Atherosclerosis is a leading issue in mortality and morbidity in the civilized world. A number of hypotheses for atherogenesis indicate the complexity of initiation and development of this multifactorial disease. Morphologic types of lesions have long since been studied in order to understand plaque evolution and determinants of plaque complication, a frequent cause of acute ischemic accidents. Chemical and pathophysiological studies defined the wide spectrum of molecular interactions between cellular elements of atherosclerotic lesions. Recently, molecular biologic investigations provide a deeper insight into genetic predispositions for the disease and have widened our understanding of the pathogenic mechanisms. Until we can diminish the high prevalence of the disease, precise information is needed on the evolution of atherosclerosis in order to slow progression, select optimal therapies and prevent plaque complications and their consequences.
RossR., The pathogenesis of arteriosclerosis: a perspective for the 1990s. Nature, 1993, 362, 801–809.
2.
SchmitzG., AslanidisC. and LacknerK.J., Recent advances in molecular genetics of cardiovascular disorders. Implications for atherosclerosis and diseases of cellular lipid metabolism. Pathology Oncology Research, 1998, 4(2), 152–160.
3.
GlagovS., BassiounyH.S., GiddensD.P., Pathobiology of plaque modeling and complication. Surg. Clin. North America, 1995, 75(4), 545–556.
4.
GimbroneM.A.Jr., ResnickN., NagelT., Hemodynamics, endothelial gene expression, and atherosclerosis. Atherosclerosis IV: recent advances in atherosclerosis research. The Fourth Saratoga International Conference on Atherosclerosis. Annals of the New York Academy of Sciences, 1997, 811, 1–11.
5.
SnidermanA.D., CianfloneK., ArnerP., The adipocyte, fatty acid trapping, and atherogenesis. Arteriosclerosis and Thrombo-Vascular Biology, 1998, 18, 147–151.
6.
EnosW.F., HolmesR.H. and BeyerJ., Coronary disease among United States soldiers killed in action in Korea: preliminary report. JAMA, 1953, 152, 1090–1093.
7.
KadarA. and MozesG., IllyesGy., WHO-ISFC Pathobiological Determinants of Atherosclerosis in Youth Study. Histomorphometry and histochemistry of atherosclerotic lesions in coronary arteries and in the aorta in young populations. Nutrition, Metabolism and Cardiovascular Diseases, 1999, 9, 220–227.
8.
VirchowR.IV, Thrombose und Embolie. Gefäßentzündung und septische Infektion. In Gesammelte Abhandlungen zur Wissentschaftlichen MedizinMeidinger Sohn, Berlin1856, pp. 495–507.
9.
JellinekH., DetreZ. and VeressB.Transmural Plasma Flow in AtherogenesisPublishing House of the Hungarian Academy of Sciences, Budapest, 1983.
10.
StaryH.C., ChandlerA.B., GlagovS., A definition of initial, fatty streak and intermediate lesions of arteriosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis American Heart Association. Circulation, 1994, 89, 2462–2478.
11.
StaryH.C., BlankenhornD.H., ChandlerA.B., A definition of advanced arteriosclerotic lesions and a classification of arteriosclerosis. Circulation, 1995, 92(5), 1355–1374.
12.
KadarA. and BjoerkerudS., Arterial remodelling following mechanical injury. The role of the nature of SMC. Pathology Research and Practice, 1985, 180, 342–347.
13.
KerenyiT., VossB., LehmannR., Monocyte-endothelial cell interactions following vascular injuries. Pathology Research and Practice, 1987, 182(4), 509.
14.
JellinekH. and TakacsE., Die Wirkung von Magnesiumorotat auf die Herzmuskulatur und die Koronarien bei verschiedenen Tierarten in Modellexperimenten. Documenta Angiologorum, 1995, 24, 7–25.
15.
KerenyiT., MerkelV., SzabolcsZ., Local enzymatic treatment of atherosclerotic plaques. Experimental Molecular Pathology, 1988, 49, 330–338.
16.
GlagovS., ZarinsC.K., GiddensD.P., Hemodynamics and atherosclerosis: Insights and perspectives gained from studies of human arteries. Archives of Pathology Laboratory Medicine, 1988, 112, 1018–1031.
17.
KuD.N., ZarinsC.K., GiddensD.P., Pulsatile flow and atherosclerosis in the human carotid bifurcation: positive correlation between plaque localisation and low and oscillating shear stress. Atherosclerosis, 1985, 5, 293–302.
18.
ZarinsC.K., GiddensD.P., BjaradajB.K., Carotid bifurcation atherosclerosis. Quantitative correlation of plaque localisation with flow velocity profiles and wall shear stress. Circulation Research, 1983, 53, 502–514.
19.
DaviesM.J. and ThomasA.C., Thrombosis in acute coronary artery lesions in sudden ischaemic death. New England Journal of Medicine, 1984, 310, 1137–1140.
20.
CookP.J. and LipG.Y.H., Infectious agents and atherosclerotic vascular disease. Quarterly Journal of Medicine, 1996, 89, 727–735.
21.
FaggiottoA. and RossR., Studies of hypercholesterolemiain the nonhuman primate, part II: fatty streak conversion to fibrous plaque. Atherosclerosis, 1984, 4, 341–356.
22.
MoreR.M., MovatH.Z. and HaustD.M., Role of mural fibrin thrombi of aorta in genesis of artriosclerotic plaques: report of two cases. Archives of Pathology, 1957, 63, 612–621.
23.
BendittE.P. and BendittJ.M., Evidence for a monoclonal origin of human atherosclerotic plaques. Proceedings of the National Academy of Science USA, 1973, 70, 1753–1759.
24.
NichollsA.C. and ThomasM., Coxackie virus infection in acute myocardial infarction. Lancet, 1977, i, 883–884.
25.
BendittE.P., BarrettT. and McDougallJ.K., Viruses in the etiology of atherosclerosis. Proceedings of the National Academy of Science USA, 1983, 80, 6386–6389.
26.
MendallM.A., GogginP.M., MolineauxN., Relation of Helicobacter pylori in coronary heart disease. British Heart Journal, 1994, 71, 437–439.
27.
GraystonJ.T., KuoC.C., CampbellL.A., Chlamydia pneumoniae sp. nov. for Chlamydia sp. strain TWAR. International Journal of System Bacteriology, 1989, 39(1), 88–90.
28.
SaikkuP., LeinonenM., ManilaK., Serologic evidence of an association of a novel Chlamydia, TWAR, with chronic coronary heart disease and acute myocardial infarction. Lancet, 1988, ii, 983–986.
29.
McDonaldK., RectorT.S., BraunlinE.A., Association of coronary artery disease in cardiac transplant recipients with cytomegalovirus infection. American Journal of Cardiology, 1989, 64, 359–362.
30.
GaffneyD., ReidJ.R., CameronI.M., Independent mutations at codon 3500 of the apolipoprotein B gene are associated with hyperlipidemia. Arteriosclerosis and Thrombo-Vascular Biology, 1995, 15, 1025–1029.
31.
PajukantaP.E., ValstaL.M., AroA., The effects of the apolipoprotein B signal peptide (ins/del) and Xbal polymorphisms on plasma lipid response to dietary change. Atherosclerosis, 1996, 122, 1–10.
32.
WangX.L., McCredieR.M. and WilckenD.E.L., Polymorphisms of the apolipoprotein E gene and severity of coronary artery disease defined by angiography. Arteriosclerosis and Thrombo-Vascular Biology, 1995, 15, 1030–1034.
33.
GavishD., ZrolanN. and BreslowJ.L., Plasma Lp(a) concentration is inversely correlated with the ratio of kringle IV/krigle V encoding domains in the Apo(a) gene. Journal of Clinical Investigation, 1989, 84, 2021–2027.
34.
BrownM.S. and GoldsteinJ.L., Lipoprotein metabolism in the macrophage: implications for cholesterol deposition in atherosclerosis. Annual Reviews in Biochemistry, 1983, 52, 223–261.
35.
SandkampM., FunkeH., SchulteH., Lipoprotein(a) is an independent risk factor for myocardial infarction at a young age. Clinical Chemistry, 1990, 36, 20–23.
36.
ThornJ.A., ChamberlainJ.C., AlcoladoJ.A., Lipoprotein and hepatic lipase gene variants in coronary atherosclerosis. Atherosclerosis, 1990, 85, 55–60.
37.
SerratoM. and MarianA.J., A variant of human paraoxonase/arylesterase (HUMPONA) gene is a risk factor for coronary artery disease. Journal of Clinical Investigation, 1995, 96, 3005–3008.
38.
MarklundS.L., NilssonP., IsraelssonK., Two variants of extracellular superoxide-dismutase: relationship to cardiovascular risk factors in an unselected middle-aged population. Journal of Internal Medicine, 1997, 242, 5–14.
39.
YeS., WattsG.F., MandaliaS., Preliminary report: genetic variations in human stromelysin promoter is associated with progression of coronary atherosclerosis. British Heart Journal, 1995, 73, 209–215.
40.
WenzelK., BlackburnA., ErnstM., Relations of polymorphisms in the renin-angiotensin system and E-selectin of patients with early severe coronary heart disease. Journal of Molecular Medicine, 1997, 75, 57–61.
41.
WenzelK., FelixS., KleberF.X., E-selectin polymorphism and atheriosclerosis: an association study. Human Molecular Genetics, 1994, 11, 1935–1937.
42.
WangX.L., SimA.S., BadenhopR.F., A smoking-dependent risk of coronary artery disease associated with a polymorphism of the endothelial nitric oxide synthase gene. National Medicine, 1996, 2, 41–45.
43.
ThybergJ., CalaraF., DimayugaP., Role of caveolae in cholesterol transport in arterial smooth muscle cells exposed to liporoteins in vitro and in vivo. Laboratory Investigation, 1998, 78, 825–837.
44.
OramJ.F. and YokoyamaS., Apoliporotein-removal of cellular cholesterol and phospholipids. Journal of Lipid Research, 1996, 37, 2473–2491.
45.
VasileE., SimionescuM. and SimionescuN., Visualization of the binding, endocytosis, and transcytosis of low-density lipoprotein in the arterial endothelium in situ. Journal of Cell Biology, 1983, 96, 1677–1689.
46.
WightT.N., The vascular extracellular matrix. In Atherosclerosis and Coronary Heart Disease, eds FusterV., RossR. and TopolE. J.. Lippincott-Raven Publishers, Philadelphia1996, pp. 421–440.
47.
PennM.S., RangaswamyS., SaidelG.M., Macromolecular transport in the arterial intima: comparison of chronic and acute injuries. American Journal of Physiology, 1997, 272, H1560–H1570.
48.
PennM.S., SaidelG.M. and ChisolmG.M., Relative significance of endothelium and internal elastic lamina in regulating the entry of macromolecules into arteries in vivo. Circulation Research, 1994, 74, 74–82.
49.
HajjarD.P. and HaberlandM.E., Lipoprotein trafficking in vascular cells. Journal of Biological Chemistry, 1997, 272, 22975–22978.
50.
OwensG.K., Role of alterations in the differetiated state of vascular smooth muscle cells in atherogenesis. In Atherosclerosis and Coronary Heart Disease, eds FusterV., RossR. and TopolE. J.. Lippincott-Raven Publishers, Philadelphia1996, pp. 401–420.
51.
ThybergJ., Phenotypic modulation of smooth muscle cells during formation of neointimal thickenings following vascular injury. Histology and Histopathology, 1998, 13, 871–891.
52.
KruthH.S., The fate of lipoprotein cholesterol entering the arterial wall. Current Opinion in Lipidology, 1997, 8, 246–252.
53.
ChaoF.F., Blanchette-MackieE.J., TertovV.V., Hydrolysis of cholesteryl ester in low density lipoprotein converts this lipoprotein to a liposome. Journal of Biological Chemistry, 1992, 267, 4992–4998.
54.
PihaM., LindstedtL. and KovanenP.T., Fusion of proteolyzed low-density lipoprotein in the fluid phase: a novel mechanism generating atherogenic lipoprotein particles. Biochemistry, 1995, 34, 10120–10129.
55.
YasruelZ., CianfloneK., SnidermanA.D., Effect of acylation stimulating protein on the triacylglycerol synthetic pathway of human adipose tissue. Lipids, 1991, 26, 495–499.
56.
StaryH.C., BlankenhornD.H., ChandlerA.B., A definition of the intima of human arteries and of its atherosclerosis-prone regions: a report from the Committee on Vascular Lesions of the Council of Arteriosclerosis American Heart Association. Circulation, 1992, 85, 391–405.
57.
GerrityR.G., The role of the monocyte in atherogenesis, I: transition of blood-borne monocytes into foam cells in fatty lesions. American Journal of Pathology, 1981, 103, 181–190.
58.
GerrityR.G., The role of the monocyte in atherogenesis, II: migration of foam cells from atherosclerotic lesions. American Journal of Pathology, 1981, 103, 191–200.
59.
ZinserlingW.D., Untersuchungen uber Atherosklerose, 1: Uber die Aortaverfettung bei Kindern. Virchows Archiv Pathologie, Anatomie, Physiobgie und Klinike Medizin, 1925, 255, 677–705.
60.
AnitschkowN., Uber die Veranderungen der Kaninchenaorta bei experimenteller Cholesterinsteatose. Beitrage Pathologie, Anatomie und Allgemeine Pathologie, 1913, 56, 379–404.
61.
StaryH.C., Coronary artery fine structure in rhesus monkeys: the early atherosclerotic lesion and its progression. Primates Medicine, 1976, 9, 359–395.
62.
SimionescuN., VasileE., LupuF., Prelesional events in atherogenesis: accumulation of extracellular cholesterol-rich liposomes in the arterial intima and cardiac valves of the hyperlipidemic rabbit. American Journal of Pathology, 1986, 123, 109–125.
63.
SmallD.M., George Lyman Duff memorial lecture: progression and regression of atherosclerotic lesions: insights from lipid physical biochemistry. Arteriosclerosis, 1988, 8, 103–129.
64.
KatzS.S., ShipleyG.G. and SmallD.M., Physical chemistry of the lipids of human atherosclerotic lesions: demonstration of a lesion intermediate between fatty streaks and advanced plaques. Journal of Clinical Investigation, 1976, 58, 200–211.
65.
SmithE.B. and SmithR.H., Early changes in aortic intima. In Atherosclerosis Reviews I, eds PaolettiR. and GottoA. M.. Raven Press, New York1976, pp. 119–236.
66.
GlagovS., WeisenbergE., ZarinsC.K., Compensatory enlargement of human atherosclerotic coronary arteries. New England Journal of Medicine, 1987, 316, 1371–1375.
67.
van der WalA.C., BeckerA.E., van der LoosC.M., 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.
68.
HenneyA.M., WakeleyP.R., DaviesM.J., Localisation of stromelysin gene expression in atherosclerotic plaques by in situ hybridization. Proceedings of the National Academy of Science USA, 1991, 88, 8154–8158.
69.
NobuyoshiM., TanakaM., NosakaH., Progression of coronary atherosclerosis: is coronary spasm related to progression?Journal of the American College of Cardiology, 1991, 18, 904–910.
70.
RichardsonP.D., DaviesM.J. and BornG.V., Influence of plaque configuration and stress distribution on fissuring of coronary atherosclerotic plaques. Lancet, 1989, 2, 941–944.
71.
FalkE., Why do plaques rupture?Circulation, 1992, 86(Suppl III), 30–42.
72.
GimbroneM.A.Jr., Culture of vascular endothelium. Progress in Hemostatic Thrombosis, 1976, 3, 1–28.
73.
SteinbergD., Antioxidants and atherosclerosis. A current assessment. Circulation, 1991, 84, 1420–1425.
74.
FurchgottR.F., Role of endothelium in responses of vascular smooth muscle. Circulation Research, 1983, 53, 557–573.
75.
LuescherT.F., Imbalance of endothelium-derived relaxing and contracting factors. A new concept in hypertension?American Journal of Hypertension, 1990, 3, 317–330.
76.
MinorR.L., MyersP.R., GuerraR.Jr., Diet-induced atherosclerosis increases the release of nitrogen oxides from rabbit aorta. Journal of Clinical Investigation, 1990, 86, 2109–2116.
77.
ChesterA.H., O'NeilG.S., MoncadaS., Low basal and stimulated release of nitric oxide in atherosclerotic epicardial coronary arteries. Lancet, 1990, 336, 897–900.
78.
RossR., MasudaJ., RainesE.W., Localization of PDGF-B protein in macrophages in all phases of atherogenesis. Science, 1990, 248, 1009–1012.
79.
CarewT.E., SchwerkeD.C. and SteinbergD., Antiatherogenic effect of probucol unrelated to its hypocholesterolemic effect: evidence that antioxidants in vivo can selectively inhibit low density lipoprotein degradation in macrophage-rich fatty streaks and slow the progression of atherosclerosis in the Watanabe heritable hyperlipidemic rabbit. Proceedings of the National Academy of Science USA, 1987, 84, 7725–7729.
80.
KitaT., NaganoY., YokodeM., Probucol prevents the progression of atherosclerosis in Watanabe heritable hyperlipidemic rabbit, an animal model for familial hypercholesterolemia. Proceedings of the National Academy of Science USA, 1987, 84, 5928–5931.
81.
RossR. and FusterV., The pathogenesis of atherosclerosis. In Atherosclerosis and Coronary Heart Disease, eds FusterV., RossR. and TopolE. J.. Lippincott-Raven Publishers, Philadelphia1996, pp. 441–460.
82.
NicholsonA.C. and HajjarD.P., Transforming growth factor-beta up-regulates low density lipoprotein receptor-mediated cholesterol metabolism in vascular smooth muscle cells. Journal of Biological Chemistry, 1992, 267, 25982–25987.
83.
GongQ. and PitasR.E., Synergistic effects of growth factors on the regulation of smooth muscle cell scavenger receptor activity. Journal of Biological Chemistry, 1995, 270, 21672–21678.
84.
FieldingC.J. and FieldingP.E., Intracellular cholesterol transport. Journal of Lipid Research, 1997, 38, 1503–1521.
85.
IkonenE., Molecular mechanisms of intracellular cholesterol transport. Current Opinion in Lipidology, 1997, 8, 60–64.
86.
LupuF., DanaricuI. and SimionescuN., Development of intracellular lipid deposits in the lipid-laden cells of atherosclerotic lesions: a cytochemical and ultrastructural study. Atherosclerosis, 1987, 67, 127–142.
87.
StaryH.C., The sequence of cell and matrix changes in atherosclerotic lesions of coronary arteries in the first forty years of life. European Heart Journal, 1990, 11(Suppl E), 3–19.
88.
TimplR. and DziadekM., Structure, development and molecular pathology of basement membranes. International Reviews in Experimental Pathology, 1986, 29, 1–112.
89.
JonassonL., HolmJ., SkalliO., Regional accumulations of T cells, macrophages, and smooth muscle cells in the human atherosclerotic plaque. Arteriosclerosis, 1986, 6, 131–138.
90.
PalinskiW., RosenfeldM.E., Yla-HerttualaS., Low density lipoprotein undergoes oxidative modification in vivo. Proceedings of the National Academy of Science USA, 1989, 86, 1372–1376.
91.
BassiounyH.S., DavisH., MasawaN., Critical carotid stenosis: morphological and chemical similarity between symptomatic and asymptomatic plaques. Journal of Vascular Surgery, 1989, 9, 202–212.
92.
YockP.G., FitzgeraldP.J., LinkerD.T., Intravascular ultrasound guidance for catheter-based coronary interventions. Journal of the American College of Cardiology, 1991, 17, 39B–45B.
93.
BradenG.A., HerringtonD.M., DownesT.R., Qualitative and quantitative contrasts in the mechanisms of lumen enlargement by coronary baloon angioplasty and directional coronary atherectomy. Journal of the American College of Cardiology, 1994, 23, 40–48.
DonerC.T. and JudkinsM.P., Transluminal treatment of atherosclerotic obstructions: description of a new technique and a preliminary report of its application. Circulation, 1964, 30, 654–670.
FranklinS.M. and FaxonD.P., Pharmacological prevention of restenosis after coronary angioplasty: review of randomized clinical trials. Coronary Artery Disease, 1993, 4, 232–242.
98.
GlagovS., Intimal hyperplasia, vascular modeling, and the restenosis problem. Circulation, 1994, 89(6), 2888–2891.
99.
RensingB.J., HermansW.R.M., VosJ., Angiographic nsk factors of luminal narrowing after coronary baloon angioplasty using baloon measurements to reflect stretch and recoil at the dilatation site. American Journal of Cardiology, 1992, 69, 584–591.
100.
GarrattK.N., HolmesD.R.Jr., BellM.R., Restenosis after directional coronary atherectomy: differences between primary atheromatous and restenosis lesions and influence of subintimal tissue reaction. Journal of the American College of Cardiology, 1990, 16, 1665–1671.
101.
JohnsonD.E., HinoharaT., SelmonM.R., Primary peripheral arterial stenoses and restenoses excised by transluminal atherectomy: a histopathologic study. Journal of the American College of Cardiology, 1990, 15, 419–425.
102.
WallerB.F., PinkertonC.A., OrrC.M., Morphological observations late (>30 days) after clinically successful coronary baloon angioplasty. Circulation, 1991, 83(Suppl I), 128–141.
103.
FischmanD.L., LeonM.B., BairnD.S., A randomized comparison of coronary stent placement and baloon angioplasty in the treatment of coronary artery disease. New England Journal of Medicine, 1994, 331, 496–501.
104.
SerruysP.W., de JaegereP., KiemeneijF., A comparison of baloon expandable stent implantation of baloon angioplasty in the treatment of coronary artery disease. New England Journal of Medicine, 1994, 8, 489–495.
105.
LanskyA.J., MintzG.S., PopmaJ.J., Remodeling after directional coronary atherectomy (with and without adjunct percutaneous transluminal coronary angioplasty): a serial angiographic and intravascular ultrasound analysis from the optimal atherectomy restenosis study. Journal of the American College of Cardiology, 1998, 32(2), 329–337.
106.
HinoharaT., RobertsonG.C., SelmonM.R., Restenosis after directional coronary atherectomy. Journal of the American College of Cardiology, 1992, 20, 623–632.
107.
MillerM.J., KuntzR.E., FriedrichS.P., Frequency and consequences of intimal hyperplasia in specimens retreived by directional atherectomy of native primary coronary artery stenoses and subsequent restenosis. American Journal of Cardiology, 1993, 71, 652–658.
108.
WeintraubW.S., BrownC.L., LibermanH.A., Effect of restenosis at one previously dilated coronary site on the probability of restenosis at another previously dilated coronary site. American Journal of Cardiology, 1993, 72, 1107–1113.
109.
NicholsonA.C. and HajjarD.P., Herpesviruses in atherosclerosis and thrombosis: etiologic agents or ubiquitous bystanders?Arteriosclerosis and Thrombo-Vascular Biology, 1998, 18, 339–348.
