 52–60.CrossRefGoogle Scholar
  22. 22.
    Blum, A., Sclarovsky, S., Rehavia, E., & Shohat, B. (1994). Levels of T-lymphocyte subpopulations, interleukin-1 beta, and soluble interleukin-2 receptor in acute myocardial infarction. American Heart Journal, 127, 1226–1230.CrossRefGoogle Scholar
  23. 23.
    Boag, S. E., Das, R., Shmeleva, E. V., Bagnall, A., Egred, M., Howard, N., Bennaceur, K., Zaman, A., Keavney, B., & Spyridopoulos, I. (2015). T lymphocytes and fractalkine contribute to myocardial ischemia/reperfusion injury in patients. The Journal of Clinical Investigation, 125, 3063–3076.CrossRefGoogle Scholar
  24. 24.
    Boag, S. E., Andreano, E., & Spyridopoulos, I. (2017). Lymphocyte Communication in Myocardial Ischemia/Reperfusion Injury. Antioxidants and Redox Signaling, 26(12), 660–675.CrossRefGoogle Scholar
  25. 25.
    Lin, J., Xue, B., Li, J., Xu, H., Huang, X., Yao, Z., Li, X., & Xia, J. (2017). Neutrophil to lymphocyte ratio may be a helpful marker to evaluate disease activity in NMOSD. Neurological Sciences, 38, 1859–1863.CrossRefGoogle Scholar
  26. 26.
    Annane, D., Chevret, S., Jars-Guincestre, C., Chillet, P., Elkharrat, D., Gajdos, P., & Raphael, C. (2001). Prognostic factors in unintentional mild carbon monoxide poisoning. Intensive Care Medicine, 27, 1776–1781.CrossRefGoogle Scholar
  27. 27.
    Cervellin, G., Comelli, I., Rastelli, G., Picanza, A., & Lippi, G. (2014). 4.Initial blood lactate correlates with carboxyhemoglobin and clinical severity in carbon monoxide poisoned patients. Clinical Biochemistry, 47, 298–301.CrossRefGoogle Scholar
  28. 28.
    Hampson, N. B. (2018). Carboxyhemoglobin: a primer for clinicians. Undersea and Hyperbaric Medicine, 45(2), 165–171.CrossRefGoogle Scholar
  29. 29.
    Yelken, B., Tanriverdi, B., Cetinbaş, F., Memiş, D., & Süt, N. (2009). The assessment of QT intervals in acute carbon monoxide poisoning. Anadolu Kardiyoloji Dergisi, 9, 397–400.Google Scholar
  30. 30.
    Kaya, H., Coşkun, A., Beton, O., Zorlu, A., Kurt, R., Yucel, H., Gunes, H., & Yılmaz, M. B. (2016). COHgb levels predict the long-term development of acute myocardial infarction in CO poisoning. The American Journal of Emergency Medicine, 34(5), 840–844.CrossRefGoogle Scholar
  31. 31.
    Tikuisis, P., Kane, D. M., McLellan, T. M., Buick, F., & Fairburn, S. M. (1985). Rate of formation of carboxyhemoglobin in exercising humans exposed to carbon monoxide. Journal of Applied Physiology, 72, 1311–1319.CrossRefGoogle Scholar
  32. 32.
    Bossard, M., Thériault, S., Aeschbacher, S., Schoen, T., Kunz, S., von Rotz, M., Estis, J., Todd, J., Risch, M., Mueller, C., Risch, L., Paré, G., & Conen, D. (2017). Factors independently associated with cardiac troponin I levels in young and healthy adults from the general population. Clinical Research in Cardiology, 106, 96–104.CrossRefGoogle Scholar
  33. 33.
    Alazzoni, A. Al-Saleh,A., Shalash, S. A., Ye, C., Mbuagbaw, L., Thabane, L., Sanjit, S., & Jolly (2014). Performance of the high-sensitivity troponin assay in diagnosing acute myocardial infarction: systematic review and meta-analysis. CMAJ Open, 2(3), E199–E207.CrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2019

Authors and Affiliations

  1. 1.Department of Emergency MedicineChonnam National University Medical SchoolDonggu, GwangjuSouth Korea

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