Coronary artery thrombosis in patients with unstable angina.

This report describes the clinical course, coronary artery anatomy, and ventricular function of 16 patients in whom coronary artery thrombosis was detected at the time of cardiac catheterisation. All patients had an unstable clinical course in which accelerated angina occurred a mean of four weeks (range four days to 12 weeks) before catheterisation, and four patients had recent subendocardial myocardial infarction. In all patients severe coronary artery disease was documented at catheterisation. Fifteen patients had segmental wall motion abnormalities involving the left ventricular wall that was supplied by the coronary artery in which there was thrombus. Three patterns of coronary artery thrombus were noted: (1) Thrombus proximal to high-grade coronary artery stenosis; (2) thrombus distal to high-grade coronary artery stenosis; and (3) thrombus in segments of the arterial tree in which there was no high-grade coronary artery stenosis. Though the precise cause of the coronary artery thrombosis in our patients is unknown, it may have been a result of stasis, a ruptured atherosclerotic plaque, or coronary spasm. The common clinical course with unstable angina of acute onset suggests the possibility that the thrombus may have been responsible for the abrupt change in clinical condition or may have been a contributing factor in the patients' course.     

Coronary anatomy and arteriography in patients with unstable angina pectoris.

A prospective series of 188 patients with the syndrome of unstable angina pectoris undergoing coronary arteriography was reviewed to determine the spectrum of anatomic coronary artery disease, suitability for coronary revascularization and in-hospital morbidity and mortality. Thirty-two patients demonstrated normal to moderately diseased coronary arteries. None of these patients sustained myocardial infarction or died. Twenty patients (10.6 percent) had normal coronary arteriograms. Of the 156 patients having severe coronary artery disease (greater than 70 percent stenosis), 20 patients (13 percent) had left main coronary artery disease. One hundred forty-two patients (91 percent) were potential candidates for coronary surgery; 14 were not candidates because of distal vessel disease or poor left ventricular function. During cardiac angiography or in the subsequent hospital period 12 patients sustained a myocardial infarction and 7 of these died. Of these seven, six had left main coronary artery disease and one had three vessel disease. In three patients who died (1.9 percent of those with severe coronary artery disease) the death may have been related to cardiac catheterization because evidence of myocardial necrosis began within 24 hours of study. Thus, patients with the syndrome of unstable angina pectoris usually presented with severe coronary artery disease and were candidates for coronary revascularization. The anatomic severity of coronary artery disease appeared to be the most important factor contributing to myocardlal infarction or death after cardiac catheterization. Mortality after catheterization was primarily associated with left main coronary artery disease.     

Coronary hemodynamic effects of systemic thrombolysis in patients with unstable angina.

Intracoronary (i.c.) thrombus is a frequent finding in patients with unstable angina (UA). Accordingly, thrombolytic treatment could be beneficial, as resolution of thrombus might result in increased delivery of blood flow to the ischemic regions. To test this hypothesis, we studied 13 patients with active UA and ST-segment shift in the anterior leads. Coronary angiography was performed and great cardiac vein blood flow (GCVF; thermodilution) was measured in all patients 25 +/- 14 h after the last chest pain episode. Following angiography, patients received i.v. urokinase (UK: 1,000,000 IU/30 min); aortic pressure and GCVF were measured before and every 10 min following drug infusion, for a total time of 90 min. At baseline angiography, 5 of 13 patients (Group 1) had evidence of i.c. thrombus (intraluminal filling defect or thrombotic subocclusion) in the ischemia-related left coronary artery, whereas 8 patients (Group 2) did not. Group analysis showed that UK increased GCVF and decreased anterior coronary resistance in Group 1 (respectively, from 86 +/- 33 to 114 +/- 41 ml/min: p less than 0.005; and from 1.37 +/- 0.68 to 1.01 +/- 0.44 mmHg/ml/min: p less than 0.05) but not in Group 2 (both: p = NS). In conclusion, UK has been shown to increase regional coronary blood flow in selected patients presenting with active UA, as well as evidence of i.c. thrombus at early angiography. Heterogeneity of angiographic findings could explain controversies in trials dealing with thrombolysis in UA.     

血管内超声技术对不稳定性心绞痛患者冠状动脉临界病变形态学评价

目的应用血管内超声技术探讨不稳定性心绞痛患者冠状动脉临界病变的形态学特征。方法入选98例不稳定性心绞痛（uA,56例）或稳定性心绞痛（SA,42例）患者,经冠状动脉造影检查证实至少一支冠状动脉主要分支存在〉20％且〈70％局限狭窄,对符合条件的冠状动脉进行血管内超声检查。结果在病变部位,斑块面积（7．85±2．83）mm^2比（6．53±2．92）mm^2、斑块负荷（60．92±11．04）％比（53．87±17．52）％、重构指数（0．93±0．16）比（0．86±0．10）及偏心指数（0．74±0．17）比（0．66±0．21）,在uA组高于SA组。正性重构在UA组比SA组更多见（28．6％±9．5％）,偏心斑块及软斑块发生率在UA组更高（89．3％比71．4％）和（3．9％比16．7％）。结论冠状动脉临界病变的斑块负荷和重构指数在UA患者高于SA患者,uA组具有更多正性重构的患者,提示斑块的形态学与临床心绞痛的状态密切相关。     

Coronary microcirculatory vasoconstriction during ischemia in patients with unstable angina

OBJECTIVE: To verify the behavior of coronary microvascular tone during spontaneous ischemia in patients with unstable angina (UA). BACKGROUND: In UA, the pathogenetic role of vasoconstriction is classically confined at the stenotic coronary segment. However, microcirculatory vasoconstriction has been also suggested by previous experimental and clinical studies. METHODS: The study included 10 patients with UA (recent worsening of anginal threshold and appearance of angina at rest) and single-vessel CAD. Blood flow velocity was monitored by a Doppler catheter in the diseased artery. Transstenotic pressure gradient was monitored by aortic and distal coronary pressure monitoring. Stenosis resistance was calculated as the ratio between pressure gradient and blood flow, microvascular resistance as the ratio between distal pressure and blood flow. Measurements were obtained at baseline, following intracoronary adenosine (2 mg) and during transient ischemia. Aortic and distal coronary pressures were also measured during balloon coronary occlusion. RESULTS: Adenosine did not affect stenosis resistance, while it decreased (p < 0.05) microvascular resistance to 52 +/- 22% of baseline. Angina and ischemic ST segment shift were associated with transient angiographic coronary occlusion in 7 of 10 patients; however, in no case was ischemia associated with interruption of flow. Despite markedly different flow values, distal coronary pressure was similar during adenosine and during spontaneous ischemia (48 +/- 15 vs. 46 +/- 20 mm Hg, respectively, NS). During ischemia, a marked increase in the resistance of both coronary stenosis and coronary microcirculation was observed (to 1,233% +/- 1,298% and 671% +/- 652% of baseline, respectively, p < 0.05). Distal coronary pressure was markedly reduced during balloon coronary occlusion (14 +/- 7 mm Hg, p < 0.05 vs. both adenosine and ischemia), suggesting the absence of significant collateral circulation. CONCLUSIONS: In patients with UA, transient myocardial ischemia is associated with vasoconstriction of both stenotic arterial segment and downstream microcirculation.     

Coronary angioplasty of 'complex lesions' in patients with unstable angina

Out of 55 patients subjected to coronary angioplasty over the past 12 months, there were 33 (60%) who had unstable angina. Amongst these, 22 patients had coronary lesions classified as 'complex' on coronary angiography. These included tandem lesions, branch stenoses, distal lesions, total occlusions, vein graft stenoses, lesions with ulceration and intraluminal clot and associated with valvular lesions. We describe our experience of coronary angioplasty in these 22 patients of unstable angina having 'complex lesions'. All were males with a mean age of 48.7 +/- 13 years. Fourteen patients had single vessel and 8 multivessel disease. A total of 35 lesions were subjected to dilatation. The angiographic primary success was achieved in 85.7% of the lesions attempted. Except total occlusions and very distal lesions, all other types of 'complex lesions' could be dilated with a success rate of greater than 75%. There were 4 (11.4%) failures because of inability to cross the lesion with the guidewire or balloon catheter. One patient developed non-Q wave inferior wall infarction. There were no deaths. We conclude that coronary angioplasty of various types of 'complex lesions' can be performed with a good primary success and negligible complications in our setting.     

Coronary angioplasty for unstable angina.

Coronary angioplasty is an effective treatment for subgroups of patients with unstable angina. The procedure has a high initial success rate but there is an increased risk of major complications resulting from a higher incidence of acute closure presumably related to additional injury of the underlying plaque with augmented platelet and clotting activity, and ensuing spasm. Newer agents that inhibit platelet aggregation or thrombin may provide a safer use of coronary angioplasty in patients with unstable angina. Coronary angioplasty is indicated if a stenosis, technically suitable for dilation, is found to be responsible for the unstable state. The decision in favor of coronary angioplasty in patients with single-vessel disease is easy to make. Patients with left main stem disease or severe multivessel disease should primarily be scheduled for bypass surgery. In the presence of other multivessel disease, uncertainty remains. However, in selected patients with multivessel disease, one might prefer dilation of the ischemia-related vessel "the culprit vessel" only, rather than total revascularization by multiple dilatations or bypass surgery, since this can be performed faster and thus shorten the hospital stay. Thrombolytic treatment in the management of patients with unstable angina may be indicated in patients with pre-existing intracoronary thrombi or when procedural acute closure occurs associated with intracoronary thrombus formation.     

Immunoinflammatory factors in unstable angina. Possibility of influence of atorvastatin

In 101 patients with ischemic heart disease (unstable angina class I and II - III) with hypercholesterolemia at the background of standard therapy (51 patients) and after administration of atorvastatin (50 persons) prescribed from first day of hospitalization in mean dose 10.8 +/- 0.1 mg/day immune status was studied in accordance with 3 stage scheme of examination. In dynamics (before onset of treatment and after 6 months of therapy) a concentrations of a row of cytokines was studied: a-factor of tumor necrosis (TNFa) and C-reactive protein (CRP). At correlation analysis of parameters of plasma lipid composition and immune profile it has been established that in patients with unstable angina (in the presence of hypercholesterolemia) together with elevation of CRP level substantial signs of dysbalance in immune system are observed. These signs appear as elevation of levels of TNFa, interleukin-4, and especially interferon g with simultaneous depression of cells of immune defense. In has been demonstrated that atorvastatin not only exerts good hypolipidemic effect, but is capable to diminish immunoinflammatory shifts in patients with acute coronary pathology.     

Coronary venous retroperfusion support during high risk angioplasty in patients with unstable angina: preliminary experience

Synchronized coronary venous retroperfusion was used during coronary balloon angioplasty to support the ischemic myocardium of 20 patients with unstable angina and anatomy at high risk of a coronary event. Hemodynamics and left ventricular function were the major end points of the study. Coronary venous catheterization and retroperfusion were successfully performed in 15 patients. The target vessel was an unprotected left main artery in 2, left anterior descending artery in 10, left circumflex coronary artery in 1 and right coronary artery in 2 patients. A nonsupported balloon inflation (mean 44 +/- 13 s) was compared with a later retroperfusion-supported inflation (mean 145 +/- 21 s). Right anterior oblique left ventriculograms, aortic blood pressure, pulmonary artery pressure and thermodilution cardiac output were obtained before and during peak untreated and treated balloon inflations and on completion of angioplasty. All patients had either a baseline left ventricular ejection fraction less than 0.40 or greater than 40% of contracting myocardium estimated to be at risk for severe ischemia during angioplasty. The cardiac (liters/min per m2) and stroke work (g.m/m2) indexes decreased from mean baseline values of 2.5 +/- 0.52 and 52 +/- 15 to 1.7 +/- 0.47 and 27 +/- 12 (mean +/- SD), respectively, during nonsupported balloon inflations but decreased only to 2.1 +/- 0.52 (p less than 0.01 vs. nonsupported) and to 36 +/- 14 (p = 0.01 vs. nonsupported), respectively, during retroperfusion-supported inflations. Ejection fraction (n = 8) decreased from a baseline value of 55 +/- 13% to 27 +/- 7.3% during nonsupported inflations but only to 39 +/- 10% during retroperfusion-supported inflations (p = 0.01 vs. nonsupported). Regional wall motion (area change) in the ischemic (target) region was reduced from a baseline value of 49 +/- 17% to 11 +/- 16% during nonsupported inflations but only to 27 +/- 15% during retroperfusion-supported inflations (p less than 0.01 vs. nonsupported). All but two patients had a favorable hemodynamic response to retroperfusion. There were no serious adverse effects related to the procedures and no hospital deaths. It is concluded from this preliminary study that coronary venous retroperfusion appears to be safe, to provide hemodynamic support and to improve left ventricular function during angioplasty in patients with unstable angina and anatomy at high risk of a coronary event.     

Serum neopterin and complex stenosis morphology in patients with unstable angina

OBJECTIVES: We sought to assess the relation between serum neopterin concentration and complex coronary artery stenosis in patients with unstable angina. BACKGROUND: Monocyte activation is associated with acute atheromatous plaque disruption and acute coronary syndromes. Angiographically demonstrated complex coronary stenosis is often an expression of plaque disruption. Increased serum concentration of neopterin, a pterydine derivative secreted by macrophages after stimulation by interferon-gamma, has been observed in patients with acute coronary syndromes as compared with control subjects and patients with stable angina pectoris. METHODS: We studied 50 patients with unstable angina (32 men) who underwent coronary angiography after hospital admission. All coronary stenoses with > or =30% diameter reduction were assessed and classified as "complex" (irregular or scalloped borders, ulceration or filling defects suggesting thrombi) or "smooth" (absence of complex features). Serum neopterin levels were assessed within 24 h of hospital admission using a commercially available immunoassay (enzyme-linked immunosorbent assay kit, IBL, Hamburg, Germany). RESULTS: Thirty-nine patients were classified in Braunwald class IIIb, four in class IIb and seven in class Ib. The number of complex lesions per patient was 2.6+/-1.8 (mean +/- SD). The mean neopterin concentration was 7.76+/-3.62 nmol/liter. A significant correlation was observed between neopterin serum concentration and the presence of complex coronary stenoses (r = 0.35, p = 0.015). Multiple regression analysis showed that serum neopterin (p < 0.0001) was independently associated with the number of complex lesions. Other variables associated with complex lesions were the number of vessels with > or =75% stenosis (p < 0.0001), plasma creatinine (p = 0.003), triglycerides (p = 0.014) and a history of unstable angina (p = 0.032). CONCLUSIONS: Serum neopterin concentration is associated with the presence of angiographically demonstrated complex lesions in patients with unstable angina and may represent a marker of coronary disease activity.     

不稳定型心绞痛患者介人术后对比剂肾病的危险因素

目的探讨不稳定型心绞痛患者冠状动脉(冠脉)介入诊断及治疗术后对比剂肾病(CIN)的发生率及危险因素。方法连续入选2007年1～8月因不稳定型心绞痛入院并接受择期冠脉介入手术的患者232例。排除标准:(1)血压<120/70 mm Hg;(2)心功能(NYHA)分级>Ⅲ级。术中使用低渗非离子型对比剂碘普罗胺。介入术后24～72 h血肌酐(Scr)较基础值增高25%或44.2 μmol/L定义为CIN。分析CIN发生率与各项危险因素的相关性。结果 CIN总发生率为14.7%。冠脉钙化、术前Scr水平≥132.6 μmol/L、内生肌酐清除率(Ccr)<60 ml/min、NYHA Ⅲ级、糖尿病及年龄≥70岁的患者CIN发生率均明显增高。多变量回归分析显示,基线Scr≥132.6μmol/L、Ccr<60 ml/min、NYHA Ⅲ级与CIN的相关性最强。结论不稳定型心绞痛患者接受冠脉介入术后CIN是常见的并发症;高龄、肾功能不全、心功能不全、糖尿病及造影发现冠脉钙化是CIN发生的危险因素。     

Coronary angiographic findings and troponin T in patients with unstable angina pectoris

This study sought to identify differences in coronary anatomic pathology in patients with unstable angina and elevated versus nonelevated serum troponin T values. Previous studies have shown a worse prognosis in unstable angina patients with elevated serum troponin T values. Consecutive patients (n = 117) with Braunwald class IIIB angina were included in the study. Serum samples for troponin T were obtained at admission and every 6 to 8 hours for 18 to 24 hours. Acute myocardial infarction was excluded by routine creatine kinase measurements. All patients underwent coronary angiography before discharge. Cardiac events including cardiac death and myocardial infarction were recorded. Two thirds of the patients with unstable angina had no increase in serum troponin T (<0.1 microg/L) (n = 80). They had a lower incidence of 3-vessel disease (26% vs 46%, p <0.001), left main disease (5% vs 16%, p = 0.04), visible thrombus (4% vs 22%, p = 0.006), and less severe stenosis of the culprit artery (65% vs 84%, p <0.004) than patients with elevated serum troponin T values (> or =0.1 microg/L) (n = 37). The 1-year cardiac event rate was 0% versus 19% in patients with troponin T values <0.1 microg/L compared with patients with serum troponin T values > or =0.1 microg/L (p <0.0001). It was concluded that patients with unstable angina and no release of troponin T have less severe coronary artery disease, and have an excellent prognosis. It is suggested that these patients may be managed more conservatively and without invasive evaluation before discharge.     

Angiographic morphology in unstable angina pectoris

Complex morphology occurs frequently in unstable angina; however, its relation to symptomatic presentation, timing of angiography and hospital outcome has not been investigated. Accordingly, coronary angiography was performed 5 +/- 2 days after qualifying rest pain in 101 consecutive patients presenting with acute coronary insufficiency (n = 67) or crescendo angina (n = 34). Significant coronary artery disease was defined as any greater than or equal to 50% stenosis, and complex morphology as any stenosis with irregularity, overhang or thrombus. Eight of the 67 patients presenting with acute coronary insufficiency later proved to have a myocardial infarction as the qualifying event (creatine kinase twice normal with elevation of MB fraction). There were no myocardial infarctions in the crescendo angina group. Complex morphology occurred in 61% of patients. Thrombus alone occurred in 27% of patients with unstable angina without myocardial infarction, with similar frequencies between the 2 clinical groups. In contrast, intraluminal thrombi were identified in 78% of patients with acute coronary insufficiency who later proved to have a myocardial infarction as the qualifying event. The need for urgent catheterization (less than 48 hours) prompted by recurrent symptoms was associated with the angiographic findings of intraluminal thrombus (46%) and complex morphology (83%). The presence of complex morphology and intracoronary thrombus was associated with a higher incidence of in-hospital cardiac events, i.e., revascularization, myocardial infarction and death, independent of the incidence of multivessel disease.     

非高压扩张和无抗凝植入冠状动脉内支架治疗不稳定型心绞痛

目的 :评估 Wiktor- Gx Hepamed冠状动脉内支架的临床疗效。方法 :对 15例不稳定型心绞痛患者植入冠状动脉内支架。植入支架的压力为 (982 .9± 182 .4) k Pa。术后即刻残余狭窄 (10 .3± 9.8) % ,支架术的急性获得 (1.96± 0 .5 1) m m,后期丢失 (0 .5 8± 0 .91) mm。术后未给肝素和华法令 ,仅服抗血小板药物。结果 :术后住院 (3± 1) d。随访 (378± 6 6 ) d,其中 2例再狭窄。在住院期和随访期 ,无一例发生严重心脏事件及出血、血栓形成、再阻塞。结论 :非高压扩张和无抗凝的 Wiktor- GX Hepamed冠状动脉内支架术是安全和有效的。     

Validated risk stratification model accurately predicts low risk in patients with unstable angina

BACKGROUND: In the mid 1990s, two unstable angina risk prediction models were proposed but neither has been validated on separate population or compared. OBJECTIVES: The purpose of this study was to compare patient outcome among high, medium and low risk unstable angina patients defined by the Agency for Health Care Policy and Research (AHCPR) guideline to similar risk groups defined by a validated model from our institution (RUSH). METHODS: Four hundred sixteen patients consecutively admitted to the hospital with unstable angina between January 1, 1995, and December 31, 1997, were prospectively evaluated for risk factors. The presence of major adverse events such as myocardial infarction (MI), death and heart failure was assessed for each patient by chart review. RESULTS: The composite end point of heart failure, MI or death occurred in 3% and 5% of the RUSH and AHCPR low risk categories, respectively, and in 8% and 10% of AHCPR and RUSH high risk categories, respectively. Recurrent ischemic events were best predicted by the RUSH model (high: 24% vs. medium: 12% and low: 10%, p = 0.029), but not by the AHCPR model (high: 14% vs. medium: 13% and low: 9%, p = 0.876). The RUSH model identified five times more low risk patients than the AHCPR model. CONCLUSIONS: Both models identify patients with low and high event rates of MI, death or heart failure. However, the RUSH model allowed for five times more patients to be candidates for outpatient evaluation (low risk) with a similar observed event rate to the AHCPR model; also, the RUSH model more successfully predicted ischemic complications. We conclude that the RUSH model can be used clinically to identify patients for early noninvasive evaluation, thereby improving cost effectiveness of care.     

Coronary angioplasty of the unstable angina related vessel in patients with multivessel disease

This study is a retrospective analysis of the efficacy of percutaneoustransluminal coronary angioplasty of the ischaemia-related vesselin patients with unstable angina. Forty-three patients had multivesseldisease with dilatation of the ischaemia-related vessel only(group I; partial revascularization) while 111 patients hadsingle vessel disease only (group II; total revascularization).The initial success rate in both groups was identical (88 versus88%). The need for emergency coronary artery bypass surgerywas similar in the two groups (group 112% versus group II 9%;NS). The total post PTC A myocardial infarction rate (despiteurgent CABG) was also similar in the two groups (group 19% versusgroup II 10%; NS). The results of electrocardiographic exercise testing and Thallium-201scintigraphy provide objective evidence for incomplete revascularizationin group I. The maximum workload achieved was lower, and thefrequency of exercise induced angina, ST-segment depressionand reversible perfusion defect was higher than in group II.Moreover, at 6 months follow-up the recurrence rate of anginapectoris rate was higher in group I than in group II (29% versus16% P<0.05). It is concluded that dilatation of the ischaemia related vesselonly in patients with unstable angina and multivessel diseaseis as effective in the management of the acute phase of unstableangina as is dilatation of the ischaemia related vessel in patientswith single vessel disease. However, due to only partial revascularizationthe recurrence rate of angina pectoris is higher.     

光学相干断层扫描比较不稳定性和稳定性心绞痛患者粥样硬化斑块特征

Objective To compare the characterization of coronary atherosclerotic plaques in patients with unstable angina pectoris (UAP) and stable angina pectoris (SAP) by optical coherence tomography (OCT). Methods OCT was performed in 47 patients (23 UAP and 24 SAP) undergoing coronary angiography. Lipid-rich plaque (defined by ≥ 2 quandrants of the cross-section area), thin cap fibroatheroma (TCFA), thickness of fibrous cap, plaque rupture, calcification and thrombus visualized by OCT were compared between UAP and SAP patients. Results OCT imaging was successfully in 44 out of 47 patients (22 UAP, 22 SAP). Proportion of lipid-rich plaques was similar between UAP and SAP groups [91% (20/22) vs, 73% (16/22),P =0. 741]. The minimum thickness of fibrous cap in the UAP group was significantly thinner than that in SAP group [(69.5±34.7) μm vs. (141.1±68.5) μm, P = 0.000] and the rate of fibrous cap erosion in the UAP group was significantly higher than that in the SAP group [59% (13/22) vs. 9% (2/22), P=0.000]. Percents of TCFA [73% (16/22) vs. 14% (3/22) ,P = 0.000] and plaque rupture [50% (11/22) vs.9% (2/22) , P = 0.003] were significantly higher in UAP group compared those in SAP group. Incidence of thrombus and calcification were similar between two groups. Conclusions OCT imaging can clearly define plaque characterization of coronary atherosclerosis. UAP patients have thinner fibrous cap, higher incidences of fibrous cap erosion, plaque rupture and TCFA compared patients with SAP.     

光学相干断层扫描比较不稳定性和稳定性心绞痛患者粥样硬化斑块特征

Objective To compare the characterization of coronary atherosclerotic plaques in patients with unstable angina pectoris (UAP) and stable angina pectoris (SAP) by optical coherence tomography (OCT). Methods OCT was performed in 47 patients (23 UAP and 24 SAP) undergoing coronary angiography. Lipid-rich plaque (defined by ≥ 2 quandrants of the cross-section area), thin cap fibroatheroma (TCFA), thickness of fibrous cap, plaque rupture, calcification and thrombus visualized by OCT were compared between UAP and SAP patients. Results OCT imaging was successfully in 44 out of 47 patients (22 UAP, 22 SAP). Proportion of lipid-rich plaques was similar between UAP and SAP groups [91% (20/22) vs, 73% (16/22),P =0. 741]. The minimum thickness of fibrous cap in the UAP group was significantly thinner than that in SAP group [(69.5±34.7) μm vs. (141.1±68.5) μm, P = 0.000] and the rate of fibrous cap erosion in the UAP group was significantly higher than that in the SAP group [59% (13/22) vs. 9% (2/22), P=0.000]. Percents of TCFA [73% (16/22) vs. 14% (3/22) ,P = 0.000] and plaque rupture [50% (11/22) vs.9% (2/22) , P = 0.003] were significantly higher in UAP group compared those in SAP group. Incidence of thrombus and calcification were similar between two groups. Conclusions OCT imaging can clearly define plaque characterization of coronary atherosclerosis. UAP patients have thinner fibrous cap, higher incidences of fibrous cap erosion, plaque rupture and TCFA compared patients with SAP.