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| 1 | 他汀类药物、高密度脂蛋白胆固醇和冠状动脉粥样硬化减退显示文摘背景:他汀类药物可降低低密度脂蛋白胆固醇(LDL-C)水平并延缓冠状动脉粥样硬化的进展。但目前尚无资料描述他汀类药物所致高密度脂蛋白胆固醇(HDL-C)变化与疾病进展之间的关系。目的:研究LDL-C及HDL-C水平变化与粥样斑块负荷之间的关系。设计、机构和参与者:对4项前瞻性随机试验(1999-2005年分别在美国、北美、欧洲和澳大利亚进行)的原始资料进行事后分析。这些试验共纳入1455例经血管造影确诊冠心病的患者,患者均在接受他汀类药物治疗18个月或24个月时进行系列血管内超声检查。所有研究的超声分析均在同一个中心实验室进行。 | Nicholls S.J. Tuzcu E.M. Sipahi I. 奚群英 | 2007 | 世界核心医学期刊文摘(心脏病学分册)2007，3，7： | 4 |
| 2 | 他汀类药物治疗、LDL胆固醇、C反应蛋白与冠状动脉疾病的关系 | Nissen S.E. Tuzcu E.M. Schoenhagen P. 丁倩 | 2005 | 世界核心医学期刊文摘(心脏病学分册)2005，0，5： | 0 |
| 3 | 降脂治疗过程中动脉壁重构的决定因素:REVESAL(强化降脂治疗逆转动脉粥样硬化)试验中的连续血管内超声观察 | Schoenhagen P. Tuzcu E.M. Apperson-Hansen C. 杜媛 | 2007 | 世界核心医学期刊文摘(心脏病学分册)2007，0，1： | 0 |
| 4 | 动脉粥样硬化进展时冠状动脉代偿性扩张与粥样斑块负荷无关:REVERSAL试验中连续血管内超声观察结果显示文摘Aims: On the basis of the evidence from autopsy studies, it is accepted that compensatory enlargement(remodelling) of coronary arteries during progression of atherosclerosis diminishes once atheroma burden(cross-sectional area stenosis) reaches ~40%. Our aim was to evaluate whether atheroma burden is a limiting factor for coronary arterial remodelling using in vivo serial intravascular ultrasound(IVUS). Methods and results: From the cohort of the Reversal of Atherosclerosis with Aggressive Lipid Lowering(REVERSAL) trial, we identified 210 focal coronary lesions at baseline IVUS. Of these, 128 lesions that had an increase in atheroma area at the 18-month follow-up IVUS were included in the analysis. Lesions were matched at baseline and follow-up. The increase in external elastic membrane(EEM) area for each mm2 increase in atheroma area was not significantly different in lesions with< 40 and ≥40%atheroma burden at baseline(1.62 vs. 1.28 mm2, P=0.30). There were no correlations between atheroma burden at baseline and change in EEM(r=0.02, P=0.86) or change in lumen(r=0.04, P=0.64) areas. Conclusion: Assessment of coronary arterial remodelling by serial IVUS revealed that compensatory remodelling is not limited by atheroma burden. Atheroma burden is not a determinant of arterial enlargement during the progression of atherosclerosis. | Sipahi I. Tuzcu E.M. Schoenhagen P. 郭俊 | 2006 | 世界核心医学期刊文摘(心脏病学分册)2006，，12： | 0 |
| 5 | 心血管危险因素和血管内超声评定动脉粥样硬化病变负荷的关系 | Nicholls S.J. Tuzcu E.M. Crowe T. S.E. Nissen 郭俊 | 2006 | 世界核心医学期刊文摘(心脏病学分册)2006，0，7： | 0 |
| 6 | ACAT抑制对冠状动脉粥样硬化进展的影响显示文摘Background: The enzyme acyl-coenzyme A:cholesterol acyltransferase(ACAT) esterifies cholesterol in a variety of tissues. In some animal models, ACAT inhibitors have antiatherosclerotic effects. Methods: We performed intravascular ultrasonography in 408 patients with angiographically documented coronary disease. All patients received usual care for secondary prevention, including statins, if indicated. Patients were randomly assigned to receive the ACAT inhibitor pactimibe(100 mg per day) or matching placebo. Ultrasonography was repeated after 18 months to measure the progression of atherosclerosis. Results: The primary efficacy variable analyzing the progression of atherosclerosis-the change in percent atheroma volume-was similar in the pactimibe and placebo groups(0.69 percent and 0.59 percent, respectively; P=0.77). However, both secondary efficacy variables assessed by means of intravascular ultrasonography showed unfavorable effects of pactimibe treatment. As compared with baseline values, the normalized total atheroma volume showed significant regression in the placebo group(-5.6 mm3, P=0.001) but not in the pactimibe group(-1.3 mm3, P=0.39; P=0.03 for the comparison between groups). The atheroma volume in the most diseased 10-mm subsegment regressed by 3.2 mm3 in the placebo group, as compared with a decrease of 1.3 mm3 in the pactimibe group(P=0.01). The combined incidence of adverse cardiovascular outcomes was similar in the two groups(P=0.53). Conclusions: For patients with coronary disease, treatment with an ACAT inhibitor did not improve the primary efficacy variable(percent atheroma volume) and adversely affected two major secondary efficacy measures assessed by intravascular ultrasonography. ACAT inhibition is not an effective strategy for limiting atherosclerosis and may promote atherogenesis.(ClinicalTrials.gov number, NCT 00268515). | Nissen S.E. Tuzcu E.M. Brewer H.B. 杜媛 | 2006 | 世界核心医学期刊文摘(心脏病学分册)2006，2，9： | 0 |
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