Study On Stability Of Atherosclerotic Plaque Of Patients With Coronary Heart Disease By Coronary Angioscopy

IntroductionCoronary atherosclerosis is a concealed disease, which can last without symptoms for a long time. The clinical abnormality take place only when the plague enlarges to some degree, or the plague ruptures and following thrombus forms, which can reduce the perfusion of myocardium. Pathological studies show that the plague rupture and the following thrombus formation are the important pathological basis for the acute narrow or occlusion of coronary artery that can cause acute coronary syndrome ( unstable angina pectoris, acute myocardial infarction , sudden cardiogenic death). Some scholars found from autopsy that there is plague ruptures at two or more sites in one patient, and some ruptures didnt result in severe narrow of coronary artery or clinical symptoms which is proved by pathological study. There are only a few biopsy studies on the coronary artery, especially the study on the risk factors of coronary intima abnormality. Recently the ACS incidence has an increasing tendency and some documents show that the increases are relative with the increasing risk factors of CHD. But which risk factors is closely related with ACS is not well known.Coronary angioscopy(CAS) is a new method for CHD pathological diagnosis which is applied clinically in recent years. As a new method , it is being widely applied clinically especially in the study of ACS and the PCI of CHD. Clinical application shows that to make accurate pathological diagnosis of the coronary intima by naked eyes is possible by CAS with the features of high resolution and fresh colors. It helps determine the aetiology of different coronary artery disease and predict the cardiovascular events which coronary angiograpy cannt.In this study, the relationship between plague stability in the culprit artery and the thrombus formation is explored in the patients with UAP and AMI to determine the pathological basis and pathogenesis of UAP and AMI. At the same time, the non - culprit branches in the patients with OMI and stable angina are also investigated by CAS to determine the relationship between the intima abnormality and CHD risk factors such as hypertension^diabetes^ smoking., abnormal lipid metabolism >, family history,, homocysteine^ox - LDL and the benefitial effect of controlling risk factors on the asymptomatic intima abnormality further more.Objects and Methods1. Objects114 patients diagnosed as ACS who had received PCI treatment from 2004. 1 to 2004. 12 are studied, male 76 cases, female 38 cases with an average age 61.68^ 8.56;UAP 68 cases, AMI 46 cases;120 patients diagnosed OMI and SA who had repeived PCI treatment are also studied, male 79 cases, female 41 cases with an average age of 54. 01 ,,12. 63. The culprit and non - culprit branches are investigated by CAS in all the patients during PCI.2. The operation of CASAfter PCI, 0.014"guiding wire is introduced to the target coronary branch;the CAS catheter is positioned at the target site under the guidance of the guiding wire and X - ray;the balloon is dialated to occlude the blood flow and warm heparin NS is injected to the vessel at a rate of 0. 5 -0. 8ml/s;the vessel can be observed by moving the catheter forward several centimeters or backward;what is observed is recorded. One branch can be investigated several times and 5 ~60s for each time.3. Findings in vessels by angioscopyThere are three types of intima atherosclerosis plagues and thrombi classified by color, activity, surface features and whether protrusion into lumen or not.1) Atherosclerosis plague : classified into yellow plague, buff plague and white plague by color. Yellow plagues ordinarily called unstable plague, are fullof more cholesterol (fat pool)under thin fibrous cap. White plagues are ordinarily called stable plague, with thick fibrous cap and less cholesterol.2) Rupture of plague: Intima injures ( broken, exfoliation, float) can be observed and sometimes accompanied by internal bleeding.3) Thrombus: Thrombi were classified into red thrombus ( mainly red) , white - red mixed thrombus, white thrombus and pink thrombus ( mainly white). The former two are fresh thrombus and latter two are old thrombus. Thrombus are divided into non - occlusion and occlusion types by whether protrusion into lumen and its degree.Intima lesions exist when yellow plague , plague rupture and thrombosis are observed (picture 1). The studied patients were divided into intima lesion group (including yellow plague group and complex plague group) and non - intima lesion group (including plague rupture group and/or thrombosis group) .4. Risk factors of CHDTo explore the relationships between asymptomatic intima lesions and the risk factors of CHD ( hypertension, DM, smoking, blood cholesterol disorders;family history, plasma Hey levels and ox - LDL levels). Automatic fluorescent partial - vibration immunoassay was used to determine the plasma Hey levels, and ox - LDL levels ( ELISA).5. Statistic analysisSAS V8 was applied. All data were recorded as x ± s. The t test and x test were applied to analyze, and p <0.05 means significant difference.Results1. The relationship between atherosclerosis plaque stability and thrombus formation in the culprit artery of ACS patients.1) There are yellow plaques in 48 cases (70.59% ) , ruptured plaques in 46 cases (67. 65% ) , thrombi in 63 cases (92. 64 % ) observed among the culprit arteries of 68 patients with UAP. The thrombi are all non - occlusive, among which there are red or mixed thrombi in 11 cases(11.18% ), pink thrombi in 52 cases(76.47 % ).2 ) There are yellow plaques in the culprit arteries of all patients with AMI,among which ruptured plaques in 32 cases (69. 57% ) , red or mixed thrombi in 36 cases (78.26% ) , occlusive thrombi in 24 cases (66. 67% ) , non - occlu-sive in 12 cases (33. 33% ). There are more ruptured plaque in NSTEMI group than in STEMI group ( p < 0. 05 );more red or mixed thrombi in STEMI group than in NSTEMI group(p <0.05). In STEMI group, the occlusive thrombi predominates (p <0. 05) , compared with NSTEMI group;in NSTEMI group, the non - occlusive thrombi predominates ( p < 0.05).2. The relationship between asymptomatic coronary intima lesions and CHD risk factors.1) Among 155 non - culprit branches in 120 patients, intima lesions are observed in 80 cases (66.67% ) ,no intima lesions in 40 cases (33. 33% ). In the group with intima lesions, simple yellow plaques are obserued in 30 cases (25.00% ) , complex plaques in 50 cases(41. 67% ).2) The hypertension^high LDL -C^diabetes are more common in 80 cases with intima lesions than in 40 cases without intima lesions (p <0. 0001;p <0. 0001;p<0.05).3) High LDL - C >, high TC are more common in the yellow plagues group (30 cases) than in the non - intima lesions group( p < 0. 0001;p <0. 05).4) The hypertension^high LDL -C^diabetes are more common in complex plagues group (50 cases) than in non - intima lesions group (p <0.0001;p < 0.005;p<0.05).5) The plasma Hey is much higher in the intima lesion group than in non -intima lesion group (p <0. 0001 ). The same change is also observed in both yellow plague and complex plague group ( p < 0. 0001;p < 0. 0001). The ox -LDL - C is much higher in the intima lesion group than in non - intima lesion group ( p < 0. 0001 );The same change is also observed in complex plague group ( P < 0.0001);but there is no significantly difference in the ox - LDL - C levels between yellow plague group and non - intima lesion group( P >0.05 ).3. The prevention of asymptomatic intima lesion by controlling risk factors. 1) The incidence of complex intima lesson such as plague rupture can belowered obviously if the blood pressure is controlled under 140/90 mmHg in the patients with hypertension ( P < 0.05 ).2) The incidence of intima lesion, yellow plague, plague rupture is lower if LDL - C is less than lOOmg/dl in patients with high LDL - C.3 ) The incidence of intima lesion, plague rupture is lower if the blood sugar is well controlled than if the blood sugar is badly controlled in the patients with diabetes, ( P < 0. 05 ).Conclusion1. The pathological basis of ACS is the yellow atherosclerosis plague and the following thrombus formation when plague ruptured. The patients with UAP have the same possibility of thrombus formation as the patients with AMI. Old pink and ( or) white non - occlusive thrombi predominate in the patients with UAP, and fresh and (or) mixed thrombi in the patients with AMI. There is the same possibility of plague rupture in the patients with UAP and AMI. But the patients with AMI suffer from plague rupture more severely than with UAP. There is more plague rupture in NSTEMI than in STEMI, more red or mixed thrombi in STEMI than in NSTEMI. Occlusive thrombi predominates in STEMI and non - occlusive thrombi in NSTEMI.2. Hypertension and diabetes take part in the formation of asymtomatic intima lesion and plague rupture, especially hypertension. TC and LDL — C is the basis of formation of yellow plague which take part in the plague rupture. Hey and ox - LDL as new risk factors for CHD also take part in the formation and rupture of atherosclerosis plague.3. The possibility of formation and rupture of atherosclerosis plague can be reduced obviously, which can prevent the onset of ACS, by controlling the BP in hypertension and controlling blood sugar in diabetes.