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Trimethylamine N-oxide (TMAO), a metabolite of intestinal flora, can promote Atherosclerosis (AS) in various ways. Current studies have found that it has a close relationship with plaque stability in clinical practice, but its molecular mechanism remains unclear at present. Extracellular matrix metalloproteinase inducers (CD147) / matrix metalloproteinases (MMPs) regulate a signal pathway highly related to plaque stability, which can promote plaque instability and lead to cardiovascular adverse events by weakening the thickness of the fibrous cap. Therefore, in this study, the mouse macrophageRAW264. 7 was stimulated by TMAO to establish a cell model to observe the effects on CD147, MMP2, and MMP9, and the CD147 gene silencing model was further constructed by using the siRNA transfection method to explore the interaction between CD147 and MMP2 and MMP9. Rt-qPCR and Western blotting results showed that there was no significant change in the gene expression level of CD147 in mouse macrophage RAW264. 7, but significantly increased in protein levels (P < 0. 05), while MMP2 andMMP9 were increased in mRNA and protein levels (P<0. 05). The expression of CD147, MMP2, andMMP9 was significantly inhibited in CD147 siRNA transfected cells (P<0. 05). In conclusion, TMAO significantly increases the expression of MMP2 and MMP9 in mouse macrophages RAW264. 7, and this effect may be partially realized through the CD147/ MMP pathway.
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Objective At present, there are few reports on the stability of carotid plaque and left ventricular function at home and abroad. The article investigated the factors influencing the stability of left ventricular function on carotid atherosclerotic plaque. Methods 90 patients with carotid atherosclerosis (carotid intima-media thickness >0.2 cm) admitted in the Department of Neurology, Jiangsu Provincial Hospital of Traditional Chinese Medicine from June 10, 2017 to January 8, 2019 were selected and their stability of plaques was graded by contrast-enhanced ultrasound (CEUS). The patients were divided into two groups according to the stability of plaque. The differences of general clinical data, related biochemical indexes and left ventricular function indexes between the two groups were compared. The effects of left ventricular structural function on plaque stability were examined by logistic multivariate regression analysis. Results Univariate analysis showed that E peak (χ2=2.170, P=0.034), ventricular septal thickness (χ2=-1.972, P=0.049), diabetes history (χ2=10.102, P=0.001) were the risk factors of plaque stability and the differences were statistically significant (P < 0.05). Multivariate analysis showed that E peak (OR=0.022, P=0.014) and diabetes history (OR=0.185, P=0.002) were independent influencing factors of plaque stability. Conclusion There is an independent correlation between left ventricular function and plaque stability, and plaque stability can predict changes in ventricular structural function.
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In the background of the high incidence and high mortality of cardiovascular diseases,atherosclerosis is the main pathological feature of cardiovascular diseases and the core pathological basis for disease progression. In the evolution of atherosclerotic plaques,the rupture of unstable plaques,plaque shedding and formation of thrombosis are the most dangerous parts. In this process,the formation of plaque fibrosis is the core mechanism regulating plaque stability. Additionally,fibrosis reflects dynamic changes in the inflammatory processes and pathological changes. In view of the inflammation regulation and fibrosis regulation,this paper clarified the process of atherosclerotic plaque,explained the roles of relevant inflammatory cells and cytokines in plaque stability,and summed up drug researches related with stable plaque in recent years. In the future,improving the fibrosis will be a new idea for stabilizing plaque in atherosclerosis drug development.
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Humans , Atherosclerosis , Drug Therapy , Pathology , Cytokines , Fibrosis , Inflammation , Plaque, Atherosclerotic , Drug Therapy , Pathology , Thrombosis , Drug Therapy , PathologyABSTRACT
Objective To investigate the correlation between serum HCY (Homocysteine) and carotid artery stenosis,plaque stability in patients with ischemic cerebrovascular disease.Methods 154 patients with ischemic cerebrovascular disease in Tangdu Hospital were enrolled in the study from June to December 2016.The serum levels of HCY were detected.CT angiography (CTA) was uesd for patients with neck vascular scanning.According to the difference of serum HCY level,patients were divided into 80 cases of high HCY group (observation group) and 74 cases of normal HCY group (control group).The degree of carotid artery stenosis,number and stability of plaque were compared between the two groups and the correlation between serum HCY level and degree of carotid artery stenosis and plaque stability were analyzed.Results The total stenosis rate in the observation group was significantly higher than that in the control group,the moderate stenosis rate and severe stenosis rate in the observation group were significantly higher than those in the control group,with the statistically significant differences (x2 =5.594～ 22.506,all P＜0.05).The levels of serum HCY in mild,moderate and severe stenosis group were 13.16 ± 6.73,15.19± 5.93 and 26.13 ±11.18 μmol/L respectively.The levels of H CY in moderate stenosis group and severe stenosis group were significantly higher than that in mild stenosis group,and the levels of HCY in severe stenosis group was significantly higher than that in moderate stenosis group,with the statistically significant differences (t=2.684～ 5.270,all P＜0.01).The rate of carotid plaque in the observation group was significantly higher than that in the control group,and the differences statistically significant (x2 =25.053,P＜0.01).The rate of unstable plaque and mixed plaque in the observation group was significantly higher than that in the control group,and the rate of stable plaque was significantly lower than that in the control group (x2 =4.067～ 14.95,all P＜0.05).The levels of serum HCY in stable plaque group,mixed plaque group and unstable plaque group were 16.14±5.49,21.91 ± 6.32 and 26.74 ± 10.59 μmol/L respectively.The levels of HCY in mixed plaque group and unstable plaque group were significantly higher than that in stable plaque group,and the differences were statistically significant (t=4.370,4.628,all P＜0.01).The level of HCY in unstable plaque group was significantly higher than that in mixed plaque group,and the difference was statistically significant (t =2.249,P＜ 0.05).Conclusion Serum HCY levels were closely related to carotid artery stenosis and plaque stability.Hyperhomocysteinemia can increase the incidence and degree of carotid artery stenosis as well as the number of carotid plaques and unstable plaques.
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Objective To investigate the relationship between plasma level of platelet derived growth factor-BB (PDGF-BB), coronary heart disease (CHD) and the severity of coronary artery stenosis. Methods A total of 262 patients hospitalized in Department of Cardiology, Tianjin Chest Hospital were collected in this study. According to the medical history, symptoms, laboratory examination and the results of coronary angiography, patients were divided into stable angina pectoris (SAP) group (n=57), acute coronary syndrome (ACS) group (n=119) and normal control group (n=86). The ACS group was divided into three subgroups:single vessel group (n=38), double vessel group (n=35) and multiple vessel group (n=46). The general clinical data, biochemical parameters and plasma PDGF-BB levels were compared between SAP group, ACS group and control group. Spearman correlation analysis was used to analyze the relationship between PDGF-BB level, high-sensitivity C-reactive protein (hs-CRP) and Gensini scores. Logistic regression analysis was used to analyze the risk factors of coronary heart disease. Results (1) The plasma levels of hs-CRP and PDGF-BB were significantly higher in ACS group than those in control group and SAP group (P0.05). (3) There was no significant difference in plasma level of PDGF-BB between single vessel group, double vessel group and multiple vessel group (P > 0.05). (4) Logistic regression analysis showed that high plasma level of PDGF-BB was the risk factor for coronary heart disease. Conclusion PDGF-BB plasma level is associated with the pathogenesis of coronary heart disease, which may reflect the instability of coronary atherosclerotic plaques, but it is not an index to evaluate the severity of coronary stenosis.
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Objective To study the relationship between the lipoprotein associated phospholipase A2 (LP-PLA2) with the carotid plaques cerebral infarction,and study the predictive value of LP-PLA2 in carotid artery plaque stability.Methods According to the results of color doppler ultrasound examination of carotid artery,169 patients with cerebral infarction were random divided into cerebral infarction with carotid plaques group (101 patients) and cerebral infarction without carotid plaques group(68 patients) groups.According to the nature of plaque stability of carotid plaques.101 cases of cerebral infarction with carotid plaques group was divided into plaques group 30 cases and 71 cases of unstable plaque group.Set healthy control groups at the same time.Then detected level of LP-PLA2 for each patient by the method of double antibody sandwich enzyme-linked immunosorbent (ELISA).To evaluate the predictive value of LP-PLA2 in carotid artery plaque stability by mapping the receiver-operating characteristic (ROC) curve.Results The level of LP-PLA2 (212.90± 117.69 ng/ml) in carotid plaques group were significantly higher than those without plaque group (127.70 ± 57.96 ng/ml,t=3.016,P ＜0.01).It was not show significantly difference between no plaque group and healthy control group (108.34 ± 42.58 ng/ml,t=0.779,P＞0.05).But it showed significantly different between the unstable plaque group (236.24 ± 128.33 ng/ml)and stability plaques group (157.65±59.27 ng/ml,t=3.442,P＜0.01).Conclusion The LP-PLA2 of plasma could be involved in the development of atherosclerosis plaques.The LP-PLA2 can certain correlation with cerebral infarction of carotid plaques,can well evaluate the stability of carotid plaques.
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Objective To use high-resolution magnetic resonance imaging (HR-MRI) for studying the vascular remodeling and plaque characteristics of two types of basilar atherosclerotic infarction; branch occlusive disease (BOD) and nonBOD. Methods Thirty-two patients with symptomatic basilar artery stenosis were divided into BOD and non-BOD groups, with 18 patients in BOD group and 14 in non-BOD group. All the patients received 3. 0T HR-MRI enhancement scanning for the basilar artery wall. The wall thickness and plaque area of steno-occlusive basilar artery at the maximal stenosis were measured and analyzed, so as to assess the vascular remodeling and plaque characteristics. Results HR-MRI scanning showed that the stenosis of non-BOD group was more obvious than that of BOD group ([68. 9 ± 19. 1]% vs [43. 8 ± 18. 8]%, P = 0. 017). Compared with BOD group, positive remodeling wasmore frequently observed in non-BOD (57. 2% vs 16. 7%, P = 0. 036). The wall area index of BOD group was also significantly lower than that of non-BOD group (P<0. 001). Eccentric enhancement was the main form for the two types of basilar atherosclerotic infarction in study, and the plaque enhancements were not significantly different between BOD and non-BOD groups (P = 0. 196); however, the enhancement degree of BOD group was significantly milder than that of the non-BOD group ([39. 9 ± 23. 2]% vs [65. 3 ± 21. 1]%, P=0. 004). Conclusion BOD and non BOD have different vascular remodelings and plaque characteristics.
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The tumor necrosis factor receptor superfamily (TNFRSF), which includes CD40, LIGHT, and OX40, plays important roles in the initiation and progression of cardiovascular diseases, involving atherosclerosis. CD137, a member of TNFRSF, is a well-known activation-induced T cell co-stimulatory molecule and has been reported to be expressed in human atherosclerotic plaque lesions, and plays pivotal roles in mediating disease processes. In this review, we focus on and summarize recent advances in mouse studies on the involvement of CD137 signaling in the pathogenesis and plaque stability of atherosclerosis, thereby highlighting a valuable therapeutic target in atherosclerosis.
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Animals , Humans , Mice , Atherosclerosis , Cardiovascular Diseases , Negotiating , Plaque, Atherosclerotic , Receptors, Tumor Necrosis FactorABSTRACT
Objective The aim of our study was to investigate the effects and mechanisms of ghrelin on neovascularization in atherosclerosis plaque. Methods 30 male New Zealand rabbits were randomly divided into normal control group ( CON group) , atherosclerosis model group ( AS group) , and ghrelin treatment group ( ghrelin group) , and each group of 10 rabbits. The AS group and ghrelin group underwent balloon-induced arterial wall injury and then fed with high fat diet, the CON group was fed only on a regular diet. They were all fed for 3 months. Then the ghrelin group was given ghrelin 25μg·kg-1 ·d-1 , the other two groups received the same amount of sterile normal saline only. Four weeks later, body weight and blood lipids were detected. The thickness ratio of the intima to media was measured by HE staining. Degree of intra-plaque angiogenesis was evaluated by CD31+ cells immunohisto-chemistry. The vascular endothelial growth factor ( VEGF ) and vascular endothelial growth factor receptor 2 ( VEGFR2) were detected by quantitative realtime PCR and Western blot. The expressions of matrix metalloproteinase ( MMP)-2 and MMP-9 were detected by immunohistochemistry and Western blot. Results ( 1 ) No significant differences in body weight and blood lipids were found between the AS group and the ghrelin group(P>0. 05), but both items were significantly higher than those of the CON group(P<0. 05). (2)The thickness ratio of the intima to media in the ghrelin treated group was distinctly less than that in the AS group(P<0. 05). (3)Compared with the AS group, the ghrelin group showed significantly decreased microvascular density and the expressions of VEGF and VEGFR2 (P<0. 05). (4)Compared with the AS group, ghrelin dramatically inhibited the plaque contents of MMP-2 and MMP-9 ( P<0. 05 ). Conclusions Ghrelin is able to inhibit the growth of neovascularizationin in the atherosclerotic plaque and the development of plaque. And these beneficial effects derive from downregulation of VEGF, VEGFR2, MMP-2, and MMP-9 at the advanced stage of atherosclerosis in rabbits.
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by lfow cytometry. According to CAG morphology, the plaques included 3 types as Type I, Type II and TypeⅢ. The patients also received coronary CT angiography (CTA), upon CTA value, the plaques were classiifed by soft plaque, ifbrous plaque and calciifed plaque. Expressions of platelet surface EMMPRIN and GPVI among different groups were compared. Results:①Compared with Control group, ACS and SAP groups had increased expressions of EMMPRIN (5.82 ± 0.81 and 3.45 ± 0.48) vs (1.35 ± 0.15) and GPVI (16.22 ± 5.27 and 8.20 ± 2.87) vs (4.14 ±1.17); the expressions in ACS group were higher than those in SAP group, allP Conclusion: Expression levels of platelet surface EMMPRIN and GPVI were closely related to the stability of coronary plaque, both of them were the risk factors for severe coronary lesions. EMMPRIN and GPVI may have certain predictive value for early diagnosis of arteriosclerosis in ACS patients.
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Objective: To observe the relationship between the dynamic changes of plasma levels of urotensin II (UII) and the stability of coronary atherosclerotic plaque in patients with acute coronary syndrome (ACS). Methods: Our research included 2 groups: ACS group,n=135 consecutive patients treated in our hospital from 2013-03 to 2013-08 that including unstable angina pectoris (UAP) sub-group,n=7, non-ST segment elevation myocardial infarction (NSTEMI) sub-group,n=22 and STEMI sub-group,n=106. In addition, there was a Control group,n=48 healthy subjects. Plasma levels of UII, hs-CRP and NT-proBNP were examined and compared among different groups at different time points. Results: Compared with Control group at immediate admission, ACS group had increased plasma level of UII (39.82 ± 22.28) pg/ml vs (26.88 ± 6.09) pg/ml,P Conclusion: Plasma levels of UII have been changing in different type of ACS patients at immediate admission, UII presented decreasing trend from UAP to NSTEMI to STEMI, while it had increasing trend upon stabilized condition; the admission level of UII had no correlation to inflammatory marker hs-CRP and ventricular overload marker NT-proBNP. UII is not only related to the extent of atherosclerosis, but also related to the nature of atherosclerosis or the stability of plaques.
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Objective To investigate the efficacy of statin on carotid plaque stability in elderly patients assessed by K trans (the combination of E and F) of dynamic contrast material enhanced (DCE) magnetic resonance (DCE MR) imaging.Methods 37 elderly patients with carotid artery of low echo or mixed echo plaque in carotid artery patches were screened by B type ultrasound.According to the standard of 2011 ESC/EAS guidelines,all patients were divided into two groups:normal level of LDL-C group achieving LDL-C target and high level of LDL C group not achieving target of LDLC.Plaque area and size of lipid-rich necrotic core were measured by 3.0T enhancement magnetic resonance,and K trans was measured by DCE-MR dynamic contrast material enhanced (DCE) magnetic resonance (MR) imaging.and serum hs-C-reactive protein level was detected within 1 week.Results Plaque area,size of lipid-rich necrotic core,ratio of lipoid core over plaque area,K trans and serum level of hs-CRP were less in normal LDL-C level group than in high LDL-C level group [(2.06±0.45) mm2 vs.(3.63±0.62) mm2,(0.52±0.05) mm2 vs.(1.49±0.01) mm2,2 cases (11.8％) vs.14 cases (70.0％),(0.041±0.009) min1 vs.(0.079±0.011) min-1,(1.60±0.27) mmol/L vs.(2.80 ± 0.34),all P＜0.05].Linear regression analysis revealed that there was no significant correlations of K trans with the size of lipid necrotic core (r=0.19,P＞0.05) and hs-CRP (r=0.23,P＞0.05).Conclusions Dynamic contrast material enhanced (DCE) magnetic resonance (MR) imaging is a quantitative method assaying atheromatous plaque components; K trans may be a new indicator to measure the stability of plaques; Statin can stabilize plaques through inhibiting the proliferation of Vasa vasorum in plaque angiogenesis,anti-inflammatory and reducing the size of lipidrich necrotic core.
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objective To observe the influence of hemodynamic changes caused by extracranial carotid stenosis on the plaque stability, and analyze the relationship of cerebral infarction classification,criminal artery stenosis degree and plaque stability to offer evidence for evalu-ating nosogenesis,clinical diagnosis,treatment and prevention of cerebral infarction. Methods CDFI,CTA were performed in 168 patients with acute cerebral infarction,some moderate and severe and occlusive carotid artery which were demonstrated by CTA and CDFI were further checked by DSA during convalescence. Totally 168 acute cerebral infarction patients were divided into 5 groups based on the criminal artery stenosis degree. To evaluate the plaque stability and flow field changes with CDFI and CTA,OCSP clinical classification and brain image clas-sification were finished according to CTA. Patients were classified into 4 subtypes,namely cortical infarction,basal ganglion infarction,corona radiata infarction and posterior infarction,according to the lesion distributions. Observe the changes of flow field and stability of plaque,and compare the relationship between different degree of stenosis and the classification of lesion of infarction. Results Among the 168 criminal arteries,there was 17. 9% of normal,22. 6% of mild stenosis,30. 9% of moderate stenosis,14. 8% of severe stenosis,and 14. 3% of occlu-sion,and the moderate stenosis proportion was the highest. When the stenosis degree was over 50%,it may lead to the changes of flow field, speeding up of blood flow,forming of turbulent flow,and increasing of plaque instability in which lipid plaque and admixture plaque was the highest. PACI is the commonest in all moderate groups. Admixture plaque is usually seen in severe stenosis and occlusion, while fibrous plaque is usually seen in mild stenosis. Conclusion Moderate carotid stenosis may lead to the increase of plaque instability as a result of the changes of flow field,and it may prone to artery-artery embolization.
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Objective: To investigate the expression of CD40 and MMP9 in carotid atherosclerotic plaques, so as to assess the role of CD40 in the stability of the plaque and the possible mechanism. Methods: The expression of CD40 and MMP9 mRNA and protein in carotid atherosclerotic plaques obtained from carotid eversion endarterectomy (CEE) of 28 patients with high-grade stenosis (>70%) (stroke group, n=15; non-stroke group, n=13) and 8 normal postmortem arteries (control group) were detected by real-time quantification polymerase chain reaction (PCR) and Western blotting. The correlation between expression of CD40 and MMP9 was analyzed. Results: The expression of CD40 mRNA and MMP9 mRNA in the non-stroke group and stroke group was significantly higher than that in control group (P<0.01); and that of the stroke group was significantly higher than that of the non-stroke group (P<0.01). There was a linear correlation between expression of CD40 and MMP9 mRNA (r=0.964, P<0.01). Extremely rare expression of CD40 and MMP9 protein wet found in the normal carotid artery; the protein expression was evidently higher in the carotid artery atherosclerosis than in the normal carotid artery, and the expression in carotid artery atherosclerosis in the stroke group was higher than that in the non-stroke group. Conclusion: The increased expression of CD40 and MMP9 in the carotid atherosclerositic plaques may be closely related to the stability of plaques.
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Plaque rupture,platelet aggregation,and thrombogenesis are the main mechanisms of acute coronary syndrome (ACS),and inflammation factors play key roles in plaque unstability.Psychological stress promotes acute inflammatory response,leading to increased circulating levels of C-reactive protein (CRP),IL-6,and serum intercellular adhesion molecule (sICAM)-1.But it is not clear that whether psychological stress has a direct effect on atherosclerotic plaque stability.The purpose of this study was to investigate effects of chronic psychological stress on inflammatory marker (ICAM-1 ) in atherosclerotic plaque,and inflammatory markers in peripheral blood.Materials and methods Sixty male rabbits were randomized into 2 groups:the control group (n =10) and the atherosclerotic group (n =50).The latter were fed on high fatty diet and were given a large dose of vitamin D3 (3 600 000IU/kg) via intraperitoneal injection.After 8 weeks,the atherosclerotic model was estaslished.Then the 50 atherosclerotic model rabbits were divided into 3 subgroups:no-stress subgroup (n = 16),physiological stress subgroup (n = 16) and psychological stress subgroup (n =18).In physiological stress subgroup and psychological stress subgroup,drinking was cut from twice a day to once a day.At the same time,psychological stress subgroup was given empty bottle stress,and this process lasted for 2 weeks.One hour after the last stress,the blood samples were collected and the serum levels of CRP,IL-6 amd ICAM-1 were tested by radioimmunoassay or enzyme linked immunosorbent assay.The aorta and heart were extracted for pathology examination,and the express of ICAM-1 was tested by immunohistochemical examination.Results (1) After effective atherosclerotic animal model construction,the expression of ICAM-1 in aorta was higher in atherosclerotic group than that in control group (P＜0.01),and was notably higher in psychological stress subgroup than that in no-stress subgroup or in physiological stress subgroup (2.18±0.17 vs 1.58±0.22,1.22±0.15,P＜0.001,respectively).The expression in physiological stress subgroup was higher than that in no-stress subgroup (584±0.22 vs 1.22±0.15,P=0.001).(2) The serum level of IL-6 (51.80±4.60 pg/ml vs 27.60±4.19 pg/ml,8.01±1.39 pg/ml,7.83±1.37 pg/ml),sICAM-1 ( 1.24±0.25 vs 0.85±0.09,0.62±0.17,0.57±0.11),CRP ( 1.004±0.37 vs 0.90±0.29,1.01±0.22,0.71±0.13) in psychological stress group were significantly higher than that in other groups (All P＜0.05).There was a positive relationship between the serum level of CRP,IL-6 and ICAM-1 and the expression of ICAM-1 in aorta wall ( r =0.59,r =0.75,r =0.87,P＜0.01,respectively).Conclusions Psychological stress induces an increased expression of ICAM-1 in aortic atherosclerotic plaque,a higher serum level of CRP,IL-6,and sICAM-1 expression.Psychologial stress has a direct effect on the transition from stability to unstability through in-plaque and out-plaque inflammation.The serum level of CRP,IL-6 and ICAM-1 can reflex the inflammatory degree in atherosclerotic plaque.(J Geriatr Cardiol 2008;5:235-242)
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Objective To find the changes and effects of nitric oxide synthase activity in atherosclerotic rabbit models. Methods Thirty rabbits were divided into 3 groups at random: control group, atherogenic diet group, balloon-injury+ atherogenic diet group. Three months later underwent pharmacological triggering with Chinese Russell’s viper venom and histamine to make the plaque rupture. Lipid concentrations and the levels of nitric oxide (NO), NOS and hydroxy radical (OH) in the serum were obtained at different period, and pathologic changes were observed. Results In atherogenic diet group and balloon-injury+ atherogenic diet group, serum lipid concentrations markedly increased, but the levels of NO did not show any difference. The activity of NOS and OH levels were obviously increased after the atherogenic diet. But it reduced after pharmacological triggering and plaque rupture. Conclusion In early period of atherosclerosis, NOS activity up regulated and endothelium functions were compensated. But, When the atherosclerotic plaques were unstable, the activity of NOS descended obviously and endothelium function goes into incompensation.
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BACKGROUND: Lipoprotein (a) concentration is mainly determined by apo (a) genotype, but elevated in the atherosclerotic vascular disease more than in normal group with the same apo (a) phenotype. It has been known that Lp (a) has independent metabolism in contrast with other lipoproteins and that the use of cholesterol lowering agent such as HMG-CoA reductase inhibitor for 6 months does not change the level of Lp (a). The results of several studies suggests that Lp (a) may be related to inflammation of atherosclerotic plaque and therefore, long term use of cholesterol lowering agents make plaque stable by reduction of inflammation at plaque. We hypothesized that there is a relationship between long term use of HMG-CoA reductase inhibitor and change of Lp (a) level. We prospectively measured Lp (a), lipids and inflammatory markers before and after long term use of HMG-CoA reductase inhibitor to examine our hypothesis. METHODS: Forty-nine subjects (M:F=28:21, age=59.1+/-12.0) with hyperlipidemia were administered HMG-CoA reductase inhibitor for 15 months (minimum 6 months, maximun 44 months), and Lp (a), lipids and inflammatory markers were measured before and after use of the HMG-CoA reductase inhibitor. In control group (ninty-nine subjects, M:F=60:39, age=61.2+/-9.2), these parameters were measured more than 6 months. RESULTS: In the hyperlipidemia group who were given HMG-CoA reductase inhibitor, baseline levels of total cholesterol, TG, LDL were significantly elevated more than those of the control group, but Lp (a) and inflammatory markers were not significantly different. After use of HMG-CoA reductase inhibitor, the level of Lp (a) was reduced significantly (before 28.9+/-29.3 mg/dl, after 20.0+/-19.0 mg/dl, p=0.009), but not significantly in the control group. There was a minimal relation between baseline Lp (a) levels and percent changes of Lp (a) levels. Total cholesterol and LDL levels reduced significantly after use of the drug, but inflammatory markers did not. CONCLUSION: These data showed that Lp (a) level in the hyperlipidemia group after the long term use of HMG-CoA reductase inhibitor decreased significantly. We suggest that these changes of Lp (a) level may be one of reliable markers for plaque stability in atherosclerotic vascular disease.