药物洗脱支架治疗冠脉无保护左主干病变的近中期疗效

目的：评价药物洗脱支架治疗冠脉无保护左主干病变的临床疗效。方法：回顾性分析2009年1月～2011年1月完成的65例无保护左主干病变药物洗脱支架置入术患者的临床资料。结果：65例无保护左主干病变患者全部成功置入支架,住院期间无主要心血管事件发生;术后6个月冠脉造影随访28例（43.1%）,其中2例发生再狭窄,再狭窄率7.1%;3年电话随访54例（83.1%）,其中8例患者心绞痛复发（14.8%）;2例（3.7%）行冠状动脉旁路移植术,余均无症状生存,3年生存率为100%。结论：药物洗脱支架治疗经选择的冠脉无保护左主干病变是安全可行的,有较理想的近期和中期疗效。     

唐山地区汉族人群血管紧张素转换酶基因多态性与冠心病的相关性研究

目的探讨血管紧张素转换酶(ACE)基因插入/缺失(insertion/deletion,I/D)多态性与冠状动脉粥样硬化性心脏病(冠心病)及冠状动脉(冠脉)病变支数间的关系。方法选取住院患者332例,其籍贯均为河北唐山地区,行冠脉造影术检查判定其是否患有冠心病及其冠脉病变支数。根据造影结果分为冠心病组(至少有一支冠脉主支血管狭窄≥50%)233例(稳定型心绞痛亚组150例、急性冠脉综合征组亚组83例)和对照组99例(任一冠脉主支血管狭窄50%)。应用聚合酶链式反应技术检测患者ACE基因I/D多态性,包括II型(插入型纯合子)、ID型(插入与缺失型杂合子)、DD型(缺失型纯合子)三组,并分析不同组别间I/D多态性差异。结果冠心病组及急性冠脉综合征亚组ACE基因DD型和D等位基因频率显著高于对照组(P0.05)。稳定型心绞痛组与对照组比较DD基因型和D等位基因频率间并无显著差异(P0.05)。不同冠脉病变支数在ACE基因型间差异无统计学意义(P0.05)。结论唐山地区汉族人群ACE基因I/D多态性中DD型和D等位基因发生率冠心病及急性冠脉综合征患者中增高,但与冠脉病变支数无关。     

无保护左主干病变支架介入治疗后冠状动脉造影随访结果分析

目的观察无保护左主干病变,应用药物洗脱支架介入治疗后冠状动脉造影随访结果,并分析其影响因素。方法选择无保护左主干病变患者150例,其中48例在平均(10.0±7.5)个月进行了冠状动脉造影复查,根据冠状动脉造影显示有无狭窄分为:再狭窄组12例和无再狭窄组36例。结果与无再狭窄组比较,再狭窄组患者随访时最小管腔直径明显减小[(2.7±1.0)mm vs (3.5±0.4)mm,P=0.0001]、直径狭窄率明显升高[(31.4±26.4)% vs (8.3±5.3)%,P=0.0000]、晚期管腔丢失明显升高[(0.8±0.7)mm vs (0.2±0.3)mm,P=0.0000];双支架置入术的再狭窄率明显高于单支架置入术[(75.0% vs 13.9%),P=0.0011]。结论左主干远端分叉病变双支架置入术的疗效较差,冠状动脉旁路移植术应作为首选。     

药物洗脱支架联用普通金属支架治疗多支冠状动脉病变的疗效评价

目的探讨多支冠状动脉病变患者药物洗脱支架与普通金属支架(普通支架)联用预防再狭窄的疗效及安全性。方法801例行多支冠状动脉内支架置入术达到完全血运重建的冠心病患者分3组。药物洗脱支架组206例、药物洗脱支架与普通支架联用组(联用组)158例及普通支架组437例。比较3组支架术后近期及远期结果。结果3组患者冠心病危险因素、心功能、冠状动脉病变程度、支架术成功率及并发症发生率均无显著差异。术后平均随访(17.3±10.9)个月,总随访率和造影随访率无显著差异。联用组普通支架置入于31.3%的前降支病变(均为A、B1型病变)及81.6%的回旋支病变和69.9%的右冠状动脉病变。与普通支架组相比,药物洗脱支架组和联用组造影再狭窄率明显降低,分别为20.3%vs7.3%和8.8%(P均<0.05),且主要不良心脏事件发生率均较低,分别为18.4%vs6.5%和9.9%(P均<0.05)。但药物洗脱支架组与联用组相比上述各指标无显著差异。结论多支冠状动脉病变患者单用药物洗脱支架或合理联用普通支架后再狭窄率降低,安全性近似,均优于单用普通支架。     

血管紧张素转换酶基因多态性与冠脉病变严重程度的相关性研究

目的探讨血管紧张素转换酶(ACE)基因I/D多态性与冠心病及冠脉病变严重程度的关系.方法对122例冠心病患者进行冠状动脉造影,判定冠脉病变支数(狭窄程度≥75%)和危险记分.用聚合酶链式反应(PCR)技术检测病例组和80例健康人群ACE基因多态性.结果ACE基因型分布和等位基因频率在病例组和对照组间差异有显著性,病例组DD基因型(38.5%)和D等位基因频率(55%)显著高于对照组(13.7%,41%;P＜0.05).冠脉病变支数和危险记分在ACE基因型间差异无显著性(P＞0.05).结论ACE基因多态性中DD型和D等位基因是冠心病发病的独立危险因素,但与冠脉病变严重程度不相关.     

药物洗脱支架与金属裸支架对非糖尿病患者冠状动脉局限病变的8个月疗效

目的评估非糖尿病冠心病患者,药物洗脱支架与金属裸支架对于治疗冠状动脉局限病变的8个月疗效.方法自身冠状动脉首次介入治疗病变(在线定量冠状动脉造影分析直径≥3.0 mm,长度≤15 mm)的非糖尿病患者入选本研究,148例患者分为药物洗脱支架组(n=81)和金属裸支架组(n=67),两组的基本临床特征和冠状动脉造影结果无显著差异.术前、术后和8个月随访时进行定量冠状动脉造影分析,并在住院期间,30天和8个月时观察不良心脏事件的发生.结果支架置入成功率均为100%.住院期间靶病变重复血管重建率,在药物洗脱支架组和金属裸支架组无显著性差异(1.2%和0%,P=0.36).在术后30天时两组均无支架内血栓形成.8个月随访时,定量冠状动脉造影分析显示,支架内最小管腔直径药物洗脱支架组明显大于金属裸支架组,有极显著性差异(P＜0.01);支架内远期管腔丢失、病变内远期管腔丢失、支架内狭窄直径、病变内狭窄直径药物洗脱支架组明显低于金属裸支架组有显著性差异(P＜0.05～0.001).两组支架内再狭窄率(8.64% vs 17.91%,P=0.09)和病变节段再狭窄率(11.11% vs 17.91%,P=0.24)均无显著性差异,但支架内再狭窄率比数比为0.8985(95%的可信区间0.7887;1.0237).结论药物洗脱支架对于治疗非糖尿病、自身冠状动脉局限病变患者安全有效,两组支架内再狭窄率虽无显著性差异,但药物洗脱支架有降低再狭窄率的趋势.     

急性冠脉综合征支架置入术后应用血脂康对再狭窄影响的研究

目的研究急性冠脉综合征支架置入术后应用血脂康调脂及预防再狭窄的作用。方法对通化市人民医院2001-01~2003-01安置冠脉内支架的冠心病患者,分辛伐他汀治疗组及血脂康治疗组,所有患者均由股动脉穿刺途径以Judkin s法完成冠状动脉造影检查,以1支血管管腔狭窄≥70%定为有意义的狭窄病变,进行支架置入术,12个月时再次进行冠状动脉造影检查。结果血脂康治疗及辛伐他汀治疗组在性别、年龄、血压、糖尿病等方面差异无统计学意义。两组病人的冠脉造影病变的特征差异无统计学意义。经过12个月的随访观察,两组的降血脂作用和预防再狭窄的程度相似。结论应用辛伐他汀和血脂康治疗后使血脂浓度明显降低,介入治疗后血脂康与辛伐他汀预防再狭窄作用相似。     

普罗布考对合并糖尿病患者冠状动脉药物洗脱支架置入术后再狭窄及炎症因子的影响

目的评价普罗布考对合并糖尿病的冠心病患者药物洗脱支架置入术后再狭窄发生率及炎症因子的影响,初步探讨普罗布考预防再狭窄的临床价值及可能机制。方法入选72例合并糖尿病并接受药物洗脱支架置入术的冠心病患者,随机分为普罗布考组（36例）和对照组（36例）。普罗布考组在常规药物的基础上加服普罗布考（0.25 g,每日2次）,连续服药至PCI术后6个月,所有患者行冠状动脉造影复查。支架内再狭窄定义为支架内或两端5 mm内出现≥50%狭窄程度的病变。测定术前及术后6个月的血清超敏C反应蛋白、白细胞介素-6、肿瘤坏死因子-α的浓度变化。结果对照组中10例（27.8%）发生再狭窄,普罗布考组仅3例（8.3%）发生再狭窄,两组间比较,差异有统计学意义（P=0.032）;术后6个月时两组患者炎症因子水平较术前均有下降,普罗布考组下降更显著,差异具有统计学意义（P〈0.05）。结论普罗布考能够有效降低合并糖尿病的冠心病患者置入药物洗脱支架置入后再狭窄的发生,其机制可能与抗炎作用有关。     

冠心病合并糖尿病患者金属裸支架置入术后再狭窄的临床和造影预测因素

目的探讨冠心病合并糖尿病患者支架术后再狭窄发生的危险因素,建立冠心病合并糖尿病患者支架术后再狭窄发生概率的预测模型,为中国冠心病合并糖尿病患者药物洗脱支架的合理使用提供循证医学证据。方法分析我院2002-2004年1126例冠状动脉内非药物洗脱支架置入术患者（2376处病变）,使用多元逻辑回归分析比较术后出现再狭窄组和无再狭窄组冠心病合并糖尿病患者临床数据和造影资料,并使用上述数据库建立支架术后再狭窄发生概率预测表。结果在889例（78．9％）有6个月随访冠状动脉造影资料的患者中,151例（17％）有糖尿病。再狭窄定义为支架内及前后5mm范围内狭窄≥50％参考管腔直径。在非糖尿病组（738例）,再狭窄的发生率为21．2％,糖尿病组（151例）再狭窄的发生率为35．9％（P〈0．001）。多元逻辑分析结果显示参考血管直径（≤3．0mm）,病变长度（〉15mm）和胰岛素治疗是冠心病合并糖尿病患者术后再狭窄的可预见危险因素（P〈0．05）。支架术后再狭窄发生概率的预测表结果显示冠心病合并糖尿病患者再狭窄发生概率首要依赖于参考血管直径。结论冠心病合并糖尿病患者支架术后再狭窄发生概率显著增加。参考血管直径、病变长度和需要胰岛素治疗是冠心病合并糖尿病患者支架术后再狭窄的可预见危险因素。非糖尿病患者合并短病变（〈15mm）而无论参考血管直径,糖尿病患者合并冠状动脉大直径血管（〉3．0mm）合并短病变（〈15mm）预期再狭窄发生率〈15％,可以考虑使用金属裸支架。除此之外,建议使用药物洗脱支架。     

高血压人群中ACE、ADRB1基因多态性与冠状动脉狭窄程度的相关性研究

目的探讨高血压人群中血管紧张素转换酶(ACE)基因多态性及β1肾上腺素能受体(ADRB1)基因多态性与冠状动脉(冠脉)狭窄程度的相关性。方法选取2017年7月至2019年4月于徐州医科大学附属医院心血管内科住院的280例高血压患者的临床资料进行回顾性分析,行冠脉造影或冠脉CT血管造影(CTA)检查判定其是否患有冠心病(CHD),并依据结果判定其冠脉病变支数及给予Gensini评分。根据冠脉检查结果将上述患者分为CHD组(n=145)和对照组(n=135)。所有入选病例均给予了ACE及ADRB1基因多态性检测,并根据结果分为ACE II型纯合子、ID型杂合子、DD型纯合子和ADRB1 GG型纯合子、GC型杂合子、CC型纯合子。结果在研究的高血压人群中,ACE DD基因型携带者在冠脉病变支数中的多支病变组及Gensini得分分组中的重度病变组的占比明显高于ACE II及ACE ID基因型(P<0.05);ADRB1基因多态性在冠脉病变支数分组及Gensini得分分组的对比中无明显相关性(P>0.05);CHD组与对照组一般临床资料对比中显示年龄、高密度脂蛋白胆固醇(HDL-C)和糖尿病与CHD存在相关性,且有统计学意义(P<0.05)。结论ACE基因多态性与高血压人群冠状动脉狭窄程度密切相关,ADRB1基因多态性无明显相关性。     

Predictors of coronary in-stent restenosis: importance of angiotensin-converting enzyme gene polymorphism and treatment with angiotensin-converting enzyme inhibitors

OBJECTIVES: This study aimed to clarify the role of the angiotensin-converting enzyme (ACE) gene polymorphism in the development of in-stent restenosis. BACKGROUND: In-stent restenosis occurs after treatment of coronary artery stenosis in 12% to 32% of coronary interventions with stents. Experimental and clinical studies have suggested that the deletion/insertion (D/I) polymorphism of the ACE gene plays a role in this. METHODS: Quantitative coronary angiography before, immediately after and six months after stent implantation were compared in 369 patients, in whom D/I typing of the ACE gene was performed. RESULTS: At follow-up we found no differences between the three genotypes in minimal lumen diameter (homozygotes with two deletion alleles in the ACE gene [DD], 2.20 mm; heterozygotes with one deletion and one insertion allele in the ACE gene [DI], 2.19 mm; and homozygotes with two insertion alleles in the ACE gene [II], 2.25 mm). The corresponding diameter stenoses were: DD: 25%, DI: 27%, II: 27% (p = NS), and the frequency of restenosis (>50% diameter stenosis) was: DD: 15.7%, DI: 11.0% and II: 16.4% (p = NS). Logistic regression analysis identified diabetes (odds ratio [OR]: 3.0, 95% confidence interval [CI]: 1.0 to 8.7), lesion length (OR: 1.1, 95% CI: 1.01 to 1.30) and minimal lumen diameter immediately after the intervention (OR: 0.3, 95% CI: 0.14 to 0.85) as predictors of in-stent restenosis. In a post hoc analysis of patients treated versus those not treated with an ACE-inhibitor antagonist or an angiotensin receptor antagonist, we found an increased frequency of in-stent restenosis in the DD genotypes (40% vs. 12%, p = 0.006). CONCLUSIONS: The D/I polymorphism is not an independent predictor of coronary in-stent restenosis in general, but it may be of clinical importance in patients treated with ACE inhibitors or angiotensin receptor antagonists.     

D/D genotype of the gene for angiotensin converting enzyme as a risk factor for post-stent coronary restenosis]

INTRODUCTION: Although intracoronary stenting has decreased restenosis rate compared to percutaneous balloon angioplasty, still a high number of patients develop in-stent restenosis, which is an entity primarily due to tissue proliferation. Experimental studies have indicated that the renin-angiotensin system is involved in neointimal hyperplasia. Plasma and cellular levels of ACE are associated with an I/D polymorphism in the ACE gene. Indeed, DD subjects have the higher ACE levels. The purpose of this study was to explore the possibility that the I/D polymorphism might be related with in-stent restenosis. METHODS: We studied the ACE polymorphism in 48 consecutive patients who underwent successful implantation of an elective coronary stent in native coronary vessels and had a 6 month angiographic follow up. Restenosis (50% of the reference vessel) was observed in 23/48 patients. Patients with or without restenosis did not differ in demographic or clinical variables like diabetes, plasma cholesterol levels or in quantitative angiographic parameters such as vessel reference size or minimal lumen diameter after stent implantation. RESULTS: I/D polymorphism was distributed as follows: 22.9% of the patients were D/D; 14.5% were I/I and 62.5% of the patients were heterozygous I/D. The presence of restenosis was strongly related with the I/D polymorphism: 81.8% of the patients with D/D genotype had restenosis, compared with 40.0% of I/D patients and only 14.2% of the I/I patients (chi 2 p < 0.01). CONCLUSIONS: In this limited cohort, homocygous D/D of the ACE gene was significantly associated with in-stent restenosis, whereas restenosis was infrequent in patients with the I/I genotype.     

ACE gene polymorphism and coronary restenosis.

In humans, circulating levels of angiotensin-converting enzyme (ACE) are linked with an insertion (I)/deletion (D) polymorphism in the ACE gene: DD genotype bearers have higher levels of ACE than either ID or II genotype bearers. Recent studies have suggested that the ACE DD genotype might be associated with a higher risk of coronary artery disease. The aim of this paper is to review studies on the influence of the I/D polymorphism on coronary restenosis. The renin-angiotensin system has been implicated in the pathogenesis of neointimal hyperplasia in experimental models. In humans, the I/D polymorphism is not associated with restenosis after balloon angioplasty, but is strongly associated with restenosis after coronary stent implantation. This may be explained by the fact that the contribution of neointimal hyperplasia to restenosis is much more important after coronary stent implantation than after balloon angioplasty.     

Angiotensin I-converting enzyme (ACE) inhibitors and restenosis after coronary artery stenting in patients with the DD genotype of the ACE gene

OBJECTIVES: We tested the hypothesis that patients with the DD genotype of the angiotensin I-converting enzyme (ACE) gene who are treated with ACE inhibitors are at a higher risk of restenosis after coronary stent placement than patients who do not receive ACE inhibitors. BACKGROUND: Two recent studies with a limited series of patients carrying the DD genotype suggested an unfavorable impact of the use of ACE inhibitors on the restenotic process after implantation of stents in coronary arteries. Because these findings may question the use of ACE inhibitors after coronary stenting, we examined this important issue in a large series of patients. METHODS: We determined the ACE gene I/D genotype of 2,222 consecutive patients with symptomatic coronary artery disease who underwent stent implantation. The patients with the DD genotype (n = 612) constituted the study population. The primary end point was in-stent restenosis, which was assessed as angiographic restenosis (> or =50% diameter stenosis at six-month follow-up) and clinical restenosis (need for target vessel revascularization due to symptoms or signs of ischemia in the presence of angiographic restenosis over one year after the intervention). RESULTS: Of the 612 patients with the DD genotype, 403 (65.8%) were treated with ACE inhibitors and 209 (34.2%) did not receive ACE inhibitors. The angiographic and clinical restenosis rates were not significantly different between the group treated with ACE inhibitors and the group not receiving ACE inhibitors (p = 0.55). Continuous measures of restenosis, minimal lumen diameter, diameter stenosis, late lumen loss, and loss index were also similar in both groups (p > or = 0.55). In addition, one-year survival free of myocardial infarction was not significantly different between the two groups (p = 0.27). CONCLUSIONS: In contrast to previous reports, our study provides evidence that patients carrying the DD genotype are not exposed to an increased risk of restenosis after stent placement when treated with ACE inhibitors.     

Angiotensin-converting enzyme insertion/deletion polymorphism does not influence the restenosis rate after coronary stent implantation

BACKGROUND: Experimental studies have shown an activation of the angiotensin-converting enzyme (ACE) system as a response to endothelial injury. Recent publications have elucidated the hypothesis that the ACE gene polymorphism may influence the level of late luminal loss after coronary stent implantation. It is still unclear whether the polymorphism of the angiotensin gene is a major predictor of the extent of neointimal hyperplasia. In this multicenter study, we therefore tested the relationship between the ACE gene polymorphism and the restenosis rate after coronary stent implantation. METHODS: As a substudy of the optimization with intracoronary ultrasound (ICUS) to reduce stent restenosis (OPTICUS) study, we analyzed ACE serum levels and the ACE gene polymorphism in 154 patients at 9 different centers. All patients underwent elective coronary stent implantation in a stenosis of a major coronary vessel. Balloon inflations were repeated until a satisfactory result was achieved in on-line quantitative coronary angiography or ICUS fulfilling the OPTICUS study criteria. After follow-up of 6 months, all patients underwent reangiography under identical projections as the baseline procedure. A blinded quantitative analysis of the initial procedure as well as the follow-up examinations were performed by an independent core laboratory. ACE gene polymorphism and ACE serum activity were measured at the 6-month follow-up in a double-blinded setting. RESULTS: With respect to the ACE gene polymorphism, there were three subgroups: DD genotype (48 patients), ID (83 patients) and II (23 patients). The subgroups did not differ in regard to age, gender, extent of coronary artery disease, stenosis length, initial degree of stenosis or degree of stenosis after stent implantation. In all, 39 patients (25.3%) had significant restenosis: 12 DD patients (25.0%), 18 ID patients (21.7%) and 9 II patients (39.1%) (odds ratio 2.164, 95% confidence interval 0.853-5.493). We obtained the following results for ACE serum levels: 0.53 micromol/l/s in the DD subgroup, 0.29 micromol/l/s in the ID subgroup and 0.09 micromol/l/s in the II subgroup (p < 0.001). Multivariate logistic regression analysis of the influence of ACE gene polymorphism on the restenosis rate after coronary stent implantation adjusted for lesion length (>12 mm), ACE inhibitor or hydroxymethylglutaryl coenzyme A reductase (CSE) inhibitor treatment, age, male gender, diabetes mellitus, hypertension, high cholesterol, family history, smoking and three-vessel disease did not uncover any statistic significance. CONCLUSIONS: In contrast to other study groups, we were unable to disclose that the DD polymorphism of the ACE gene was associated with a higher rate of restenosis after coronary stent implantation in this multicenter study. In addition, patients with higher ACE serum levels did not show a higher restenosis rate in this trial. We conclude that the pathogenesis of restenosis is a multifactorial process involving various genetic and nongenetic factors.     

The relationship between angiotensin converting enzyme gene polymorphism, coronary artery disease, and stent restenosis: the role of angiotensin converting enzyme inhibitors in stent restenosis in patients with diabetes mellitus

Patients with diabetes mellitus (DM) have advanced atherosclerosis compared with nondiabetics. Restenosis after intracoronary stent implantation occurs frequently in diabetic patients. Angiotensin II is an important growth factor for the development of neointimal hyperplasia after vascular injury. The aim of our study was to evaluate the relationships between angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and coronary artery disease (CAD) and stent restonosis in diabetic patients. One hundred and thirty consecutive patients with CAD and 47 consecutive patients (14 males, mean age, 58.0 +/- 10.0) without CAD were enrolled in the study. All patients had type 2 (noninsulin dependent) DM. The patients with CAD underwent percutaneous transluminal coronary angioplasty (PTCA) and stenting. Ninety-four (59 males, mean age, 60.3 +/- 9.8) underwent control coronary angiography at the end of the follow-up period (mean duration, 9.1 +/- 2.9 months). ACE gene I/D genotyping was identified in all patients. No significant difference was found among patients with and without CAD with respect to ACE gene I/D polymorphism (P = 0.460). In the control coronary angiography, stent restenosis and new lesion development were comparable in each genotyping subgroup. However, a significant relationship was observed between restenosis and the use of ACE inhibitors (ACEI) in patients with D allele (ACEI ratio, 43.5% in the restenosis group and 56.5% in non-restenotic group, P < 0.05). We did not find any relationship between ACE gene I/D polymorphism and CAD and stent restenosis and new lesion development in diabetic patients. On the other hand, ACEI treatment may reduce stent restenosis in type 2 diabetic patients with D allele (DD or ID).     

Intracoronary β-irradiation prevents excessive in-stent neointimal proliferation in de novo lesions of patients with high plasma ACE levels. The BetAce randomized trial

BACKGROUND: This study evaluated vascular brachytherapy (VBT) as a potent antiproliferative treatment to prevent in-stent restenosis (ISR) after coronary angioplasty of de novo lesions in patients carrying the D allele of the I/D polymorphism of the ACE gene and high ACE plasma levels (>34 U/l). METHODS AND MATERIALS: A prospective randomized trial was designed to detect a 30% improvement in the minimal lumen diameter (MLD) of the stenotic artery, as measured by quantitative coronary analysis (QCA), 6 months following VBT at the time of stented angioplasty. All patients were carriers of the D allele of the ACE gene, with plasma ACE levels >34 U/l. RESULTS: Thirty-one patients (33 stenoses) were allocated to stent implantation (control group) and 30 patients (31 stenoses) to VBT and stented angioplasty. After angioplasty, in-stent MLD was similar in the two groups. At 6 months in the control group, in-stent MLD had decreased to 1.74+/-0.8 versus 2.25+/-1.05 mm in the VBT group (P=.04). The mean in-stent diameter was 2.3+/-0.8 mm in the control group versus 2.9+/-1.05 mm after VBT (P=.02), and the restenosis rate was 37.5% versus 17.9%, respectively (P=.08). At 6 months, a higher need for target vessel revascularization (TVR) was observed in the control group: 35.5% versus 13.3% (P=.04). CONCLUSIONS: This randomized study confirms that patients with high plasma ACE concentrations are exposed to an increased risk for ISR after coronary stenting. The preventive use of VBT in these patients reduced neointimal formation by 65% such that the MLD at follow-up was increased by 29% compared with the control group.     

Relation between the insertion/deletion polymorphism of the angiotensin I converting enzyme gene and restenosis after coronary stenting

BACKGROUND: Observations with intravascular ultrasound demonstrated that neointimal hyperplasia is the predominant factor responsible for in-stent restenosis. Experimental data suggest that angiotensin I converting enzyme (ACE) plays a role in the thickening of neointima after balloon denudation. Insertion/deletion (I/D) polymorphism of the ACE gene is significantly associated with plasma level of ACE and subjects with D/D genotype have significantly higher plasma levels of ACE than normal. OBJECTIVE: To investigate whether this polymorphism influences the risk of restenosis after coronary stenting. METHODS: We genotyped 158 patients who had undergone single-vessel coronary stenting for the ACE I/D polymorphism. RESULTS: Of the 158 patients, 56 (35%) had the D/D genotype, 71 (45%) had the I/D genotype and 31 (20%) had the I/I genotype. Prevalences of genotypes were compatible with Hardy-Weinberg equilibrium and distributions of ACE genotype among patients and 132 healthy controls from the same geographic area did not differ. At follow-up (after a median duration of 5.4 months), overall rates of angiographic restenosis and of revascularization of target lesion (RTL) were 32.3 and 22.8%, respectively. Of 51 patients with angiographic restenosis, 31 (60.8%) had focal and 20 (39.2%) had diffuse patterns of restenosis. Diffuse in-stent restenosis was significantly more prevalent among patients with D/D genotype (P = 0.016). Multiple stepwise logistic regression analysis identified ACE I/D polymorphism as the independent predictor of angiographic restenosis and RTL. Relative risk of angiographic restenosis was 6.29 [95% confidence interval (CI), 1.80-22.05, P = 0.0004] for D/D genotype and 3.88 (95% CI 1.11-13.12, P = 0.029) for I/D genotype, whereas relative risk of RTL was 7.44 (95% CI 1.60-34.58, P = 0.01) for D/D genotype and 3.88 (95% CI 0.083-18.15, P = 0.085) for I/D genotype. CONCLUSIONS: The ACE I/D polymorphism is significantly associated with risk of angiographic and clinical restenosis after coronary stenting. Angiographic pattern of restenosis is also significantly associated with I/D polymorphism, diffuse type being more prevalent among subjects with D/D genotype.     

单核细胞趋化蛋白-1基因多态性与冠状动脉介入治疗后再狭窄的相关性研究

目的 探讨单核细胞趋化蛋白-1(MCP-1)启动子区-2518A/G基因多态性与冠状动脉(冠脉)粥样硬化病变进程及经皮冠脉腔内成形术(PCI)后再狭窄的相关性.方法 对276例接受PCI并进行冠脉造影随访的患者,采用PCR-RFLP方法进行MCP-1 -2518A/G多态性检测;按冠脉造影结果分为再狭窄组(113例)和无再狭窄组(163例),判定冠脉血管病变及再狭窄与MCP-1 -2518A/G多态性的相关性.结果 MCP-1 -2518A/G基因型频率为:AA纯合子21.0%,GG纯合子34.1%,AG杂合子44.9%,3种基因型血管病变支数和血管平均狭窄程度,差异均无统计学意义(P＞0.05).再狭窄组中AA、AG和GG基因型频率分别为23.9%、40.7%和35.4%,无再狭窄组分别为19.0%、47.9%和33.1%,差异无统计学意义(P=0.446).再狭窄组中-2518A和G等位基因频率分别为44.2%和55.8%,无再狭窄组分别为42.9%和57.1%,差异无统计学意义(P=0.761).结论 冠脉粥样硬化进程及PCI术后再狭窄可能与MCP-1 -2518A/G基因多态性无相关性.     

Balloon angioplasty for the treatment of coronary in-stent restenosis: immediate results and 6-month angiographic recurrent restenosis rate

Objectives. The purpose of this prospective study was to evaluate the immediate results and the 6-month angiographic recurrent restenosis rate after balloon angioplasty for in-stent restenosis.Background. Despite excellent immediate and mid-term results, 20% to 30% of patients with coronary stent implantation will present an angiographic restenosis and may require additional treatment. The optimal treatment for in-stent restenosis is still unclear.Methods. Quantitative coronary angiography (QCA) analyses were performed before and after stent implantation, before and after balloon angioplasty for in-stent restenosis and on a 6-month systematic coronary angiogram to assess the recurrent angiographic restenosis rate.Results. Balloon angioplasty was performed in 52 patients presenting in-stent restenosis. In-stent restenosis was either diffuse (≥ 10 mm) inside the stent (71%) or focal (29%). Mean stent length was 16 ± 7 mm. Balloon diameter of 2.98 ± 0.37 mm and maximal inflation pressure of 10 ± 3 atm were used for balloon angioplasty. Angiographic success rate was 100% without any complication. Acute gain was lower after balloon angioplasty for in-stent restenosis than after stent implantation: 1.19 ± 0.60 mm vs. 1.75 ± 0.68 mm (p = 0.0002). At 6-month follow-up, 60% of patients were asymptomatic and no patient died. Eighteen patients (35%) had repeat target vessel revascularization. Angiographic restenosis rate was 54%. Recurrent restenosis rate was higher when in-stent restenosis was diffuse: 63% vs. 31% when focal, p = 0.046.Conclusions. Although balloon angioplasty for in-stent restenosis can be safely and successfully performed, it leads to less immediate stenosis improvement than at time of stent implantation and carries a high recurrent angiographic restenosis rate at 6 months, in particular in diffuse in-stent restenosis lesions.