Predictive Value of Ultrasensitive C-Reactive Protein in Ischemic Cerebrovascular Accident and Its Relation to Atherosclerosis of Carotid Arteries

Czech version

Authors: I. Vlachová ¹; R. Herzig ¹; H. Vaverková ²; D. Novotný ³; V. Krčová⁴; A. Bártková ¹; B. Křupka ¹; D. Šaňák ¹; K. Urbánek ¹ ; M. Budíková⁵; E. Sovová⁶; P. Kaňovský ¹
Authors‘ workplace: Neurologická klinika LF UP a FN v Olomouci ¹; III. Interní klinika LF UP a FN v Olomouci ²; Oddělení klinické biochemie FN v Olomouci ⁴Hemato-onkologická klinika LF UP a FN v Olomouci ⁵Klinika nukleární medicíny LF UP v FN v Olomouc ⁶I. interní klinika LF UP a FN v Olomouci ³
Published in: Cesk Slov Neurol N 2007; 70/103(1): 49-55
Category: Original Paper

Vytvořeno za podpory grantu IGA MZ ČR NF7492-3/2003.

Overview

Introduction:
Atherosclerosis plays an essential role in the etiopathogenesis of ischemic cerebrovascular accident (iCVA). A chronic inflammatory process shares significantly in its development. Among the inflammation indices, ultrasensitive C-reactive protein (hsCRP) has been considered an independent risk factor of ictus, predictor of a more severe affection, relapses as well as other cardiovascular disorders. The research aimed at judging the effects of hsCRP on the severity of iCVA in the acute phase, the relation to the iCVA subtypes, atherosclerosis of carotid arteries, and its possible predictive value.

A set of patients and methods:
The plasma hsCRP levels were determined in 110 probands (66 men, 44 women, mean age 61.5 ± 9.9 years) in the acute phase of iCVA. The accident severity was evaluated according to NIHSS criteria. A set was divided, according to etiology, into three groups (atherothrombotic – AT, embolic arterio-arterial – EA, cardioembolic – EC ictuses) and according to the degree of atherosclerotic affection of carotid arteries (≤ 30 %, 30 – 69 %, ≥ 70 %). Three months after the acute phase of the disease hsCRP was examined in 78 probands (44 men, 34 women). A control set (CS) consisted of 58 healthy subjects (32 men, 26 women, mean age 57.1 ± 9.9 years).

Results:
If compared with CS, higher levels of hsCRP were revealed in: (1) probands in the acute phase (p < 0.0001), (2) patients with NIHS < 10 (p = 0.001) as well as NIHSS ≥ 10 (p < 0.0001), (3) subtype of AT ictus (p < 0.0001), less in EC (p = 0.01) and EA (p = 0.01), (4) degrees of carotid stenoses ≤ 30 % (p = 0.008), 30 – 69 % (p = 0.004) and ≥ 70 % (p = 0.001), (5) probands after three months (p < 0.0001). No difference was found with regard to the Glasgow Outcome Scale (GOS).

Conclusion:
The study has confirmed the connection of higher hsCRP levels in the acute phase of iCVA and severity of a neurological deficit as well as that of higher hsCRP levels and carotid artery atherosclerosis.

Key-words:
ischemic ictus, atherosclerosis, ultrasensitive CRP, carotid stenosis

Sources

1. Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis. Circulation 2002; 105: 1135-43.

2. Dvořáková A, Poledne R. Ultrasenzitivně měřený C-reaktivní protein – nový parametr kardiovaskulárního rizika. Vnitř lék 2004; 11: 852-7.

3. Ridker PM, Buring JE, Shih J et al. Prospective study of C-reactive protein and the risk of future cardiovascular events among apparently healthy woman. Ciculation 1998; 98: 731-3.

4. Rost NS, Wolf PA, Kase CS at al. Plasma concentration of C-reactive protein and risk of ischemic stroke and transient ischemic attack: the Framingham study. Stroke 2001; 32: 2575-9.

5. Van Exel E, Gussekloo J, de Crean AJ et al. Inflammation and stroke: the Leiden 85-plus Study. Stroke 2002; 33: 1135-8.

6. Di Napoli M, Papa F, Bocola V. C-reactive protein in ischemic stroke an independent prognostic factor. Stroke 2001; 32: 917-24.

7. Anuk T, Assayag EB, Rotstein R et al. Prognostic implications of admission inflammatory profile in acute ischemic neurological events. Acta Neurol Scand 2002; 106: 196-9.

8. Van DM, I, De Maat MP, Hak AE et al. C-reactive protein predicts progression of atherosclerosis measured at various sites in the arterial tree: the Rotterdam Study. Stroke 2002; 33: 2750-5.

9. Pearson TA, Mensah GA, Alexander RW et al. Markers od inflammation and cardiovascular disease: application to clinical and public healt practice: a statement for healtcare professionals from the Centers for Disease Control and Prevention and the Am Heart Association. Circulation 2003; 107: 499-511.

10. Mendal MA, Patel P, Ballam L et al. C-reactive protein and its relation to cardiovascular risk factors: a population based cross-sectional study. BMJ 1996; 312: 1061-5.

11. Ridker PM, Buring JE, Cook NR et al. C-reactive protein, the metabolic syndrome and risk of incident cardiovascular events: an 8-year follow-up of 14 719 initially healthy American woman. Circulation 2003; 107: 391-7.

12. Cífková R. Rizikové faktory kardiovaskulárních onemocnění v české populaci [habilitace]. Praha: Karlova Universita 2003.

13. Erren M, Reinecke H, Junker R et al. Systemic inflammatory parameters in patients with atherosclerosis of the coronary and peripheral arteries. Arterioscler Tromb Vasc Biol 1999; 19: 2355-63.

14. Solomon DH, Karlson EW, Rimm EB et al. Cardiovascular morbidity and mortality in woman diagnosed with rheumatoid arthritis. Circulation 2003; 107: 1202-7.

15. Manzi S, Meilahn EN, Rairie JE et al. Age-specific rates of myocardial infarction and angina in woman with systemic lupus erytematosus: comparison with the Framingham Study. Am J Epidemiol 1997; 145: 408-15.

16. Yudkin JS, Stenhower CD, Emeis JJ et al. C-reactive protein in healthy subjects: associacions with obesity, insulin resistence, and endotelial dysfunction: a potential role for cytokines originating from adipose tissue? Arterioscler Thromb Vasc Biol 1999; 19: 972-8.

17. Baumann H, Morella KK, Wong GH. TNF-alpha, IL-1 beta and hepatocyte growth factor cooperate in stimulating specific acute phase plasma protein genes in rat hepatoma cells. J Immunol 1993; 151: 4248-57.

18. Kuneš P. Krejsek J. Ateroskleróza a přirozené autoprotilátky. 2. část: Přirozené autoprotilátky a C-reaktivní protein. Cor Vasa 2004; 46(10): 484-91.

19. Marquardt L, Ruf A, Mansmann U et al. Inflammatory response after acute ischemic stroke. J Neurol Aci 2005; 236(1-2): 65-71.

20. Emsley HC, Smith CJ, Gavin CM et al. An early and substained peripheral inflammatory response in acute ischaemic stroke: relationship with infection and atherosclerosis. J Neuroimmunol 2003; 139: 93-101.

21. Beamer NB, Coull BM, Clark WM et al. Persistent inflammatory response in stroke survivors. Neurology 1998; 50: 1722-8.

22. Chlumský J, Holá D, Kratochvílová R. Zánětlivé parametry u nemocných s cévní mozkovou příhodou. Vnitř lék 2002; 10: 956-8.

23. Smith CJ, Emsley HC, GavinCM et al. Peak plasma interleukin-6 and other peripheral markers of inflammation in the first week od ischaemic stroke correlate with brain volume, stroke severity and long-term outcome. BMC Neurol 2004; 4:2.

24. Chapman CM, Beilby JP, McQuillan BM et al. Monocyte count, bat not C-reactive protein or interleukin-6, is as independent risk marker for subclinical carotid atherosclerosis. Stroke 2004; 35: 1619-24.

25. Cao JJ, Manolio TA,Psaty BM et al. C-reactive protein, carotid intima-media thickeness, and incidence of ischemic stroke in the elderly: the Cardiovascular Health Study. Circulation 2003; 108: 166-70.

26. Sitzer M, Markus HS, Mendal MA et al. C-reactive protein and carotid intimal media thickness in a community population. J Cardiovasc Risk 2002; 9: 97-103.

27. Rerkasem K, Sherman CP, Williams JA et al. C-reactive protein is elevated in symptomatic compared with asymptomatic patients with carotid artery disease. Eur J Vasc Endovasc Surg 2002; 23: 505-9.

28. Di Napoli M, Schwaninger M, Cappelli R et al. Evaluation of C-reactive protein measurment for assesing the risk and prognosis in ischemic stroke. A statement for health care professionals from the CRP pooling project members. Stroke 2005; 36: 1316-29.