微栓子的组成和大小与脑缺血性损伤程度的相关性研究

目的:探讨微栓子不同组成和大小与脑缺血损伤程度的相关性。方法:将不同组成(钙化斑块、纤维斑块和全血凝块)和不同大小(75～105μm和55～74μm)的微栓子混悬液注入SD大鼠右侧颈内动脉。采用苏木精-伊红染色、TUNEL细胞凋亡检测及caspase-3蛋白免疫组化染色观察术后24h脑缺血损伤程度。结果:相同大小的微栓子,其脑缺血损伤程度钙化斑块>纤维斑块>全血凝块(P<0.01),相同组成的微栓子,75～105μm微栓子组的脑缺血损伤程度明显>55～74μm微栓子组(P<0.01)。结论:微栓子的组成和大小与脑缺血损伤程度密切相关。     

氧化应激在慢性缺血性脑白质损伤中的作用

目的 阐明氧化应激是否参与大鼠慢性脑缺血所致的脑白质损伤.方法 健康雄性Wistar大鼠按照完全随机数字表法分为假手术组,持久性双侧颈总动脉结扎3 d组、7 d组、3周组及6周组,每组6只.应用大鼠双侧颈总动脉结扎制备慢性脑缺血模型,检测大鼠脑白质内超氧化物歧化酶(SOD)活性、过氧化氢酶(CAT)活性、谷胱甘肽(GSH)含量以及脂质过氧化产物丙二醛(MDA)和4-羟基壬烯醛(4-HNE)加合物的变化.结果 与假手术组比较,慢性脑缺血大鼠脑白质内MDA含量在手术后3周明显增加,手术后6周进一步增高,差异有统计学意义(P<0.05).手术后3d至6周,慢性脑缺血大鼠脑白质内4-HNE蛋白加合物逐渐增高,与假手术组比较有差异有统计学意K(P<0.05).SOD活性在手术后3周和6周才明显降低,与假手术组比较差异有统计学意义(P<0.05).此外,慢性脑缺血大鼠脑白质内GSH含量在手术后7d即开始降低,而在手术后3周及6周则进一步下降,与假手术组比较差异有统计学意义(P<0.05).结论 慢性脑缺血导致大鼠脑白质氧化性损伤增加,抗氧化防御能力降低:氧化性损伤的增加和抗氧化防御能力的降低与慢性脑缺血所致的脑白质损伤密切相关.     

活性氧在脑缺血-再灌注损伤后动态表达

目的观察活性氧(ROS)在大鼠脑缺血—再灌注损伤不同时间缺血灶周区皮质的动态表达。方法健康成年SD雄性大鼠(n=55),随机分成假手术组(n=5)和模型组(n=50),模型组按再灌注时间分为10个组,即脑缺血—再灌注1h、3h、6h、12h、1d、3d、5d、7d、14d和28d组,每组5只大鼠。通过阻塞大脑中动脉(MCAO)制作大鼠局灶性脑缺血—再灌注损伤模型,采用改良神经功能严重性评分(m NSS)对不同时间点大鼠的神经功能进行评价,采用流式细胞术检测缺血灶周区ROS和血管内皮生长因子(VEGF)动态时空表达。结果假手术组未见神经功能损伤,评分为0。脑缺血—再灌注1h大鼠出现神经损伤,3h~1d时症状加重,3~7d时症状有所改善,14~28d症状明显好转。假手术组有少量ROS和VEGF表达,脑缺血再灌注损伤后1h缺血灶周区ROS急剧上升,3~6h有所下降,但仍远高于假手术组,后逐渐下降,3d时降到最低,与假手术组相仿,随后迅速上升,5d时已超过6h数值,7d时接近1h高度,后ROS表达呈平台期,VEGF表达趋势与其相仿,ROS表达与神经功能评分呈负相关。结论 ROS可能在脑缺血损伤中起双相作用,在超早期参与脑损伤过程,后期可能参与脑修复作用。     

高温对重型颅脑损伤后乳酸、Na+-K+-ATP酶和脑水肿的影响

目的 探讨大鼠重型颅脑损伤后高温对伤灶区脑组织乳酸、Na+-K+-ATP酶和脑水肿的影响.方法 90只SD大鼠随机分为假手术组、颅脑损伤组、伤后高温组,每组又按处死时间点(伤后4 h、1 d、3 d、5 d和7 d)分为五个亚组,每亚组6只.取伤灶区脑组织测含水量、乳酸含量和Na+-K+-ATP酶活性并行电镜检查.结果 高温组脑组织含水量和乳酸含量在伤后各时间点均显著高于颅脑损伤组和假手术组(P＜0.05),而Na+-K+-ATP酶含量显著低于颅脑损伤组和假手术组(P＜0.05),电镜检查发现高温组神经细胞肿胀、血脑屏障破坏程度较颅脑损伤组明显加重.结论 颅脑损伤后高温增加脑组织乳酸生成,同时Na+-K+-ATP酶活性下降,脑水肿加重,故在颅脑损伤后应保持体温在正常范围内,避免体温升高.     

大鼠全脑缺血再灌注损伤后APC-Cdh1mRNA的表达变化

目的 研究大鼠全脑缺血再灌注损伤后APC-Cdh1的表达变化.方法 雄性SD大鼠60只,体重280-350 g,随机分成假手术组(SH组)、模型组(IR组).采用改良4-VO法建立SD大鼠全脑缺血模型,在损伤后不同时间点,免疫组化染色检测Cdh1的表达部位并且采用实时荧光定量PCR检测大鼠海马组织APC-Cdh1的表达.结果 与对照组相比,术后1d Cdh1 mRNA表达减少,术后3d显著升高,术后7d又降低.免疫组化检测显示APC-Cdh1在海马区及皮质区中均有大量表达.结论 APC-Cdh1可能与中枢神经系统的发育及损伤有着密切的关系.     

人脐带沃顿胶间充质干细胞移植对创伤性脑损伤大鼠脑损伤区微循环的影响

目的 探讨人脐带沃顿胶间充质干细胞(WJCs)对脑创伤区周围微循环的影响. 方法 72只健康SD大鼠采用随机数字表法分为4组:(1)假手术组;(2)移植对照组;(3)WJCs移植组;(4)正常组.每组18只.移植对照组和WJCs移植组采用Feeney自由落体硬脑膜外撞击法建立中度创伤性颅脑损伤模型,再分别注射0.3 mL的生理盐水和WJCs混悬液;假手术组颅骨钻孔后不损伤脑组织不移植细胞;正常组不做任何处理.分别于移植后3d及7d进行大鼠行为学评分;取移植后ld、3d、7d和2周的脑组织切片行免疫组织化学检测,检测大鼠损伤灶周围血管内皮生长因子(VEGF)及CD34的表达;实时定量PCR(RT-PCR)检测的VEGF mRNA表达;测定微血管面密度(MVD);移植后2周和4周行免疫组化观察胶质纤维酸性蛋白(GFAP)和神经元特异性烯醇化酶(NSE)蛋白表达水平. 结果 移植后7d,WJCs移植组大鼠mNSS评分明显高于移植对照组,差异有统计学意义(P＜0.05).WJCs移植组移植后3d、7d和2周损伤灶周围皮层脑组织VEGF和CD34的表达均高于移植对照组,差异有统计学意义(P＜0.05).移植后2周和4周WJCs移植组损伤区免疫组织化学染色均发现GFAP和NSE阳性细胞,其他3组均未发现.RT-PCR检测到WJCs组VEGF mRNA的表达量高于移植对照组,差异有统计学意义(P＜0.05). 结论 WJCs移植后可增加损伤区脑组织VEGF及CD34阳性表达,参与调控损伤区微血管的变化,改善损伤区的微循环,促进大鼠神经功能的恢复.     

静脉注射人脐血间充质干细胞对脑损伤神经生长因子的影响

目的 观察TBI后静脉注射人脐血间充质干细胞(CB-MSCs)对NGF、BDNF表达的影响,探讨其脑保护的作用机制.方法 清洁级健康雄性SD大鼠90只采用完全随机数字表法分为假手术组、损伤组和治疗组,每组30只.损伤组和治疗组采用改进的Feeney自由落体法制作大鼠TBI模型,假手术组只开骨窗,不撞击硬脑膜.治疗组尾静脉注入3×106个Brdu标记的CB-MSCs,损伤组及假手术组注入等体积的PBS液.在移植后3、7、14、21、28 d,采用HE染色、免疫组化染色、原位杂交法对TBI大鼠脑组织形态学变化、Brdu标记情况、NGF和BDNF表达情况进行检测.结果 假手术组仅有极少量的NGF、BDNF阳性表达细胞.损伤组表达明显增加,以损伤周边区最为明显,注射后14d达到高峰(NGFA值为8.35±1.07,BDNFA值为9.01±1.74),之后逐渐下降,但仍高于假手术组,差异有统计学意义(P＜0.05).治疗组表达趋势与损伤组相同,14d达高峰后,21 d、28 d阳性表达明显下降;各时间点均高于损伤组与假手术组,差异有统计学意义(P＜0.05).结论 在TBI中,静脉注射CB-MSCs可以增加损伤局部NGF、BDNF的分泌,改善局部微环境,促进神经元的修复.     

大鼠面神经缺血后面神经核磷酸化CREB水平的变化

目的探讨大鼠面神经缺血损伤后面神经元内环磷腺苷反应元件结合蛋白（CREB）磷酸化水平的变化及其与氧化应激的关系。方法 55只成年雄性SD大鼠随机分为正常组（5只）、假手术组（25只）和面神经缺血组（25只）,后两组又根据时间分为术后1、3、7、14、21 d 5个亚组,每亚组5只大鼠。显微手术阻断大鼠鼓室段岩动脉建立大鼠面神经缺血损伤模型。采用分光光度法测定面神经核丙二醛（MDA）含量;利用免疫印迹法测定面神经元内锰超氧化物歧化酶（Mn SOD）和磷酸化CREB（p-CREB）表达水平。结果面神经缺血后,面神经核MDA含量先增高,7 d达峰值,随后降低;而面神经元Mn SOD和p-CREB表达水平先降低,7 d达最低值,随后逐渐增高。面神经缺血组每个时间点MDA水平、Mn SOD和p-CREB表达水平均与正常组和假手术组差异显著（P〈0.05）,而假手术组与正常组之间无显著差异（P〉0.05）。结论面神经缺血损伤后造成面神经元氧化应激损伤,导致p-CREB水平先降低后增高,p-CREB水平的增高可降低ROS对面神经元的氧化损伤能力。     

2ME2对脊髓损伤大鼠运动功能及凋亡相关基因caspase-3表达的影响

目的探讨2-甲氧基雌二醇(2ME2)对脊髓损伤(SCI)大鼠运动功能及细胞凋亡相关基因caspase-3表达的影响。方法成年雄性SD大鼠72只按随机数字表法分为假手术组、脊髓损伤组和2ME2治疗组,每组24只,采用改良的Allen’s法制作脊髓损伤模型,2ME2干预组大鼠自脊髓损伤模型建立后第1天开始按24 mg/kg给予2ME2腹腔注射,连续注射7 d,在造模成功后1 d、3 d、7 d、14 d、21 d、28 d采用BBB运动评分系统对各组大鼠运动功能进行评估,造模成功后第7天应用免疫荧光技术检测各组大鼠caspase-3表达,应用TUNEL染色进行凋亡细胞计数。结果造模后14 d、21 d、28 d 2ME2治疗组BBB评分显著高于脊髓损伤组,差异具有统计学意义(P<0.05),与假手术组相比,脊髓损伤组及2ME2治疗组caspase-3表达阳性细胞数及凋亡细胞数显著增加,差异具有统计学意义(P<0.05),2ME2治疗组较脊髓损伤组caspase-3表达阳性细胞数及凋亡细胞数显著减少,差异具有统计学意义(P<0.05)。结论 2ME2治疗能改善脊髓损伤大鼠肢体运动功能,具有一定神经保护作用,其治疗机制可能与通过抑制脊髓损伤后的进一步细胞凋亡相关基因的表达有关。     

非压迫性髓核导致大鼠背根神经节的病理变化

目的 观察大鼠脊神经节自体髓核移植后,大鼠左后肢疼痛行为学和神经节非压迫性损伤的超微结构的变化.方法 78只SD大鼠随机分成空白组(6只)、假手术组(36只)和自体髓核移植模型组(36只).模型组大鼠行腰5左侧半椎板切除,暴露腰5背根神经节,取尾部的自体髓核组织置于背根神经节表面,假手术组背根神经节表面放置等量的自体肌肉,每组用yon Frey hair测鼍手术前后大鼠后肢机械刺激缩爪阈值,于术后7 d、14 d和21 d取材用光镜和电镜行病理学观察.结果 空白组和假手术组左后肢机械刺激缩爪阈值手术前后无明显降低,模型组术后有明显机械刺激缩爪阈值降低(P<0.05);模型组脊神经节出现长达21 d的病理损伤改变,表现为不同程度的神经节充血水肿,节细胞线粒体空泡变,溶酶体增多,内质网肿胀扩张,有的甚至出现细胞核皱缩;神经纤维的轴突内细胞器减少,髓鞘肿胀疏松,个别甚至崩解;假手术组仅在7 d时轻度的神经节充血水肿,细胞有轻微的粒体空泡变;空白组和假手术组的14、21 d脊神经节无病理损伤改变.结论 非机械压迫的自体髓核可引起大鼠脊神经节超微结构严重损伤和后肢机械痛敏.     

Longer duration of cardiopulmonary bypass is associated with greater numbers of cerebral microemboli

BACKGROUND AND PURPOSE: Many patients who undergo cardiac surgery assisted with cardiopulmonary bypass (CPB) experience cerebral injury, and microemboli are thought to play a role. Because an increased duration of CPB is associated with an increased risk of subsequent cerebral dysfunction, we investigated whether cerebral microemboli were also more numerous with a longer duration of CPB. METHODS: Brain specimens were obtained from 36 patients who died within 3 weeks after CPB. Specimens were embedded in celloidin, sectioned 100 microm thick, and stained for endogenous alkaline phosphatase, which outlines arterioles and capillaries. In such preparations, emboli can be seen as swellings in the vessels. Cerebral microemboli were counted in equal areas and scored as small, medium, or large to estimate the embolic load (volume of emboli). RESULTS: With increasing survival time after CPB, the embolic load declined (P<0.0001). (Lipid emboli are known to pump slowly through the brain.) Also with increasing time after CPB, the percentage of large and medium emboli became lower (P=0.0034). This decline is consistent with the concept that the emboli break into smaller globules as they pass through the capillary network. A longer duration of CPB was associated with increased embolic load (P=0. 0026). For each 1-hour increase in the duration of CPB, the embolic load increased by 90.5%. CONCLUSIONS: Thousands of microemboli were found in the brains of patients soon after CPB, and an increasing duration of CPB was associated with an increasing embolic load.     

进展性卒中与微栓子、脑血流动力学检测的相关性研究

目的探讨进展性卒中与微栓子、脑血流动力学之间的关系。方法 240例急性脑梗死患者,进展组116例,对照组124例。应用经颅多普勒(TCD)检测两组患者入院时的脑血流,并检测入院时,入院后第1、3、7天的微栓子阳性率及数量,所有数据进行统计学分析。结果进展性卒中患者的脑血流异常率与对照组比较有统计学意义(P<0.01);进展性卒中患者入院时微栓子阳性率及数量均高于对照组(P<0.01)。结论对急性缺血性卒中患者进行微栓子、脑血流动力学检测可以预测缺血性卒中的进展。     

Velocity of microemboli and transit time from the heart to the brain in patients with patent foramen ovale and artificial heart valves

There is no information about the physical behavior of microemboli en route from their source to the cerebral vessels. Microemboli could abide to a certain laminae, and have a consistent velocity, or wander between different laminae, and keep changing their velocity. Two hundred and seventy four microemboli were recorded by transcranial Doppler (TCD) in six patients with artificial valves, and 119 microemboli were recorded in response to i.v. injection of saline agitated with air in eight patent foramen ovale (PFO) patients. Transit time of microemboli, calculated based on their arrival time at the cerebral vessel (site of monitoring) was explored as a possible function of their measured velocity at the detection point. In the PFO group, the relation between embolus velocity and transit time was: embolus velocityPFO = -41.8 * transit time + 100.6, whereas for the artificial heart valve group it was: embolus velocityValve = -22.6 * transit time + 67.1. Transit time, in both clinical groups, was inversely related to velocity (p < 0.001), thus, early appearing emboli had higher velocity and vice versa. The inverse relation between transit time and measured terminal velocity implies a consistent velocity per microemboli en route, in both groups. Thus, a flow abided to a certain laminae seems to characterize microemboli.     

The Nature of Microemboli in Patients With Artificial Heart Valves

Cognitive decline has recently been found to be associated with microemboli in cerebral vessels in patients with artificial heart valves. The authors sought to determine the nature of such microemboli, that is, whether they are gaseous or solid, by comparing their characteristics to those of artificially generated air emboli in patients with patent foramen ovale (PFO). Three hundred and forty-eight microemboli were recorded in 11 patients with artificial valves (all taking coumadin), and 86 microemboli were recorded in response to intravenous injection of saline agitated with air in 8 PFO patients. No difference in intensity, duration, or relative velocity of microemboli was found between groups. The authors conclude that microemboli generated from artificial heart valves are generally gaseous and not solid.     

Cerebral microembolus detection in an unselected acute ischemic stroke population

OBJECTIVE: The aims of this study were firstly to determine prevalence, frequency, and clinical significance of cerebral microemboli in an unselected acute ischemic stroke population and secondly to examine how this information may improve ischemic stroke subtype classification. METHODS: We intended to perform transcranial Doppler (TCD) microembolus monitorings of the middle cerebral artery (MCA) in the symptomatic hemisphere for 45 min in 120 consecutive patients with internal carotid artery territory ischemia. The first examination was performed within 72 h from start of symptoms and the second 5 +/- 1 days later. Platelet and coagulation system activation were measured following TCD monitoring in 38 patients. The strokes were subtyped using the TOAST classification criteria, and the patients' clinical status was assessed at discharge using the Scandinavian Stroke Scale and the Barthel Index. RESULTS: Microembolus monitoring was technically possible in 83 (69.2%) of the 120 patients. Thirty-two (26.6%) patients had an inadequate temporal bone acoustic window or were too restless to allow long-time monitoring. In 5 (4.2%) patients the relevant MCA was occluded. Twenty-two (26.5%) of the 83 patients had microemboli despite the fact that over 90% were receiving an antiplatelet or an anticoagulant treatment. The mean frequency of microemboli was 6.7 +/- 13.6 per 45 min. Microemboli were more prevalent in assumed cardioembolic stroke than in other subtypes of ischemic stroke (p = 0.047). We found no association between the presence of cerebral microemboli and the clinical outcome or the parameters for platelet or coagulation system activation. The presence of microemboli was not associated with in-hospital deaths (p = 0.17), whereas MCA occlusion was (p = 0.01). CONCLUSIONS: Cerebral microemboli are frequent in unselected acute ischemic stroke patients despite antiplatelet or anticoagulant treatment. TCD detection of microemboli provides valuable pathophysiological information and may, therefore, improve current ischemic stroke subtype classification.     

Induction of transient neurological dysfunction in baboons by platelet microemboli.

BACKGROUND AND PURPOSE: To investigate experimental mechanisms of reversible cerebral dysfunction, we produced transient focal cerebral ischemia in five baboons by unilateral perfusion of internal carotid territories with platelet microemboli generated endogenously. METHODS: Platelet microemboli were formed by incorporating segments of Dacron vascular graft for 1 hour as unilateral carotid arterio-arterial shunts. Platelet embolization was assessed by ultrasonography and isotopic imaging; cerebral function was evaluated by measurements of somatosensory evoked potentials and clinical motor performance. RESULTS: Platelet microemboli, detected by transcranial Doppler ultrasonography, accumulated rapidly in the shunted carotid hemispheric territory. Indium-111-labeled platelets reached a maximum value of 3.2 +/- 0.8 x 10(9) platelets in the dependent hemisphere of five animals after 20 minutes of carotid blood flow through the grafts when measured in real time by continuous scintillation camera imaging. The retained 111In-platelet microemboli cleared from the cerebral vasculature within 1 hour after removing the grafts. Corresponding blood markers of in vivo thrombus formation, beta-thromboglobulin, platelet factor 4, and fibrinopeptide A, increased eightfold to 20-fold after incorporating graft segments and normalized within 1 hour after removing the grafts. Coincidently, focal neurological function was temporarily impaired, as shown by the ipsilateral loss of somatosensory evoked potentials 5 minutes after initiating platelet microembolization, with restoration 1 hour after removing the grafts in five baboons, and contralateral hemiparesis in two recovered baboons, with complete resolution by 24 hours. CONCLUSIONS: Endogenously generated platelet microemboli accumulate transiently in the dependent cerebral circulation and produce corresponding focal neurological dysfunction that resolves within hours after microembolization.     

Source of cerebral microembolic signals in occlusion of the internal carotid artery

Background and purpose: There are several possible sources of cerebral embolic ischaemia distal to an occlusion of the internal carotid artery (ICA). Our aim was to identify the source of microembolic signals in the ipsilateral middle cerebral artery (MCA) by taking simultaneous bitemporal transcranial Doppler ultrasound recordings of the ipsilateral MCA and the contralateral ACA to find the route of potential microembolic material to MCA. Subjects and methods: The study group consisted of 38 patients with an occlusion of the ICA. With extracranial duplex sonography (ACUSON 128 XP; 7 MHz), performed by an experienced sonographer, the echo intensity and echo structure of the occluded ICA in the extracranial part (proximal) were classified as homogeneous or inhomogeneous. In addition, affected segments of the ipsilateral and contralateral carotid artery with arteriosclerotic vessel walls were compared. Microembolic signals were recorded with transcranial Doppler (TCD) monitoring. The microemboli counts in the MCA and ACA were added to the sum scores. Results: The number of affected segments of the carotid artery on the ipsilateral (the bifurcation, the external or common carotid artery) and contralateral side of occluded ICA were equally distributed. In ipsilateral MCA 3.1, 7.1 microemboli (average mean, SD) with a range of between 0 and 34 were counted, in the contralateral ACA 0.3, 0.6 (range of between 0 and 2). Regression analysis confirmed the non-predictability of the microemboli variance on the ipsilateral side of the occlusion from the variance on the contralateral side (multiple r: 0.024). We found no significant correlation between the echo intensity or echo structure of the occluded artery and an increased rate of microemboli in the ipsilateral MCA. Conclusions: Our results indicate a predominantly ipsilateral source for cerebral microemboli in ICA occlusion. The rate of cerebral microembolic signals was not influenced by the echo structure and echo intensity of the occluded ICA. Received: 24 May 1996 Received in revised form: 20 January 1997 Accepted: 31 January 1997     

Acute Neuropsychological Functioning Following Cardiosurgical Interventions Associated With the Production of Intraoperative Cerebral Microemboli

Coronary artery bypass graft (CABG) and valve replacement (VR) surgical patients underwent neuropsychological assessment 1–2 days prior to surgery; 7–10 days postsurgery; and 1 month following hospital discharge. A group of matched healthy controls was tested at identical intervals. Cerebral microemboli in both middle cerebral arteries were quantified during surgery using Doppler sonography. Neuropsychological testing results revealed that the CABG and VR groups did not differ from one another at any assessment point. However, surgical patients performed more poorly than healthy controls across all assessments. Surgical patients, as a group, demonstrated a mild decline in attentional functioning and learning efficiency at the 7–10 day follow-up, but these difficulties essentially returned to baseline by the 1-month follow-up. Intraoperative microemboli counts were not significantly associated with postsurgical neuropsychological functioning in either the CABG or VR group.     

Acute neuropsychological functioning following cardiosurgical interventions associated with the production of intraoperative cerebral microemboli

Coronary artery bypass graft (CABG) and valve replacement (VR) surgical patients underwent neuropsychological assessment 1-2 days prior to surgery; 7-10 days postsurgery; and 1 month following hospital discharge. A group of matched healthy controls was tested at identical intervals. Cerebral microemboli in both middle cerebral arteries were quantified during surgery using Doppler sonography. Neuropsychological testing results revealed that the CABG and VR groups did not differ from one another at any assessment point. However, surgical patients performed more poorly than healthy controls across all assessments. Surgical patients, as a group, demonstrated a mild decline in attentional functioning and learning efficiency at the 7-10 day follow-up, but these difficulties essentially returned to baseline by the 1-month follow-up. Intraoperative microemboli counts were not significantly associated with postsurgical neuropsychological functioning in either the CABG or VR group.     

Cerebral microembolism in acute myocardial infarction

BACKGROUND AND PURPOSE: This study was undertaken to determine the frequency of cerebral microemboli (high-intensity transient signals; HITS) detected by transcranial Doppler (TCD) in patients with acute myocardial infarction (AMI) and to relate them to the various putative risk factors and clinical embolic events. METHODS: We investigated 112 consecutive patients within 72 hours of admission to an acute coronary care unit using TCD to monitor for cerebral microemboli. Twelve patients were excluded because of failure of ultrasound insonation. All patients had 2-dimensional echocardiograms within the study period. RESULTS: HITS were detected in 17% of patients, with significantly higher frequency in patients with reduced (<65%) left ventricular (LV) ejection fraction (P=0. 019), akinetic LV segments (P=0.002), and LV thrombus (P=0.015). A marginally significant (P=0.059) increase of HITS was found in patients with anterior AMI. Stroke was significantly more frequent in patients with cerebral microemboli (P=0.01). CONCLUSIONS: HITS were detected in 17% of patients in spite of adequate antithrombotic therapy and were increased in patients with reduced LV function, akinetic myocardial segments, and LV thrombus. They were present in all 3 patients with stroke and may represent a predictor of clinical embolic events.