| Background and Objective:Intravascular ultrasound (IVUS) is useful methodto evaluate coronary atherosclerosis and it can provide more details of atheroscleroticplaques and the wall of vascula.Recently,IVUS studies showed the relationship ofthe level of cholesterol,treatment of statins,cardiovascular risk factors and progressof atherosclerotic plaques,and there were also some studies to evaluate theremodeling of coronary arteries,the stability and rupture of atherosclerotic plaquewith IVUS.The projective of our study is 1.To evaluate the effects of statins onatherosclerotic plaque of coronary heart disease with mild elevation of LDL-C.2.Toquantify the different patterns of coronary calcification of patients with stable anginapectoris (SAP),unstable angina pectoris (UAP) and acute myocardial infaction (AMI).3.To evaluate the association between poststenting atherosclerotic plaqueredistribution/lumen reduction at the stent edge and stent length.Methods:1.Coronary heart disease patients with mild elevation of LDL-C were divided into threegroups:Gourp one,Forty-nine coronary heart disease patients were divided into twosub-groups,statins group and non-statins group.Group two,Fifty-seven coronaryheart disease patients were divided into two sub-groups,＞65 years old group and≤65 years old group.Group three,Seventy-eight patients with stable angina pecterisand type 2 diabetes mellitus were divided into two sub-group,statins group andnon-statins group.One 50%-70% stenosis plaque was selected as target plaque ineach patient.Coronary artery angiography (CAG) and target plaque intravascularultrasound (IVUS) were performed on admission and after 12 months later tocompare the plaque volume,lumen volume and vascular volume.2.We selected 201patients with SAP,UAP,or AMI who underwent IVUS imaging of a de novo nativeatherosclerotic lesion considered to be the culprit lesion before percutaneous coronaryintervention.The culprit lesion site for analysis was the 10-mm-long segmentincluding the smallest lumen cross-sectional area.The arc of each calcium deposit ineach image was measured with a protractor centered on the lumen and the length ofeach calcium deposit was calculated with the number of images containing thecalcium deposit minus 1,then multiplying 0.5 mm (the images were 0.5 mm apart). Finally,the AA was calculated by arc (degree) multiplying length (mm).3.Seventystents were implanted to 47 patients with stable or unstable angina and 33 stents were＜18 mm and 37 stents were＞18 mm.IVUS analysis was performed on proximalstent edge,stent area and distal stent edge.Lumen area (LA) and vascular area (VA)were measured and lumen volume (LV) and vascular volume (VV) were calculatedon the three segments.Vascular wall volume (WV) was calculated as VV—LV,volume of plaque redistribution=poststenting WV—prestenting WV.Results:1.Ingroup one,12 months later,LDL-C levels decreased by 32.8% from (3.44±0.42)mmol/L to (2.31±0.19) mmol/L in statins group and unchanged in non-statins group.These were no significant difference in vascular volume,lumen volume and plaquevolume between the two groups on admission.In non-statins group,plaque volumeincreased from (82.1±14.5) mm~3 to (95.9±20.5) mm~3(p＜0.05),lumen volumedecreased from (55.1±7.8) mm~3 to (44.6±6.6) mm~3(p＜0.05) and vascular volumeunchanged.All the indexes showed no changes after 12-months thearapy in statinsgroup.In group two,after 12 months,LDL-C in＞65 years old group and≤65years old group LDL-C decreased to 2.39 mmol/L and 2.23 mmol/L,i.e.,decreasedby 32.1% and 33.2% of the baseline values respectively.In＞65 years old group,plaque volume,lumen volume and vascular volume were unchanged,while in≤65years old group,the plaque volume decreased from (80.1±18.6) mm~3 to (69.9±21.7)mm~3 (P＜0.05),the lumen volume increased from (68.8±14.4) mm~3 to (83.6±22.5)mm~3 (P＜0.05),and the vascular volume was unchanged.There were more calcificplaques in＞65 years old group than in≤65 years old group.In group three,after12 months,LDL-C decreased 31.5% in statin group and remained unchanged innon-statin group.After 12 months,plaque volume was significantly increased [(76.1±13.0) mm~3 vs.(95.0±21.9) mm~3,P＜0.05],lumen volume was significantlydecreased [(65.0±10.9) mm~3 vs.(45.4±6.6) mm~3,P＜0.05] and vascular volumeremained unchanged in non-statins group;plaque volume was also significantlyincreased [(79.5±15.2) mm~3 vs.(87.5±17.9) mm~3,P＜0.05] while lumen volumeand vascular volume remained unchanged in statin group.Remodeling index (RI)remained unchanged in non-statin group but significantly increased in statin group (0.91±0.08 vs.0.95±0.10,P＜0.05) after 12 months.2.The average number ofcalcium deposits in the culprit lesions of patients with AMI was significantly largerthan patients with SAP or UAP and the number of calcium deposits of patients withSAP or UAP was almost same (AMI 2.21±1.98,SAP 1.15±1.01,UAP 1.20±1.15,AMI vs SAP or UAP;P＜0.0005).The average AA per calcium deposit wassignificantly different in culprit lesions of patients with SAP and UAP or AMI,thecalcium deposits were bigger in SAP than in UAP or AMI,and there were nodifferent between UAP and AMI (SAP 788.6±767.0 degree x mm,UAP 136.6±189.3degree x mm,AMI 148.4±217.1 degree x mm,SAP vs UAP or AMI;P＜0.0005).Thetotal AA of culprit lesions per patient was greatest in patients with SAP,less inpatients with AMI,and least in patients with UAP (SAP 903.3±1018.8 degree x mm,AMI 301.1±401.5 degree x mm,UAP 163.9±279.6 degree x mm,SAP vs UAP orAMI;P＜0.0005,AMI vs UAP;P＜0.01).3.Compared to prestenting,poststentingLV significantly decreased,VV remained unchanged and WV significantly increasedat proximal and distal edge of≤18 mm group and at proximal edge of＞18 mmgroup,suggesting reduced lumen due to plaque distribution.At distal edge of＞18mm group,poststenting LV,VV and WV all equally significantly increased thereforethe lumen was not effected by plaque distribution.Couclusion:1.Statins therapy canprevent the development of atherosclerotic plaque of coronary artery of coronaryheart disease patients with mild elevation of LDL-C.Statin therapy can halt thedevelopment of atherosclerotic plaque of coronary artery in old coronary heartdisease patients with mild elevation of LDL-C,but the same therapy can make theplaque regress in≤65 years old group regress.Chronic statin therapy could retardthe coronary atherosclerotic progression in patients with stable angina pectoris andtype 2 diabetes with mild elevated LDL-C.2.The culprit lesions of patients with SAP,AMI,or UAP have greatest,less,or least calcification burden,respectively.Theculprit lesions of patients with SAP have bigger and fewer calcium deposits,patientswith AMI have smaller and more numerous calcium deposits,and patients with UAPhave smaller and fewer calcium deposits.3.The poststenting lumen changes due to plaque redistribution were associated with stent length,lumen reduced at proximaland distal edge of short stents and proximal edge of long stents but not at distal edgeof long stents.
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