稳定型心绞痛冠状动脉斑块结构与重构关系的研究

目的:探讨血管内超声对稳定型心绞痛(SAP)患者冠状动脉(冠脉)病变斑块结构与血管重构关系的评估价值。方法:在冠脉介入治疗前应用血管内超声对SAP患者的冠脉病变进行研究。根据测定的重构指数(RI)将患者分为A组(负重构,RI<1.0)和B组(正重构,RI≥1.0),根据管腔面积狭窄率分为管腔面积狭窄率<70%组(轻中度狭窄组)和管腔面积狭窄率≥70%组(重度狭窄组)。结果:①与A组比较,B组近端参考段斑块负荷小,病变处的管腔面积和外弹力膜面积大、斑块负荷小,硬斑块所占比例少,病变处最大钙化弧度和长度小;②与轻中度狭窄组比较,重度狭窄组负重构多,软斑块少,病变处管腔面积小,病变处斑块面积和斑块负荷大,RI偏小,病变最大钙化弧度大。结论:不同程度管腔狭窄的SAP患者中,斑块钙化在负重构和严重管腔狭窄中占优势,负重构更常见于严重狭窄病变。     

冠状动脉造影联合血管内超声在老年急性冠状动脉综合征的临床研究

目的探讨老年急性冠状动脉综合征(ACS)的衰减斑块(AP)特点。方法选择符合条件的166例ACS患者,分为老年组92例和非老年组74例,记录一般临床资料、冠状动脉造影血管病变情况和罪犯斑块的血管内超声特点,主要包括有无AP、最大衰减回声弧度、血管外弹力膜面积、管腔面积、斑块面积,计算斑块负荷和重构指数。结果与非老年组比较,老年组3支冠状动脉病变的比例较高(50.0%vs 35.1%,P=0.038),AP更多(62.0%vs45.9%,P=0.039),最大衰减回声弧度[(142±80)°vs(115±54)°,P=0.000]、斑块面积[(14.2±3.9)mm2 vs(12.3±4.1)mm2,P=0.022]、斑块负荷[(81.1±14.2)%vs(76.4±13.5)%,P=0.042]和重构指数[(1.2±0.2)vs(1.1±0.1),P=0.031]更高。结论老年ACS患者的发病与不稳定斑块的关系更为密切,加强稳定斑块的治疗措施,将有助于老年ACS的防治。     

冠状动脉左前降支开口部病变的血管内超声观察

目的 探讨冠状动脉左前降支(LAD)开口部病变的重塑类型。方法 对31例LAD开口部病变(甲组)和24例冠状动脉造影正常的LAD(乙组)进行血管内超声检查。分别于病变远端参照部位及开口部病变处测量血管面积、管腔面积及斑块面积。重塑指数定义为开口部病变处血管面积与病变远端参照部位血管面积的比值。结果 甲组的重塑指数明显小于乙组(0.79±0.19比0.97±0.11,P<0.001)。如定义重塑指数<0.92(乙组平均重塑指数的95％可信区间的下限值)为收缩性重塑,则甲组中81％(25/31)为收缩性重塑。在发生收缩性重塑的病变中,病变处管腔面积的减少54％是由病变处血管收缩所致。病变处管腔面积的减少与血管面积的减少的相关性比病变处管腔面积的减少与斑块面积的增加的相关性更强(r=0.75,P<0.001和r=0.62,P<0.01)。结论 LAD开口部病变以收缩性重塑更常见,收缩性重塑是决定LAD开口部病变狭窄程度的重要因素。     

左主干冠状动脉病变的血管内超声研究

目的 血管内超声评价非严蕈钙化性左主干病变的形态特点,探讨开口和非开口部位形成狭窄的不同机制.方法 2004年10月至2007年10月,共入选造影确诊或可疑的狭窄病变并行血管内超声检查的153例(开口47例,非开口106例)非严重钙化性左主干病变,定性和定量分析血管内超声图像;负性重构定义为重构指数＜0.95.结果 左主干参考节段平均管腔直径和血管(外弹力膜)直径为(4.1±0.8)mm和(5.3士0.8)mm.开口病变的纤维性、钙化性和软斑块分别为70.2%、19.2%和8.5%,而非开口病变为35.8%、43.4%和3.8%,两者差异有统计学意义(P=0.01).总体来说,31.1%病例的最小管腔面积＜6 mm2,其中开口组29.5%,非开口组31.9%(P=0.87).最小管腔面积在两组相似,但非开口组的斑块面积[(13.3±5.4)mm2比(10.8±4.5)mm2,P=0.007]和斑块负荷(61.9%±14.5%比54.8%±15.9%,P=0.020)均显著大于开口组,斑块负荷＞50%的比例更高(84.8%比61.3%,P=0.002).开口病变的重构系数显著低于非开口病变(0.9±0.2比1.0.±0.2,P=0.000),而且负性重构更多见(74.5%和34.9%,P=0.000).logistic回归分析发现,病变部位(OR=4.9,P=0.004)、斑块面积(OR=1.2,P=0.01)和斑块负荷(OR=0.003,P=0.000)是左主干发生重构的独立预测因素.结论 负性重构现象在左主干开口病变中更常见,可能是其狭窄形成的机制之一.狭窄程度不确定的冠状动脉左主干病变需要血管内超声精确评价.     

急性冠状动脉综合征患者雷帕霉素洗脱支架晚期贴壁不良及其对临床预后的影响

目的 观察急性冠状动脉综合征(ACS)患者雷帕霉素洗脱支架晚期贴壁不良发生率及其对临床预后的影响.方法 观察2005年2月至2007年3月因ACS(ACS组,54例)和稳定性心绞痛(对照组,83例)行雷帕霉素洗脱支架治疗并于1年后行血管内超声检查患者,检测支架晚期贴壁不良发生率,并观察血管内超声检查后1年内主要不良心血管事件及支架内血栓发生率.结果 所有137例患者219处病变中,16例患者25处病变检测到晚期支架贴壁不良.25处晚期支架贴壁不良中ACS组和对照组分别为20处(22.2%)和5处(3.9%)(P＜0.001).两组患者参照血管外弹力膜面积、参照血管和支架段血管管腔面积和新生内膜面积均相似,但ACS组患者支架段血管外弹力膜面积[(15.34±5.44)mm2比(13.83±4.51)mm2,P=0.026]、支架段血管外弹力膜面积与参照血管外弹力膜面积比值(1.13±0.22比1.02±0.18,P＜0.001)、斑块和中膜面积[(8.43±3.93)mm2比(7.01±2.93)mm2,P:0.002]较对照组明显增大.Logistic多元回归分析显示,ACS(OR=6.477,P＜0.001)和支架长度≥23 mm(OR=3.680,P=0.025)为晚期支架贴壁不良的独立危险因素.血管内超声检查后临床随访1年,两组主要不良心血管事件发生率差异无统计学意义.结论 雷帕霉素洗脱支架置入后,ACS患者较稳定性心绞痛患者更多发生晚期支架贴壁不良,然而随访1年的主要不良心血管事件发生率差异无统计学意义.     

急性冠状动脉综合征和稳定型心绞痛患者的血管内超声显像结果

目的　采用血管内超声显像(IVUS)的方法比较急性冠状动脉综合征(ACS)和稳定型心绞痛(SAP)患者的冠状动脉病变性质。方法　共入选85例患者(男性59例,平均年龄59±1 0岁) ,其中ACS患者50例,SAP患者35例,对罪犯血管采用ClearView或Galaxy2 (BostonScientific ,USA)行IVUS检查。IVUS分析资料包括罪犯病变的定性分析和定量测定。定量测定的数据包括病变部位和参照节段的血管面积(EEMcsa)、管腔面积(Lcsa)和斑块面积(EEMcsa -Lcsa) ,斑块负荷=(EEMcsa -Lcsa) EEMcsa×1 0 0 % ,计算血管重构指数(RI)。RI >1 . 0者为正性重构,RI <1. 0者为负性重构。结果　ACS患者的罪犯病变中软斑块为主,占74 % ,明显高于SAP患者的31 % (P =0 .0 0 1 ) ,更多斑块破裂[ACS( 38% )比SAP( 8% ) ,P =0 .0 0 2 ]和血栓形成[ACS( 2 4 % )比SAP( 0 % ) ,P =0 .0 0 2 ]。ACS患者的病变处EEMcsa( 1 5 .0±4 . 4mm2 比1 1 .3±3 6mm2 ,P <0. 0 0 1 ) ,斑块面积( 1 1 . 5±4 .1mm2 比7. 6±2 . 9mm2 ,P <0 . 0 0 1 ) ,斑块负荷( 76 . 7%±1 0 . 4 %比6 6 . 8%±1 2 .6 % ,P <0 . 0 0 1 )和RI( 1 . 0 5±0 .1 1比0 . 95±0 . 1 6 ,P =0 .0 0 2 )均显著高于SAP。ACS患者冠状动脉病变部位的正性重构较SAP患者更常见( 6 7%比36 % ,     

血管内超声对急性心肌梗死相关病变的分析

目的 应用血管内超声(IVUS)研究急性心肌梗死(AMI)患者梗死相关动脉罪犯斑块与非梗死相关动脉斑块的不同.方法 用IVUS检查了20例AMI患者梗死相关动脉罪犯斑块20个与非梗死相关动脉斑块38个,IVUS分析包括对病变部位及近端参考部位的外弹力膜面积、管腔、斑块面积定量测量,血管重构指数(RI)定义为病变外弹力膜(EEM)截面积(CSA)/参考部位EEM CSA,正性重构(PR)定义为RR＞1.05、负性重构(NR)定义为RR＜0.95.梗死相关动脉及病变部位由心电图、左室壁运动异常(心室造影及超声心动结果)、冠脉造影病变形态联合鉴定.结果 罪犯斑块主要为低回声斑块(60% vs 28.9%)(P＜0.05),病变更长[(17.2±8.7) vs (10.6±5.7) mm;P＜0.05]、具有更大EEM面积[(15.8±6.0) vs (11.9±5.6) mm2;P＜0.05]及斑块面积[(13.1±6.0) vs (9.2±4.3) mm2;P＜0.05],大的斑块负荷[(82.9±6.2)% vs (77.3±7.2)%;P＜0.05],更多的正性重构(75% vs 47.4%;P＜0.05).结论 罪犯斑块具有更多的不稳定指标(正性重构、低回声斑块、大的斑块容积).     

急性冠状动脉综合征患者不稳定性斑块的血管内超声

目的观察急性冠状动脉综合征患者不稳定性斑块的血管内超声特征.方法 36例急性冠状动脉综合征患者和20例稳定型心绞痛患者进行冠状动脉造影及血管内超声检查.应用血管内超声分别观察比较冠状动脉内斑块的性质,同时测量冠状动脉病变部位及其参考部位的血管外弹力膜面积、管腔面积、斑块面积及管腔面积狭窄率,并计算斑块的偏心指数及血管重构指数.结果急性冠状动脉综合征患者中脂质斑块占77.8%(28/36),其中10例发生斑块破裂及血栓形成;稳定型心绞痛患者主要为纤维性斑块及混合性斑块,脂质斑块仅占10%(2/20),无斑块破裂及血栓形成.两组斑块的特征包括偏心性、外弹力膜面积、斑块面积及管腔面积狭窄率具有显著性差异.不稳定性斑块呈现明显的正性重构,占72.2%(26/36),而稳定性斑块主要表现为负性重构,占75%(15/20).结论血管内超声能够准确地识别动脉粥样硬化不稳定性斑块,为早期临床发现不稳定性斑块并预测斑块破裂奠定了基础.     

血管内超声显像在肾动脉介入治疗中的应用价值

评价血管内超声显像在肾动脉介入治疗中的应用价值。 15例显著肾动脉狭窄 (内径减少 >5 0 % )患者在肾动脉介入术前、术后接受肾动脉内血管超声检查。所有患者均接受肾动脉支架术治疗 (共植入 15枚支架 ) ,所选支架直径均根据术前血管内超声图像定量计算所得肾动脉参考直径选择。结果发现 ,15例患者中 13例肾动脉病变由硬性斑块构成 ,其中 2例伴严重钙化 ,剩余 2例为软斑块。血管重构方式 12例表现为负性重构 ,3例为正性重构。病变血管外弹力膜横截面积为 119.7± 2 3.1mm2 ,管腔横截面积为 34.5± 9.3mm2 ,斑块面积为 85 .2± 2 6 .0mm2 。肾动脉支架术治疗手术成功率为 10 0 %。结果提示 ,肾动脉血管内超声检查在判定肾动脉斑块性质、明确狭窄程度、测量管腔直径及指导支架植入有重要临床价值。     

Gemstone能谱冠状动脉CT血管成像诊断冠状动脉重构的临床研究

目的:探讨Gemstone能谱冠状动脉CT血管成像(CCTA)诊断冠状动脉重构的临床价值。方法:选取我院使用Gemstone能谱CCTA检查的冠心病患者76例。根据重构指数(RI)将患者分为三组,正性重构组(RI1.05)44例,无重构组(RI 0.95～1.05)21例,负性重构组(RI0.95)11例,另外,又根据斑块负荷(PB)将患者分为四组,PB 21%～40%组30例、PB 41%～60%组30例、PB 61%～80%组14例和PB80%组2例。比较各组患者的年龄、PB、RI、近端及远端参考段外弹力膜直径差异。结果:正性重构组、负性重构组、无重构组患者的病变处外弹力膜直径与近端参考段外弹力膜直径之间差异均有统计学意义(P均0.05),正性重构组和无重构组病变处外弹力膜直径明显大于负性重构组,无重构组近端参考段外弹力膜直径均明显大于正性重构组和负性重构组(P均0.05);PB三组之间差异无统计学意义(P0.05)。不同PB组RI、远端及近端参考段外弹力膜直径之间差异无统计学意义(P均0.05),病变处外弹力膜直径、病变管腔直径在不同PB组之间的差异有统计学意义(P均0.05),除BP80%组外,其他PB组(PB从20%到80%变化时)病变处外弹力膜直径和管腔直径都随PB增加而降低。结论:Gemstone能谱CCTA能精确测量与重构性质相关的各种参数,反映PB从20%到80%不同分组的冠状动脉重构变化。     

Coronary Atherosclerotic Precursors of Acute Coronary Syndromes

Background

The association of atherosclerotic features with first acute coronary syndromes (ACS) has not accounted for plaque burden.

Coronary Sarcoidosis Presenting as Acute Coronary Syndrome

Sarcoidosis is a systemic disorder of uncertain etiology characterized by noncaseating granulomatous inflammation. The disease often involves the heart on autopsy, but the antemortem diagnosis of cardiac sarcoidosis is frequently missed. Cardiac involvement usually includes granulomatous inflammation or fibrosis of the myocardium, conduction system, or pericardium. We now describe a case of epicardial coronary involvement by sarcoidosis, where the diagnosis was made by surgical biopsy of the coronary artery in an African American man presenting with acute coronary syndrome and recurrent symptomatic restenosis following coronary intervention. The case extends the spectrum of common cardiac syndromes that cardiac sarcoidosis can masquerade as and highlights the importance of maintaining a high index of suspicion for early recognition and instituting specific treatment that might improve prognosis. A review of the literature also suggests the need for improvement in diagnostic approaches and prospective clinical trials to establish the best management strategy for this disease. Copyright © 2009 Wiley Periodicals, Inc.     

Coronary Thromboembolism with Fatal Outcome Following Coronary Angiography

ABSTRACT A case of fatal thromboembolic occlusion of the left coronary artery at selective coronary arteriography is described. The course of events and the findings at autopsy suggest that thrombotic material was deposited on one intravascular catheter and transferred to a second catheter inserted over the same guide wire. Contrast injection through the second catheter into the left coronary ostium resulted in immediate and fatal occlusion of the two major branches of the left coronary artery.     

Spontaneous Multivessel Coronary Spasm During Diagnostic Coronary Angiography

Acute vasospastic angina, formerly known as Prinzmetal angina, is characterized by transient electrocardiographic changes that are not related to exertion. Its atypical presentation makes it difficult to establish the diagnosis, so it is probably underrecognized and therefore mismanaged. We treated a 49-year-old woman who presented with a 2-day history of chest pain associated with palpitations. Abnormal radionuclide stress test results prompted diagnostic coronary angiography, during which the patient reported chest pain and became hemodynamically unstable. Active coronary vasospasm at multiple sites was treated with intracoronary nitroglycerin and nicardipine, leading to immediate recovery.Our case highlights the importance of accurate, timely diagnosis of vasospastic angina, and of early recognition and management of spontaneous coronary spasm during angiography.     

Coronary microembolization

Atherosclerotic plaque rupture is a key event in the pathogenesis of acute coronary syndromes and during coronary interventions. Atherosclerotic plaque rupture does not always result in complete thrombotic occlusion of the entire epicardial coronary artery with subsequent acute myocardial infarction, but may in milder forms result in the embolization of atherosclerotic and thrombotic debris into the coronary microcirculation. This review summarizes the available morphological evidence for coronary microembolization in patients who died from coronary artery disease, most notably from sudden death. Then the experimental pathophysiology of coronary microembolization in animal models of acute coronary syndromes is detailed. Finally, the review presents the available clinical evidence for coronary microembolization in patients, highlights its key features--arrhythmias, contractile dysfunction, microinfarcts and reduced coronary reserve--, compares these features to those of the experimental model and addresses its prevention by mechanical protection devices and glycoprotein IIb/IIIa antagonism.     

Coronary microembolization

Atherosclerotic plaque rupture is the key event in the pathogenesis of acute coronary syndromes and it also occurs during coronary interventions. Atherosclerotic plaque rupture does not always result in complete thrombotic occlusion of the epicardial coronary artery with subsequent impending myocardial infarction, but may in milder forms result in the embolization of atherosclerotic and thrombotic debris into the coronary microcirculation.This review summarizes the present experimental pathophysiology of coronary microembolization in animal models of acute coronary syndromes and highlights the main consequences of coronary microembolization--reduced coronary reserve, microinfarction, inflammation and oxidative modification of contractile proteins, contractile dysfunction and perfusion-contraction mismatch.Furthermore, the review presents the available clinical evidence for coronary microembolization in patients and compares the clinical observations with observations in the experimental model.