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2014 | 14 | 1 | 43-53
Article title

Tworzenie blaszki miazdzycowej, jej destabilizacja i diagnostyka

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EN
The formation of atherosclerotic plaque, its destabilisation and diagnostics
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Abstracts
EN
According to the established medical knowledge, the atheromatous lesions occur in the arteries of large and medium diameter. Their presence in the aorta, arteries of extremities as well as extracerebral and coronal arteries is clinically relevant. The evolution of atherosclerotic plaques probably starts in the prenatal development, what may be proved by the presence of the fatty streaks in endothelium of coronal arteries in some newborns. Then it evolves through lipid accumulation, media inflammatory response, vasa vasorum proliferation, fibrination and calcification of plaques. Researches proved that the matter of atherosclerosis is exaggerated inflammatory proliferative reaction to the arterial wall damage. The oxidative stress phenomenon and infections with common pathogens play an undoubtful role in this process. Ultimately the direct damage is an effect of immune response cells infiltration and secretion of cytokines and proinflammatory factors. Among the cells of immune system responsible for formation and development of atheromatous plaque are considered: macrophages, dendritic cells, T and B lymphocytes, monocytes. Attention was also paid to the inflammatory mediators and growth factors. Scientist are interested in unstable atherosclerotic plaque and accompanying inflammatory process within the artery wall for a long time. Meanwhile, there are conducted researches on inflammation markers underlying the destabilisation of plaques. Revealing the role of these cells in evolution of atherosclerosis would enable more complex understanding of the mechanism of lesions development. Then it would facilitate an introduction of the new and upgraded methods of treatment and prevention. Also the progress of imaging examinations is meaningful for diagnostics and treatment. It is contributory to the choice of therapeutic strategy and assessment of surgical intervention urgency. In the clinical practice there are recognized standards of imaging the morphology of atheromatous plaque. Development of diagnostics aims the indirect assessment of possible dynamics of lesions progression. Targeting the complex plaque analysis is based on excellence of established standards such as ultrasound examination or computed tomography.
PL
Według powszechnej wiedzy medycznej zmiany miażdżycowe dotyczą naczyń tętniczych dużego i średniego kalibru. Kluczowe kliniczne znaczenie ma ich powstawanie w aorcie i tętnicach kończyn dolnych, tętnicach domózgowych czy tętnicach wieńcowych. Ewolucja zmian miażdżycowych rozpoczyna się prawdopodobnie już w życiu płodowym, czego dowodem może być istnienie u niektórych noworodków pasm tłuszczowych (fatty streaks) w śródbłonku naczyń wieńcowych. Obejmuje ona kolejno etapy gromadzenia lipidów, odpowiedź immunologiczną błony środkowej, proliferację vasa vasorum, włóknienie oraz wapnienie blaszek. Badania naukowe wykazały, iż istotą miażdżycy jest nadmierna zapalno-proliferacyjna odpowiedź na uszkodzenie ściany tętnicy. Niekwestionowaną rolę w tym procesie odgrywają zjawisko stresu oksydacyjnego oraz infekcje powszechnie występującymi patogenami. Jednak bezpośrednie uszkodzenie jest efektem napływu komórek odpowiedzi immunologicznej oraz wydzielanych przez nie czynników zapalnych. Wśród komórek układu immunologicznego zaangażowanych w proces tworzenia i rozwoju blaszki miażdżycowej na szczególną uwagę zasługują m.in. makrofagi, komórki dendrytyczne, limfocyty T i B oraz monocyty. Zwrócono również uwagę na mediatory zapalne i czynniki wzrostu. Od dawna naukowcy zainteresowani są niestabilną blaszką miażdżycową i związanym z nią toczącym się procesem zapalnym w obrębie ściany naczynia. W chwili obecnej trwają poszukiwania markerów zapalnych podłoża destabilizacji blaszek miażdżycowych. Poznanie roli tych komórek w procesach rozwoju miażdżycy w przyszłości pozwoliłoby na szersze oraz dogłębne zrozumienie mechanizmu powstawania blaszek miażdżycowych. To z kolei daje możliwość szybkiego wprowadzenia nowych i udoskonalonych metod leczenia tej choroby lub spowalniania jej rozwoju. Nie bez znaczenia dla diagnostyki i leczenia pozostaje także rozwój badań obrazowych. Umożliwia on przede wszystkim wybór strategii terapeutycznej i ocenę pilności interwencji chirurgicznej. Dotychczas podstawową rolę odgrywały badania określające hemodynamiczną istotność zmian. W praktyce klinicznej funkcjonują ugruntowane standardy obrazowania morfologii blaszki miażdżycowej. Celem diagnostyki jest jednak pośrednie określanie możliwej dynamiki jej zmian. Dąży się do coraz bardziej wnikliwej analizy zmian, doskonaląc takie uznane metody, jak ultrasonografia czy tomografia komputerowa.
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Year
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14
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1
Pages
43-53
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References
  • 1. Hamby R.I., Tabrah F., Wisoff B.G., Hartstein M.L.: Coronary artery calcification: clinical implications and angiographic correlates. Am. Heart J. 1974; 87: 565-570.
  • 2. Naghavi M., Libby P., Falk E. et al.: From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part I. Circulation 2003; 108: 1664-1672.
  • 3. Schmermund A., Erbel R.: Unstable coronary plaque and its relation to coronary calcium. Circulation 2001; 104: 1682-1687.
  • 4. Naghavi M., Libby P., Falk E. et al.: From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part II. Circulation 2003; 108: 1772-1778.
  • 5. Maseri A., Fuster V: Is there a vulnerable plaque? Circulation 2003; 107: 2068-2071.
  • 6. Ross R.: Atherosclerosis - an inflammatory disease. N. Engl. J. Med. 1999; 340: 115-126.
  • 7. Pearson T.A., Mensah G.A., Alexander R.W. et al.; Centers for Disease Control and Prevention; American Heart Association: Markers of inflammation and cardiovascular disease: application to clinical and public health practice: a statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association. Circulation 2003; 107: 499-511.
  • 8. Libby P., Ridker P.M.: Inflammation and atherosclerosis: role of Creactive protein in risk assessment. Am. J. Med. 2004: 116 suppl. 6A: 9S-16S.
  • 9. Ross R.: Rous-Whipple Award Lecture. Atherosclerosis: a defense mechanism gone awry. Am. J. Pathol. 1993; 143: 987-1002.
  • 10. Członkowska A., Gromadzka G.: Związek czynników immunologicznych z etiopatogenezą i przebiegiem klinicznym udaru mózgu. Neurol. Neurochir. Pol. 2000; 34 supl.: 13-26.
  • 11. Kaźmierski R., Kozubski W: Wpływ zakażenia bakterią Chlamydia pneumoniae na rozwój miażdżycy tętnic domózgowych. Neurol. Neurochir. Pol. 2002; 36: 131-142.
  • 12. Kuvin J.T., Kimmelstiel C.D.: Infectious causes of atherosclerosis. Am. Heart J. 1999; 137: 216-226.
  • 13. Libby P., Egan D., Skarlatos S.: Roles of infectious agents in atherosclerosis and restenosis: an assessment of the evidence and need for future research. Circulation 1997; 96: 4095-4103.
  • 14. Ezzahiri R., Stassen F.R.M., Kurvers H.A.J.M. et al.: Chlamydia pneumoniae infection induces an unstable atherosclerotic plaque phenotype in LDL-receptor, ApoE double knockout mice. Eur. J. Vasc. Endovasc. Surg. 2003; 26: 88-95.
  • 15. Kalimo H., Kaste M., Haltia M.: Vascular diseases. In: Graham D.I., Lantos P.L. (eds.): Greenfield’s Neuropathology. 7th ed., Arnold, London 2002: 281-355.
  • 16. Weissberg P.: Mechanisms modifying atherosclerotic disease -from lipids to vascular biology. Atherosclerosis 1999; 147 suppl. 1: S3-S10.
  • 17. Beręsewicz A., Kurzelewski M.: Patofizjologia ostrych zespołów wieńcowych. Medipress Kardiologia 2001; 8: 3-11.
  • 18. Filipiak K.J., Opolski G.: Patofizjologia ostrych zespołów wieńcowych. In: Opolski G., Filipiak K.J., Poloński L. (eds.): Ostre zespoły wieńcowe. 1st ed., Urban & Partner, Wrocław 2002: 14-31.
  • 19. de Boer O.J., van der Wal A.C., Teeling P., Becker A.E.: Leucocyte recruitment in rupture prone regions of lipid-rich plaques: a prominent role for neovascularization? Cardiovasc. Res. 1999; 41: 443-449.
  • 20. Jeziorska M., Woolley D.E.: Local neovascularization and cellular composition within vulnerable regions of atherosclerotic plaques of human carotid arteries. J. Pathol. 1999; 188: 189-196.
  • 21. Anwar A., Zahid A.A., Scheidegger K.J. et al.: Tumor necrosis factor-a regulates insulin-like growth factor-1 and insulin-like growth factor binding protein-3 expression in vascular smooth muscle. Circulation 2002; 105: 1220-1225.
  • 22. Gupta S., Pablo A.M., Jiang X. et al.: IFN-gamma potentiates atherosclerosis in ApoE knock-out mice. J. Clin. Invest. 1997; 99: 2752-2761.
  • 23. Libby P., Hansson G.K.: Involvement of the immune system in human atherogenesis: current knowledge and unanswered questions. Lab. Invest. 1991; 64: 5-15.
  • 24. Nakajima T., Schulte S., Warrington K.J. et al.: T-cell-mediated lysis of endothelial cells in acute coronary syndromes. Circulation 2002; 105: 570-575.
  • 25. Liuzzo G., Goronzy J.J., Yang H. et al.: Monoclonal T-cell proliferation and plaque instability in acute coronary syndromes. Circulation 2000; 101: 2883-2888.
  • 26. Raines E.W., Rosenfeld M.E., Ross R.: The role of macrophages. In: Fuster V., Ross R., Topol E.J. (eds.): Atherosclerosis and Coronary Artery Disease. 1st ed., Lippincott-Raven, Philadelphia 1996: 539-555.
  • 27. Hansson G.K., Jonasson L., Seifert PS., Stemme S.: Immune mechanisms in atherosclerosis. Arteriosclerosis 1989; 9: 567-578.
  • 28. Lamb D.J., El-Sankary W., Ferns G.A.A.: Molecular mimicry in atherosclerosis: a role for heat shock proteins in immunisation. Atherosclerosis 2003; 167: 177-185.
  • 29. Lombardo A., Coli S., Natale L., Crea F.: Carotid plaque inflammation in a patient with unstable angina. Ital. Heart J. 2003; 4: 125-128.
  • 30. Silva J.A., White C.J.: Plaque instability in peripheral vessels. Prog. Cardiovasc. Dis. 2002; 44: 429-436.
  • 31. Espinola-Klein C., Rupprecht H.J., Blankenberg S. et al.: Manifestationen der Atherosklerose in verschiedenen Gefäß-regionen. Gemeinsamkeiten und Unterschiede hinsichtlich Epidemiologie, Ätiologie und Prognose. Med. Klin. 2002: 97: 221-228.
  • 32. Davies M.J.: Stability and instability: two faces of coronary atherosclerosis. The Paul Dudley White Lecture 1995. Circulation 1996; 94: 2013-2020.
  • 33. Davies M.J., Thomas A.: Thrombosis and acute coronary-artery lesions in sudden cardiac ischemic death. N. Engl. J. Med. 1984; 310: 1137-1140.
  • 34. Lammie G.A., Sandercock P.A., Dennis M.S.: Recently occluded intracranial and extracranial carotid arteries. Relevance of the unstable atherosclerotic plaque. Stroke 1999; 30: 1319-1325.
  • 35. Hennerici M.G.: The unstable plaque. Cerebrovasc. Dis. 2004; 17 suppl. 3: 17-22.
  • 36. Loftus I.M., Naylor A.R., Bell P.R., Thompson M.M.: Plasma MMP-9 - a marker of carotid plaque instability. Eur. J. Vasc. Endovasc. Surg. 2001; 21: 17-21.
  • 37. Engström G., Lind P., Hedblad B. et al.: Effects of cholesterol and inflammation-sensitive plasma proteins on incidence of myocardial infarction and stroke in men. Circulation 2002; 105: 2632–2637.
  • 38. Alvarez Garcia B., Ruiz C., Chacon P. et al.: High-sensitivity Creactive protein in high-grade carotid stenosis: risk marker for unstable carotid plaque. J. Vasc. Surg. 2003; 38: 1018-1024.
  • 39. Ridker P.M.: Inflammatory biomarkers, statins, and the risk of stroke: cracking a clinical conundrum. Circulation 2002; 105: 2583-2585.
  • 40. Holven K.B., Halvorsen B., Schulz H. et al.: Expression of matrix metalloproteinase-9 in mononuclear cells of hyperhomo-cysteinaemic subjects. Eur. J. Clin. Invest. 2003; 33: 555-560.
  • 41. Schmitz S.A.: Eisenoxidverstärkte MRT inflammatorischer atherosklerotischer Läsionen: Übersicht experimenteller und erster klinischer Ergebnisse. Rofo 2003; 175: 469–476.
  • 42. Tearney G.J., Yabushita H., Houser S.L. et al.: Quantification of macrophage content in atherosclerotic plaques by optical coherence tomography. Circulation 2003; 107: 113-119.
  • 43. Carbone G.L., Mauriello A., Christiansen M. et al.: [Unstable carotid plaque: biochemical and cellular marker of vulnerability]. Ital. Heart J. Suppl. 2003; 4: 398-406.
  • 44. Falk E., Shah P.K., Fuster V: Coronary plaque disruption. Circulation 1995; 92: 657-671.
  • 45. van der Wal A.C., Becker A.E., van der Loss C.M., Das P.K.: Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology. Circulation 1994; 89: 36-44.
  • 46. Stary H.C., Chandler A.B., Glagov S. et al.: A definition of initial, fatty streak, and intermediate lesions of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Circulation 1994; 89: 2462-2478.
  • 47. Stary H.C., Chandler A.B., Dinsmore R.E. et al.: A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Circulation 1995; 92: 1355-1374.
  • 48. Stary H.C.: Natural history and histological classification lesions: an update. Arterioscler. Thromb. Vasc. Biol. 2000; 20: 1177-1178.
  • 49. Wexler L., Brundage B., Crouse J. et al.: Coronary artery calcification: pathophysiology, epidemiology, imaging methods, and clinical implications. A statement for health professionals from the American Heart Association. Writing Group. Circulation 1996; 94: 1175-1192.
  • 50. Tintut Y., Demer L.L.: Recent advances in multifactorial regulation of vascular calcification. Curr. Opin. Lipidol. 2001; 12: 555-560.
  • 51. Boström K., Watson K.E., Stanford W.P., Demer L.L.: Atherosclerotic calcification: relation to developmental osteogenesis. Am. J. Cardiol. 1995; 75: 88B-91B.
  • 52. Tanimura A., McGregor D.H., Anderson H.C.: Calcification in atherosclerosis. I. Human studies. J. Exp. Pathol. 1986; 2: 261-273.
  • 53. Anderson H.C.: Mechanism of mineral formation in bone. Lab. Invest. 1989; 60: 320-330.
  • 54. Hirota S., Imakita M., Kohri K. et al.: Expression of osteopontin messenger RNA by macrophages in atherosclerotic plaques. A possible association with calcification. Am. J. Pathol. 1993: 143:1003-1008.
  • 55. Rekhter M.D., Zhang K., Narayanan A.S. et al.: Type I collagen gene expression in human atherosclerosis. Localization to specific plaque regions. Am. J. Pathol. 1993; 143: 1634-1648.
  • 56. Fitzpatrick L.A., Severson A., Edwards W.D., Ingram R.T.: Diffuse calcification in human coronary arteries. Association of osteopontin with atherosclerosis. J. Clin. Invest. 1994; 94: 1597-1604.
  • 57. Fleet J.C., Hock J.M.: Identification of osteocalcin mRNA in nonosteoid tissue of rats and humans by reverse transcription-polymerase chain reaction. J. Bone Miner. Res. 1994; 9: 1565-1573.
  • 58. Shanahan C.M., Proudfoot D., Tyson K.L. et al.: Expression of mineralisation-regulating proteins in association with human vascular calcification. Z. Kardiol. 2000; 89 suppl. 2: 63-68.
  • 59. Berliner J.A., Navab M., Fogelman A.M. et al.: Atherosclerosis: basic mechanisms. Oxidation, inflammation, and genetics. Circulation 1995; 91: 2488-2496.
  • 60. Pawlikowski M., Pfitzner R., Wachowiak J.: Mineralization (calcification) of coronary arteries. Mater. Med. Pol. 1994; 26: 3-8.
  • 61. Proudfoot D., Shanahan C.M.: Biology of calcification in vascular cells: intima versus media. Herz 2001; 26: 245-251.
  • 62. Proudfoot D., Skepper J.N., Hegyi L. et al.: The role of apoptosis in the initiation of vascular calcification. Z. Kardiol. 2001; 90 suppl. 3: 43-46.
  • 63. Mautner G.C., Mautner S.L., Froehlich J. et al.: Coronary artery calcification: assessment with electron beam CT and histomorphometric correlation. Radiology 1994; 192: 619-623.
  • 64. Hansson G.K.: Inflammation, atherosclerosis, and coronary artery disease. N. Engl. J. Med. 2005; 352: 1685-1695.
  • 65. Weber C., Zernecke A., Libby P.: The multifaceted contributions of leukocyte subsets to atherosclerosis: lessons from mouse models. Nat. Rev. Immunol. 2008; 8: 802-815.
  • 66. Asahara T, Murohara T, Sullivan A. et al.: Isolation of putative progenitor endothelial cells for angiogenesis. Science 1997; 275: 964-967.
  • 67. Simper D., Stalboerger P.G., Panetta C.J. et al.: Smooth muscle progenitor cells in human blood. Circulation 2002; 106: 1199-1204.
  • 68. Urbich C., Dimmeler S.: Endothelial progenitor cells: characterization and role in vascular biology. Circ. Res. 2004; 95: 343-353.
  • 69. Zengin E., Chalajour F., Gehling U.M. et al.: Vascular wall resident progenitor cells: a source for postnatal vasculogenesis. Development 2006; 133: 1543-1551.
  • 70. Hristov M., Weber C.: Endothelial progenitor cells: characterization, pathophysiology, and possible clinical relevance. J. Cell. Mol. Med. 2004; 8: 498-508.
  • 71. Hillebrands J.L., Klatter F.A., Rozing J.: Origin of vascular smooth muscle cells and the role of circulating stem cells in transplant atherosclerosis. Arterioscler. Thromb. Vasc. Biol. 2003; 23: 380-387.
  • 72. Sata M., Saiura A., Kunisato A. et al.: Hematopoietic stem cells differentiate into vascular cells that participate in the pathogenesis of atherosclerosis. Nat. Med. 2002; 8: 403-409.
  • 73. Sugiyama S., Kugiyama K., Nakamura S. et al.: Characterization of smooth muscle-like cells in circulating human peripheral blood. Atherosclerosis 2006; 187: 351-362.
  • 74. Zoll J., Fontaine V, Gourdy P. et al.: Role of human smooth muscle cell progenitors in atherosclerotic plaque development and composition. Cardiovasc. Res. 2008; 77: 471-480.
  • 75. Sugiyama S., Kugiyama K., Aikawa M. et al.: Hypochlorous acid, a macrophage product, induces endothelial apoptosis and tissue factor expression: involvement of myeloperoxidase-mediated oxidant in plaque erosion and thrombogenesis. Arterioscler. Thromb. Vasc. Biol. 2004; 24: 1309-1314.
  • 76. Zernecke A., Bot I., Djalali-Talab Y. et al.: Protective role of CXC receptor 4/CXC ligand 12 unveils the importance of neutrophils in atherosclerosis. Circ. Res. 2008; 102: 209-217.
  • 77. Haley K.J., Lilly C.M., Yang J.H. et al.: Overexpression of eotaxin and the CCR3 receptor in human atherosclerosis: using genomic technology to identify a potential novel pathway of vascular inflammation. Circulation 2000; 102: 2185-2189.
  • 78. Bobryshev Y.V: Dendritic cells in atherosclerosis: current status of the problem and clinical relevance. Eur. Heart J. 2005; 26: 1700-1704.
  • 79. Yilmaz A., Lochno M., Traeg F. et al.: Emergence of dendritic cells in rupture-prone regions of vulnerable carotid plaques. Atherosclerosis 2004; 176: 101-110.
  • 80. Han J.W, Shimada K., Ma-Krupa W. et al.: Vessel wall-embedded dendritic cells induce T-cell autoreactivity and initiate vascular inflammation. Circ. Res. 2008; 102: 546-553.
  • 81. Niessner A., Shin M.S., Pryshchep O. et al.: Synergistic proinflammatory effects of the antiviral cytokine interferon-alpha and Toll-like receptor 4 ligands in the atherosclerotic plaque. Circulation 2007; 116: 2043-2052.
  • 82. Niessner A., Sato K., Chaikof E.L. et al.: Pathogen-sensing plasmacytoid dendritic cells stimulate cytotoxic T-cell function in the atherosclerotic plaque through interferon-a. Circulation 2006; 114: 2482-2489.
  • 83. Jeziorska M., McCollum C., Woolley D.E.: Mast cell distribution, activation, and phenotype in atherosclerotic lesions of human carotid arteries. J. Pathol. 1997; 182: 115-122.
  • 84. Kovanen P.T.: Mast cells: multipotent local effector cells in atherothrombosis. Immunol. Rev. 2007; 217: 105-122.
  • 85. Kovanen P.T, Kaartinen M., Paavonen T: Infiltrates of activated mast cells at the site of coronary atheromatous erosion or rupture in myocardial infarction. Circulation 1995; 92: 1084-1088.
  • 86. Lee-Rueckert M., Kovanen P.T.: Mast cell proteases: physiological tools to study functional significance of high density lipoproteins in the initiation of reverse cholesterol transport. Atherosclerosis 2006; 189: 8-18.
  • 87. Sun J., Sukhova G.K., Wolters P.J. et al.: Mast cells promote atherosclerosis by releasing proinflammatory cytokines. Nat. Med. 2007; 13: 719-724.
  • 88. Furukawa Y., Becker G., Stinn J.L. et al.: Interleukin-10 (IL-10) augments allograft arterial disease: paradoxical effects of IL-10 in vivo. Am. J. Pathol. 1999; 155: 1929-1939.
  • 89. Mallat Z., Besnard S., Duriez M. et al.: Protective role of interleukin-10 in atherosclerosis. Circ. Res. 1999; 85: e17-e24.
  • 90. Schulte S., Sukhova G.K., Libby P.: Genetically programmed biases in Th1 and Th2 immune responses modulate atherogenesis. Am. J. Pathol. 2008; 172: 1500-1508.
  • 91. Vanderlaan P.A., Reardon C.A.: Thematic review series: the immune system and atherogenesis. The unusual suspects: an overview of the minor leukocyte populations in atherosclerosis. J. Lipid Res. 2005; 46: 829-838.
  • 92. Moos M.P., John N., Gräbner R. et al.: The lamina adventitia is the major site of immune cell accumulation in standard chow-fed apolipoprotein E-deficient mice. Arterioscler. Thromb. Vasc. Biol. 2005; 25: 2386-2391.
  • 93. Caligiuri G., Nicoletti A., Poirier B., Hansson G.K.: Protective immunity against atherosclerosis carried by B cells of hyper-cholesterolemic mice. J. Clin. Invest. 2002; 109: 745-753.
  • 94. Swirski F.K., Pittet M.J., Kircher M.F. et al.: Monocyte accumulation in mouse atherogenesis is progressive and proportional to extent of disease. Proc. Natl Acad. Sci. USA 2006; 103: 10340-10345.
  • 95. Swirski F.K., Libby P., Aikawa E. et al.: Ly-6Chi monocytes dominate hypercholesterolemia-associated monocytosis and give rise to macrophages in atheromata. J. Clin. Invest. 2007; 117: 195-205.
  • 96. Tacke F., Alvarez D., Kaplan TJ. et al.: Monocyte subsets differentially employ CCR2, CCR5, and CX3CR1 to accumulate within atherosclerotic plaques. J. Clin. Invest. 2007; 117: 185-194.
  • 97. Hansson G.K., Libby P.: The immune response in atherosclerosis a double-edged sword. Nat. Rev. Immunol. 2006; 6: 508-519.
  • 98. Jóźwicka M., Głąbiński A.: Patogeneza rozwoju blaszki miażdżycowej w tętnicach szyjnych. Aktualn. Neurol. 2011; 11: 265-273.
  • 99. Ait-Oufella H., Salomon B.L., Potteaux S. et al.: Natural regulatory T cells control the development of atherosclerosis in mice. Nat. Med. 2006; 12: 178-180.
  • 100. Mallat Z., Gojova A., Brun V et al.: Induction of a regulatory T cell type 1 response reduces the development of atherosclerosis in apolipoprotein E-knockout mice. Circulation 2003; 108: 1232-1237.
  • 101. Mor A., Planer D., Luboshits G. et al.: Role of naturally occurring CD4+CD25+ regulatory T cells in experimental atherosclerosis. Arterioscler. Thromb. Vasc. Biol. 2007; 27: 893-900.
  • 102. Steffens S., Burger F., Pelli G. et al.: Short-term treatment with anti-CD3 antibody reduces the development and progression of atherosclerosis in mice. Circulation 2006; 114: 1977-1984.
  • 103. Sasaki N., Yamashita T., Takeda M. et al.: Oral anti-CD3 antibody treatment induces regulatory T cells and inhibits the development of atherosclerosis in mice. Circulation 2009; 120: 1996-2005.
  • 104. Tanigawa T., Iso H., Yamagishi K. et al.: Association of lymphocyte sub-populations with clustered features of metabolic syndrome in middle-aged Japanese men. Atherosclerosis 2004; 173: 295-300.
  • 105. Mintz G.S., Nissen S.E., Anderson WD. et al. American College of Cardiology Clinical Expert Consensus Document on Standards for Acquisition, Measurement and Reporting of Intravascular Ultrasound Studies (IVUS). A report of the American College of Cardiology Task Force on Clinical Expert Consensus Documents. J. Am. Coll. Cardiol. 2001; 37: 1478-1492.
  • 106. Yamagishi M., Terashima M., Awano K. et al.: Morphology of vulnerable coronary plaque: insights from follow-up of patients examined by intravascular ultrasound before an acute coronary syndrome. J. Am. Coll. Cardiol. 2000; 35: 106-111.
  • 107. Maehara A., Mintz G.S., Bui A.B. et al.: Morphologic and angiographic features of coronary plaque rupture detected by intravascular ultrasound. J. Am. Coll. Cardiol. 2002; 40: 904-910.
  • 108. Sukiennik A., Radomski M., Rychter M., Kubica J.: Usefulness of optical coherence tomography in the assessment of atherosclerotic culprit lesions in acute coronary syndromes. Comparison with intravascular ultrasound and virtual histology. Cardiol. J. 2008; 15: 561-563.
  • 109. Pracoń R., Pręgowski J.: Nowoczesne metody obrazowania ranliwej blaszki miażdżycowej. Post. Kardiol. Interw. 2008; 4: 20-30.
  • 110. Uchida Y., Nakamura F., Tomaru T et al.: Prediction of acute coronary syndromes by percutaneous coronary angioscopy in patients with stable angina. Am. Heart J. 1995; 130: 195-203.
  • 111. Stefanadis C., Toutouzas K., Tsiamis E. et al.: Increased local temperature in human coronary atherosclerotic plaques: an independent predictor of clinical outcome in patients undergoing a percutaneous coronary intervention. J. Am. Coll. Cardiol. 2001; 37: 1277-1283.
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