Hostname: page-component-586b7cd67f-2plfb Total loading time: 0 Render date: 2024-11-28T20:42:25.121Z Has data issue: false hasContentIssue false
  • English
  • Français

Circulating Endothelial Cells as Potential Markers of Atherosclerosis

Published online by Cambridge University Press:  02 December 2014

Yang Gao ,
Chunyan Liu ,
Xiangjian Zhang ,
Jian Gao  and
Chunyan Yang
Yang Gao
Affiliation:
Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang The Department of Neurology, The First Hospital of Shi Jia Zhuang City
Chunyan Liu
Affiliation:
The Department of Neurology, The First Hospital of Shi Jia Zhuang City
Xiangjian Zhang*
Affiliation:
Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang
Jian Gao
Affiliation:
The Department of Ophthalmology, The Hospital of Hebei Geriatrics, Hebei, China
Chunyan Yang
Affiliation:
The Department of Neurology, The First Hospital of Shi Jia Zhuang City
*
Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, China.
Rights & Permissions [Opens in a new window]

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.
Background and Purpose:

Vascular endothelial cell (VEC) injury represents a major initiating step in the process of atherosclerosis, which may lead to cerebral infarction. “Circulating endothelial cell” (CEC) is an index of ongoing endothelial injury, while intimal-medial thickness (IMT) detected by sounography was used to evaluate the severity of atherosclerosis. However, to our knowledge, there is no study that investigated the relationship of these two determinations. Our study was designed to address correlate CEC with IMT.

Methods and Results:

The study population consisted of 30 patients with acute cerebral infarction (ACI) and 30 age-and sex-matched volunteers as controls. The CEC counts were determined using Hladovec's method. All subjects underwent a 2-dimensional ultrasound examination of both carotid arteries to measure IMT. CEC counts in ACI group were significantly increased compared with control group (4.88±2.14 cells /0.9μl vs 2.73±1.95/0.9μl, P0.01); IMT in ACI patients was also significantly thicker compared with volunteers (2.72±1.07 mm vs 1.73±0.99 mm, P<0.01). There was positive correlation between CEC counts and maximal carotid artery IMT in both groups (r=0.522, P<0.01 in ACI patients and r=0.395, P<0.05 in healthy volunteers).

Conclusions:

Circulating endothelial cell counts can directly reflect the vascular injury. CEC counts parallel IMT. The CEC may be an independent predictor of cerebral infarction.

Résumé:

RÉSUMÉ:Contexte et objectif:

Une lésion des cellules endothéliales vasculaires constitue une étape majeure initiant le processus de l’athérosclérose et pouvant mener à l’infarctus cérébral. La cellule endothéliale circulante (CEC) est un témoin de la lésion endothéliale active alors que l’épaisseur intima-média (ÉIM) évaluée par ultrasonographie a été utilisée pour déterminer la sévérité de l’athérosclérose. Cependant, à notre connaissance, aucune étude n’a examiné la relation entre ces deux mesures. Le but de notre étude était d’analyser la relation entre la CEC et l’ÉIM.

Méthodes et résultats:

La population étudiée était constituée de 30 patients atteints d’un infarctus cérébral aigu (ICA) et de 30 volontaires appariés pour l’âge et le sexe. Le décompte CEC a été effectué au moyen de la méthode de Hladovec. Tous les sujets ont subi un examen bidimensionnel par ultrasons des deux artères carotides pour mesurer l’ÉIM. Le décompte CEC dans le groupe ICA était significativement plus élevé par rapport à celui du groupe témoin (4,88 ± 2,14 cellules /0,9 μL vs 2,73 ± 1,95/0,9 μL, p < 0,01); l’ÉIM dans le groupe ICA était également significativement plus épais par rapport aux témoins (2,72 ± 1,07 mm vs 1,73 ± 0,99 mm, p < 0,01). Le décompte CEC et l’ÉIM maximale de la carotide étaient corrélés positivement dans les deux groupes (r = 0,522 et p < 0,01 dans le groupe ICA et r = 0,395 et p < 0,05 dans le groupe témoin).

Conclusions:

Le décompte CEC peut refléter directement la lésion vasculaire. Le décompte CEC et l’ÉIM sont en parallèle. Le CEC peut être un prédicteur indépendant de l’infarctus cérébral.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 35 , Issue 5 , November 2008 , pp. 638 - 642
Copyright
Copyright © The Canadian Journal of Neurological 2008

References

1. Segal, MS, Bihorae, A, Koc, M. Circulating edothelial cells: tea leaves for renal disease. Am J Physiol Ren Physiol. 2002; 283(1): F11–19.Google Scholar
2. Takahashi, H, Harker, LA. Measurement of human endothelial cells in whole blood. Thromb Res. 1983; 31(1): 1–12.CrossRefGoogle ScholarPubMed
3. Pignoli, P, Longo, T. Evaluation of atherosclerosis with B-mode ultrasound imaging. J Nucl Med Allied Sci. 1988; 32(3): 166–73.Google Scholar
4. Pignoli, P, Tremoli, E, Poli, A, Oreste, P, Paoletti, R. Intimal plus medial thickness of the arterial wall: a direct measurement with ultrasound imaging. Circulation. 1986; 74(6): 1399–406.Google Scholar
5. Blankenhorn, DH, Rooney, JA, Curry, PJ. Non-invasive assessment of atherosclerosis. Prog Cardiovasc Dis. 1984; 26(4): 295–307.Google Scholar
6. Gulati, R, Lerman, A, Simari, RD. Therapeutic uses of autologous endothelial cells for vascular disease. Clin Sci. 2005; 109(1): 27–37.Google Scholar
7. Zilla, P, Von Oppell, U, Deutsch, M. The endothelium: a key to the future. Carddiovasc Surg. 1993; 8(1): 32–60.Google ScholarPubMed
8. Vanhoutte, PM. Endothelial dysfunction and atherosclerosis. Arch Mal Coeur Vaiss. 1997; 90(6): 9–19.Google Scholar
9. Wu, S, Liu, S, Zhao, R. Effect of longshoudan on serum tumor necrosis factor and circulating endothelial cell levels in acute cerebral infarction patients. Zhongguo Zhong Xi Yi Jie He Za Zhi. 2000; 20(2): 91–3.Google Scholar
10. Rubanyi, GM. The role of endothelium in cardiovascular homeostasis and diseases. J Cardiovasc Pharmacol. 1993; 22 Suppl 4: S1–14.Google Scholar
11. Lüscher, TF. The endothelium as a target and mediator of cardiovascular disease. Eur J Clin Invest. 1993; 23(11): 670–85.CrossRefGoogle ScholarPubMed
12. Ross, R. The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature. 1993; 362(6423): 801–9.Google Scholar
13. Salonen, JT, Salonen, R. Ultrasound B-mode imaging in observational studies of atherosclerotic progression. Circulation. 1993; 87 Suppl 3: II 56–65.Google Scholar
14. Pignoli, P, Tremoli, E, Poli, A Intimal plus medial thickness of the arterial wall: a direct measurement with ultrasound imaging. Circulation. 1986; 74(6): 1399–406.Google Scholar
15. Jackson, VP, Bendick, PJ. Duplex ultrasound screening for carotid atherosclerotic disease in asymptomatic patients. J Ultrasound Med. 1985; 4(8): 411–15.Google Scholar
16. Josse, MO, Touboul, PJ, Mas, JL, Laplane, D, Bousser, MG. Prevalence of asymptomatic internal carotid artery stenosis. Neuroepidemiology. 1987; 6(3): 150–2.CrossRefGoogle ScholarPubMed
17. Van Merode, T, Hick, P, Hocks, PG, Reneman, RS. Serum HDL/total cholesterol ratio and blood pressure in asymptomatic atherosclerotic lesions of the cervical carotid arteries in men. Stroke. 1985; 16(1): 34–8.Google Scholar