S-100B protein elevation in patients with the acute coronary syndrome after resuscitation is a predictor of adverse neurological prognosis

Česká verzia

Authors: K. Helánová ¹; J. Pařenica ¹; J. Jarkovský ² ; L. Dostálová ¹; S. Littnerová ²; I. Klabenešová3ihash2 ^{,4 3,4}; P. Lokaj ¹; P. Kala ¹; M. Poloczek ¹; O. Toman ¹; O. Gimunová ⁵; J. Maláska ⁵; J. Špinar ¹
Authors place of work: Interní kardiologická klinika Lékařské fakulty MU a FN Brno, pracoviště Bohunice, přednosta prof. MUDr. Jindřich Špinar, CSc., FESC ¹; Institut biostatistiky a analýz Lékařské a Přírodovědecké fakulty MU Brno, ředitel doc. RNDr. Ladislav Dušek, Ph. D. ²; Oddělení klinické biochemie FN Brno, pracoviště Bohunice, přednosta prim. doc. MUDr. Milan Dastych, CSc., MBA ³; Katedra laboratorních metod Lékařské fakulty MU Brno, přednosta doc. MUDr. Milan Dastych, CSc., MBA ⁴; Klinika anesteziologie, resuscitace a intenzivní medicíny Lékařské fakulty MU Brno a FN Brno, pracoviště Bohunice, přednosta prof. MUDr. Pavel Ševčík, CSc. ⁵
Published in the journal: Vnitř Lék 2012; 58(4): 266-272
Category: Original Contributions

Summary

Introduction:
The annual incidence of out-of-hospital cardiac arrest is around 90–190 cases per 100 000 inhabitants. The limiting factor for further prognosis of patients after out-of-hospital arrest is their neurological status. The S100B protein is mainly the nervous system cell’s product, it’s glial-specific and mostly expressed by astrocytes. It has been shown that after circulatory arrest its increased level correlates with the prognosis of patients. Work aims to determine the level of protein S100B in the group of patients with acute myocardial infarction without circulatory arrest, and compare it to the value in patients with acute myocardial infarction after out-of-hospital resuscitation.

Methods:
24 patients were evaluated after out-of-hospital resuscitation for the malignant arrhythmias during acute coronary syndrome (ACS). All patients were treated with mild therapeutic hypothermia. The control group consisted of 19 patients with ACS. The sample for the determination of S-100B was taken immediately on admission. Neurological status was evaluated according to the CPC scores (Cerebral Performance Categories) at discharge, patients were divided into 3 groups: CPC1 – good condition, CPC2 – moderate neurological disability, CPC3-5 – serious neurological impairment, coma or death.

Results:
The values of protein S-100B fluctuated, in patients with no resuscitation, in range between 0.038 to 0.204 pg/ml. In patients after resuscitation without subsequent neurological disability (CPC 1) was range 0.077 to 0.817 pg/ml, in patients with moderate to severe neurological disability (CPC 2) was range 0.132–2.59 pg/ml, patients with severe neurological disabilities or deaths had S-100B levels from 0.70 to 8.53 pg/ml. According to ROC analysis we found the cut-off value for the S-100B. Cut-off value for probably a good neurological condition is < 0.23 pg/ml (specificity 93%, sensitivity 70%), and value testify for supposed severe neurological disability or death is > 1.64 pg/ml (specificity 95%, sensitivity 83%).

Conclusion:
Protein S-100B is one of the early and sensitive markers of severe brain damage in patients after cardiac arrest. Its early determination can help in prediction of patient neurological condition and help doctors to decide further action.

Key words:
S-100B – acute coronary syndrom – cardiac arrest

Zdroje

1. Rea TD, Pearce RM, Raghunathan TE et al. Incidence of Out-of-Hospital cardiac arrest. Am J Cardiol 2004; 93: 1455–1460.

2. Straus SM, Bleumink GS, Dieleman JP et al. The incidence of sudden cardiac death in the general population. J Clin Epidemiol 2004; 57: 98–102.

3. Nolan JP, Neumar RW, Adrie C et al. Post-cardiac arrest syndrome: Epidemiology, pathophysiology, treatment, and prognostication: A Scientific Statement from the International Liaison Committee on Resuscitation; the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; the Council on Stroke. Resuscitation 2008; 79: 350–379.

4. Rosario D. S-100: a multigenic family of calcium-modulated proteins of the EF-hand type with intracellular and extracellular functional roles. Int J Biochem Cell Biol 2001; 33: 637–668.

5. Tsoporis JN, Marks A, Haddad A et al. S100B Expression Modulates Left Ventricular Remodeling After Myocardial Infarction in Mice. Circulation 2005; 111: 598–606.

6. Cai XY, Lu L, Wang YN et al. Association of increased S100B, S100A6 and S100P in serum levels with acute coronary syndrome and also with the severity of myocardial infarction in cardiac tissue of rat models with ischemia-reperfusion injury. Atherosclerosis 2011; 217: 536–542.

7. Nagao K, Havashi N, Kanmatsuse K et al. Cardiopulmonary cerebral resuscitation using emergency cardiopulmonary bypass, coronary reperfusion therapy and mild hypothermia in patients with cardiac arrest outside the hospital. J Am Coll Cardiol 2000; 36: 776–783.

8. Raabe A, Grolms C, Sorge O et al. Serum S-100B Protein in Severe Head Injury. Neurosurgery 1999; 45: 477–483.

9. Zongo D, Ribéreau-Gayon R, Masson F et al. S100-B protein as a screening tool for the early assessment of minor head injury. Ann Emerg Med 2012; 59: 209–218.

10. Ruan S, Noyes K, Bazarian JJ et al. The economic impact of S-100B as a pre-head CT screening test on emergency department management of adult patients with mild traumatic brain injury. J Neurotrauma 2009; 26: 1655–1664.

11. Moritz S, Warnat J, Bele S et al. The Prognostic Value of NSE and S100B From Serum and Cerebrospinal Fluid in Patients With Spontaneous Subarachnoid Hemorrhage. J Neurosurg Anesthesiol 2010; 22: 21–31.

12. Nash DL, Bellolio MF, Stead LG. S100 as a Marker of Acute Brain Ischemia: A Systematic Review. Neurocrit Care 2008; 8: 301–307.

13. Ali MS, Harmer M, Vaughan R. Serum S100 protein as a marker of cerebral damage during cardiac surgery. Br J Anaesth 2000; 85: 287–298.

14. Tamura A, Imamaki M, Shimura H et al. Release of serum S-100B protein and neuron-specific enolase after off-pump coronary artery bypass grafting with and without intracranial and cervical artery stenosis. Ann Thorac Cardiovasc Surg 2011; 17: 33–38.

15. Mráček J, Holečková I, Lavička P et al. Vliv neuroprotekce na mozkové metabolické parametry při karotické endarterektomii. Čas Lék Čes 2011; 150: 489–493.

16. Rosén H, Rosengren L, Herlitz J et al. Increased Serum Levels of the S-100 Protein Are Associated With Hypoxic Brain Damage After Cardiac Arrest. Stroke 1998; 29: 473–477.

17. Böttiger BW, Möbes S, Glätzer R et al. Astroglial Protein S-100 Is an Early and Sensitive Marker of Hypoxic Brain Damage and Outcome After Cardiac Arrest in Humans. Circulation 2001; 103: 2694–2698.

18. Lippi G, Aloe R, Numeroso F et al. The significance of protein S-100B testing in cardiac arrest patients. Clin Biochem 2011; 44: 567–575.

19. Derwall M, Stoppe C, Brücken D et al. Changes in S-100 protein serum levels in survivors of out-of-hospital cardiac arrest treated with mild therapeutic hypothermia: a prospective, observational study. Crit Care 2009; 13: R58.

20. Shinozaki K, Oda S, Sadahiro T et al. Serum S-100B is superior to neuron-specific enolase as an early prognostic biomarker for neurological outcome following cardiopulmonary resuscitation. Resuscitation 2009; 80: 870–875.