Influence of inflammatory agent on structure of carotid atherosclerotic plaques

  • A. Lastas Neurology and Neurosurgery Clinic of Vilnius University Emergency Hospital,
  • E. Barkauskas Neurology and Neurosurgery Clinic of Vilnius University Emergency Hospital,
  • V. Graziene Institute of Experimental and Clinical Medicine of Vilnius University
Keywords: atherosclerosis, carotid stenosis, morphology, immunohistochemistry, inflammatory signs, Chlamydia pneumonfqp

Abstract

The sonographical, morphological, and immunohistochemical Chlamydia pneumoniae characteristics of the atherosclerotic plaques from 200 patients with asymptomatic (A =59) and symptomatic (S=141) courses of carotid stenosis (A/S-1/2.4) were studied. 34 (17 %) homogeneous (HO) or stable and 166 (83%) heterogeneous (HE) or unstable plaques were found morphologically. According to the number of their histopathological signs and prevalence of inflammatory cell type, the plaques were subdivided into 3 HO and 5 HE subtypes with different sonographical characteristics. Complicated plaques, in both A and S patients, have signs of the activation of chronic inflammation (PMN), of phagocytosis (foreign body macrophages), and of atheromatosis (foam cells) all together in HE plaque subtypes (HE2, HE5, HE4) and only of atheromatosis in HO plaques (HO2). Disruptures, intraplaque haemorrhages, and thrombi were associated with the C. pneumoniae, as the inflammatory agent, found in every kind of phagocytes located in the fibrous cap, atheroma, and mainly at the boundary between the fibrous cap and atheroma. The complications strongly correlate with the abundance of C. pneumoniae (p < 0.001) and so with a greater risk of a cerebral ischaemic stroke as in A and in S patients with carotid stenosis. Reliable correlation between C. pneumoniae and the degree of carotid stenosis and plaque thickness (p < 0.06 - 0.07) as well as sufficient correlation between plaque thickness and the disease’s symptomaticity (p < 0.01) were found.

References

Sitzer M, Mueller W, Siebler M et al: Plaque ulceration and lumen thrombus are the main cources of cerebral microemboli is high-grade internal carotid artery stenosis. Stroke 1995; 26:1231-1233.

Geraulakas G, Hobson R.W and Nicolaides. Ultrasonography carotid plaque morphology in predicting stroke risk. British Journal of Surgery 1996, 83, 582-587.

Gurfiskel E, Bozovitch G. Chlamydia pneumoniae: isflam- mation and instability of atherosclerotic plaque. Atherosclerosis 1998, 140:Suppl. 1 s31-s35.

Golledge J, Greeshalgh RM, Davies AH. Symptomatic Carotid Plaque. Stroke 2000, 31: 774-781.

Bauriedel G, Welsch U, Likusgu JA et al: Chlamydia pseu- moniae in koronarem Plaquegewebe: Wermehrter Nachweis bei akutem Korosarsysdrom. DMW, 1999; 124: 375-380.

O’Cossor S, Taylor Ch, Campbell LA, Epsteis S. Potential Infectious Etiologies of Atherosclerosis: Multifactorial Perspective. Emerging Infectious Disease 2001; 7, 5: 78088.

Kadar A, Hortovanyi E, Illyes G, Glasz T. Atherosclerosis and Chlamydia pneumoniae infection. Histopathology 2002; 41 (Suppl 1) 1-63.

Kiechl S, Lorenz E, Reindhl MR et al: Toll-like receptor 4 polymorphism and Atherosclerosis. NEJM, 2002; 347(3): 185-92.

De Boer OJ, Der Wal AC, Houtkamp MA, Ossewaarde JM, Teeling, Becker AE. Unstable atherosclerotic plaques contain T-cells that respond to Chlamydia pneumoniae. Cardio- vasc Res 2000, 48(3): 402-8.

Kalman S, Mitchell W, Marathe R, Lammel C, Fan J, Hyman RW, Olinger L, Grimwood J, Davis RW, Stephens R. Comparative genomes of Chlamydia pneumoniae and C. trachomatis. Nature 2002; 21(4): 385-389.

Matturri L, Cazzullo A, Turcosi P, Roscorosi L, Grasa D, Milei J. Inflammatory cells, apoptosis and Chlamydia pseu- moniae infection in atherosclerosis. Int J Cardiol 2000; 75 (1) : 23-33.

Stary HC, Chandler AB, Dissmore RE et al: A definition of advanced types of atherosclerotic lesions and histological classification of atherosclerosis. A Report from Committee on vascular lesions of the Council of Atherosclerosis, American Heart Association. Circulation, 1995; 92; 135574.

Rothwell PM, Gibson R, Warlow CP. Interrelation between plaque surface morphology and degree of stenosis on carotid angiograms and the risk of ischemic stroke in patients with symptomatic carotid stenosis. On behalf of the Euro- peas Carotid Surgery Trialists’ Collaborative Group. Stroke; 31: 615-621.

Shah PK. Plaques disruption and thrombosis: potential role of inflammation and infection Cardiol Rev 2000; 8(1): 3139.

Siscovick DS, Schwartz SM, Corey L, Graystose JT, Ashley R, Wang SP, Psaty BM, Tracy RP, Kuller LH, Kronmal RA. Chlamydiae pneumoniae, herpes simplex virus type 1, and cytomegalovirus and incident of myocardial infarction and coronar heart disease death in older adults: the Cardiovascular Health Study. Circulation 2000; 102(19), 2335-40.

Danesh J, Whincup P, Walker M, Lennon L, Thomson A, Appleby P, Gallimore JR, Pepys MB. Low grade isflamma- tion and coronary heart disease: prospective study and up- tatet meta-asalyses. MBJ 2000; 321, (7255), 199-204.
Published
2016-05-31
How to Cite
Lastas, A., Barkauskas, E., & Graziene, V. (2016). Influence of inflammatory agent on structure of carotid atherosclerotic plaques. Bulletin of the International Scientific Surgical Association, 1(3), 58-60. Retrieved from http://surgjournal.ru/index.php/BISSA/article/view/121
Section
Original Articles