冠状动脉堵闭法建立猪心肌梗死模型

探讨运用经皮腔内冠状动脉成形术球囊堵闭猪冠状动脉建立急性心肌梗死动物模型的实验方法。选用苏中幼猪11只，麻醉后经股动脉或颈总动脉置入经皮腔内冠状动脉成形术球囊至冠状动脉左前降支远端，堵闭血流120min。观察心电图、心肌酶、心脏二维超声检查及冠状动脉和左心室造影。结果发现，存活7只猪均完成冠状动脉左前降支远端的封堵，心电图显示急性心肌梗死典型图形变化，血浆肌钙蛋白明显升高并呈动态演变：术后1h超声检查出现间隔上部及前壁局部运动异常；术后2至4周造影复查显示左心室前壁、心尖部心室壁异常运动；存活7只猪均成功地建立急性心肌梗死模型。另4只猪分别在堵闭60～100min因心室纤颤死亡。结果提示，运用经皮腔内冠状动脉成形术球囊封堵冠状动脉可成功建立猪急性心肌梗死模型，并保持封堵冠状动脉通畅；与开胸法相比更接近人体状态，具有创伤小、动物生存时间长并易于术后馒头等优点。     

非开胸法建立持续性单形性室性心动过速动物模型的研究

探讨运用经皮球囊冠状动脉成形术 (PTCA)球囊堵闭猪冠状动脉造成急性心肌梗死 (AMI)后数周建立持续性单形性室性心动过速 (VT)的非开胸法动物模型的方法。猪 1 3只 ,体重 30± 5kg ,运用PTCA球囊堵闭猪左前降支(LAD)形成AMI。存活猪在AMI后数周内进行心室程序电刺激诱发持续性单形性VT ,观察VT诱发、终止的方式及VT诱发的时间窗等。结果 :9/ 1 3只猪形成AMI,经左心室造影及心脏超声检查证实左室心尖、前间隔、左室前壁室壁瘤形成。术后 2～ 2 0周内 9只猪接受平均 1～ 2次电生理检查 ,运用程序电刺激方法 ,8只猪共成功诱发出 1 6种单形性持续性VT ,1只猪仅诱发出非持续性短阵VT。VT周长为 2 54± 65ms ,持续时间 1 8± 1 6min,最长达 62min。程序电刺激和直流电复律可终止VT ,1 0种VT表现为室房分离 ,6种VT室房均为 1∶1逆传 ;9种呈左束支阻滞型 ,7种呈右束支阻滞型。结论 :运用PTCA球囊堵闭冠状动脉造成MI后室壁瘤形成 ,通过程序电刺激的方法可成功建立持续性单形性VT非开胸动物模型 ,成功率较高 ,VT诱发的时间窗长。     

非开胸法室壁瘤相关持续性单行性室性心动过速动物模型的建立

目的:探讨运用经皮球囊冠状动脉成形术(PTCA)球囊堵闭猪冠状动脉前降支(LAD)造成急性心肌梗死(AMI)后数周,形成左心室室壁瘤(LVA)并结合程序刺激方法,建立持续性单行性室性心动过速(SMVT)的非开胸动物模型。方法:中华实验小型猪7只,体质量(35±5)kg,运用PTCA球囊堵闭猪LAD形成AMI。存活猪在AMI后数周内行心室程序刺激诱发SMVT。术中及术后观察LAD、左心室造影及超声心动图改变,SMVT诱发、终止方式及SMVT周期变化。结果:5只猪证实左心室室壁瘤形成。术后4 w对5只猪行程序刺激,诱发出11种SMVT,周长为(223.63±32.55)ms,且可被程序刺激和直流电复律终止。其中,7种SMVT为房室分离,4种SMVT为室房1:1逆传;8种呈左束支传导阻滞,3种呈右束支传导阻滞。心电图演变过程与人体心肌梗死过程基本一致。结论:运用PTCA球囊堵闭LAD造成AMI后LVA形成,并通过程序刺激成功诱发SMVT。此种非开胸法建立室壁瘤相关持续性单行性室性心动过速动物模型成功率高。研究结果提示,折返可能是室壁瘤相关室性心律失常的电生理基础,为进一步研究治疗奠定了实验基础。     

经皮穿刺球囊封堵冠脉建立犬急性心肌梗死模型的实验研究

目的:探讨应用PTCA球囊封堵冠状动脉犬急性心肌梗死动物模型的实验方法。方法:选用杂种犬20只,麻醉后经股动脉置入PTCA球囊至左前降支（LAD）和左旋支（LCX）,封堵血流90min。结果:2只因指引导管致前降支闭塞发生心室纤颤死亡,2只因球囊封堵前降支近端约30min后发生心室纤颤死亡,4只在球囊拔除后发生心室纤颤死亡,1只封堵左旋支中段犬在心肌梗死后20h死亡。其余11只动物成功建立急性心肌梗死模型。前降支封堵术后1周,行超声心动图检查出现室间上部及前壁局部运动异常,室壁也变薄。结论:运用PTCA球囊封堵冠状动脉成功建立急性心肌梗死动物模型,可为研究提供较好的实验模型。     

经皮球囊扩张封堵冠状动脉前降支制备巴马香猪急性心肌梗死模型

目的 探讨经皮球囊扩张封堵冠状动脉前降支(LAD)制备巴马香猪急性心肌梗死(AMI)模型的方法及可行性.方法 经右股动脉置入冠状动脉球囊导管至左前降支;预适应3～4次,每次球囊充盈30 s,间隔5～10 min;以3～5 atm扩张球囊封闭LAD远端血流,40 min后撤除球囊.结果 8头巴马香猪中有6头存活,造模成功率为75%.模型梗死面积变异系数为11.7%(33.2±3.9).封堵后心电图呈动态变化,心肌酶学指标(CK、CK-MB、cTnI、Myo、LDH)较术前明显升高,心脏彩超左心室舒张末内径、左心室舒张末容积及左心室收缩末容积均增大,LVEF均下降,部分实验猪出现心室壁瘤,TTC染色、HE染色证实心肌梗死模型建立成功.结论 经皮球囊扩张封堵法制备巴马香猪急性心肌梗死模型成功率高,保持了梗死区冠脉可重复进行造影,为干细胞植入梗死区心肌治疗AMI提供了较好的动物模型.     

应用开胸法建立室壁瘤动物模型

用杂种犬10只，麻醉后左侧开胸，结扎左前降支（LAD）及其第二对角支，5周后行心脏二维超声检查以明确室壁瘤形成效果。结果为10只犬均完成冠状动脉结扎手术，1只房室收缩分离术中死亡，1只心室纤颤术中死亡。存活的8只均成功建立了左室急性心肌梗死后室壁瘤的动物模型。心脏二维超声检查示左室前壁、心尖部室壁瘤形成。认为应用开胸法结扎冠状动脉可以成功建立急性心肌梗死后室壁瘤的动物模型。     

尼沙赫电图对早期心肌缺血的预先诊断价值探讨

目的 建立中国中型猪经皮冠状动脉腔内血管成形术(PTCA)球囊封堵冠状动脉急性心肌梗死模型,研究急性心肌缺血梗死过程中尼沙赫电图(saahECG)时间轴心室测量标量参数S-VS和VS-VD的变化,并探讨该变化对心肌缺血的早期诊断价值.方法 中国中型猪,体重39~67(44.5±12.70)kg,麻醉后经股动脉置入PTCA球囊至左前降支第一对角支远端,堵闭血流120 min,同步、逐波扫描记录模型建立前后及过程中saahECG和常规12导联心电图(ECG),随后对saahECG时间轴心室测量,以S-VS和VS-VD作为标量参数进行分析,并与同步记录的ECG对比分析.结果 ①运用PTCA球囊封堵法成功建立猪急性心肌梗死模型,球囊封堵12 s后saahECG即出现VS-VD改变,39 s后S-VS显著增加,而ECG的ST段改变则于24 s后出现.②saahECG心室时间轴标量参数S-VS、VS-VD改变早于心电图改变.③ 球囊封堵前及封堵2 h后,saahECG标量参数S-VS、VS-VD差异显著.结论 我们发现了一种新的监测心肌缺血的体表心电图,即saahECG,saahECG比ECG提前反应,并可以实现心肌缺血改变的数据化显示,对心肌缺血更早期的诊断有重要价值.     

小型猪急性心肌梗死经皮冠状动脉再通后无复流模型的建立

目的复制小型猪急性心肌梗死冠状动脉再通(AMI-PCI)后无复流(no-reflow)现象,提供更为接近人类心血管组织生物学特性的动物模型。方法小型猪20头,雌雄不限,行左、右冠状动脉造影和左心室造影,并记录有创血流动力学参数,通过球囊闭塞、微血栓注入造成左前降支(LAD)无复流。监测心电图变化。结果(1)制模共有16头小型猪成活,其中14头达到AMI-PCI后无复流动物模型标准[TIMI血流≤2级,校正的TIMI血流记帧法(CTFC)≥36.2帧],制模成功率为70%。(2)小型猪在无复流模型建立成功后较闭塞前心率增快、血压下降、心肌耗氧量(PRI)增加、左心室舒张期末压(LVEDP)升高、肺毛细血管楔压(PCWP)升高,较闭塞前差异均具有统计学意义(P<0.05)。(3)在整个实验中,体表心电图和冠状动脉内心电图的演变均出现类似人类急性心肌梗死缺血再灌注的心电图演变规律。结论通过选择性冠状动脉前降支急性闭塞、再灌注、微血栓注入制备的无复流小型猪模型是无复流研究中一种较理想的实验动物模型。     

急性前壁心肌梗死时下壁导联ST段改变的临床价值

目的探讨急性前壁心肌梗死病人下壁导联ST段改变的临床价值.方法对93例冠状动脉左前降支(LAD)单支病变所致急性前壁心肌梗死病人,根据早期心电图下壁导联ST段改变将其分为压低组、抬高组、无改变组3组,与冠状动脉造影结果进行分析比较.结果下壁导联ST段压低组中71.4%为LAD非包绕型近端病变;抬高组中61.5%为LAD包绕型远端病变;无改变组中LAD包绕型近端病变和LAD非包绕型远端病变所占比例相近.结论急性前壁心肌梗死病人下壁导联ST段改变与LAD形态及病变部位有关.     

球囊封堵法建立猪急性心肌梗死模型及MR判定

目的:运用球囊封堵法建立猪急性心肌梗死(AMI)模型,通过磁共振(MR)判定模型建成与否。方法:实验使用12头小型猪,麻醉后经右侧股动脉将球囊导管置入至左前降支第1对角支下方0.5~1.0 cm处堵闭90 min,直至心电图证实AMI形成,并行MR True Fisp-PSIR序列心肌延迟灌注扫描及HE染色。结果:12头小型猪中10头成功建立AMI模型,MR延迟灌注扫描在T1WI双反转序列上,室间隔呈半月形低信号。HE染色法显示,封堵血管远端的心肌细胞核淡染、胞浆溶解。结论:冠状动脉球囊堵法是一种简单安全的建立AMI模型的方法,MR可更直观地观察到梗死区面积、组织水肿及心功能改变。     

A porcine model of ischemic heart failure produced by intracoronary injection of ethyl alcohol

We have developed a porcine model of acute myocardial infarction (AMI) and ischemic heart failure by transcatheter intracoronary injection of ethyl alcohol and observed pathologic changes induced in the alcohol-injured coronary artery and infarcted myocardium. In a total of 12 female pigs, anteroseptal AMI was induced by transcatheter delivery of 1 mL of 99.9% ethyl alcohol using a 2.5 mm diameter over-the-wire balloon catheter in the left anterior descending artery (LAD). Another five pigs underwent the sham operation, and the differences in left ventricular (LV) dimension and LV ejection fraction between these pigs and those injected with ethyl alcohol were evaluated. Follow-up coronary and LV angiography, echocardiography and histopathology were performed at 4 weeks after the procedure. Myocardial SPECT using ²⁰¹Tl (and ^99mTc-MIBI) and triphenyl tetrazolium chloride (TTC) stain were performed and compared. Procedure-related death occurred in two pigs with proximal LAD occlusion. Four pigs suffered from ventricular tachycardia, which converted to sinus rhythm by DC cardioversion. Follow-up coronary angiography at 4 weeks revealed persistent total occlusion in all pigs. Echocardiogram showed decreased apicoanteroseptal wall motion with an ejection fraction of 46.5 ± 3.3% and nonsignificantly changed LV dimensions. Myocardial SPECT revealed a perfusion defect in the apicoanterior wall in all subjects (percent area of the perfusion defect = 22.1 ± 2.50%). The percentage of myocardium not stained by TTC was 23.1 ± 2.25%. Histologic examination revealed severe fibrosis in the infarcted myocardium and massive thrombus with organization and calcification in the alcohol-injured coronary artery. The porcine model of AMI obtained by intracoronary alcohol injection provides a safe and reproducible method for the research and development of new therapeutic modalities for MI and end-stage heart failure.     

尿激酶原对急性心肌梗死模型大鼠心功能的保护作用及机制探究

目的 探究尿激酶原对急性心肌梗死(AMI)模型大鼠心功能的保护作用及可能机制.方法 36只SD大鼠,采用随机数字法分为Sham组(n=12)、AMI组(n=12)和尿激酶原组(n=12).采用结扎左冠状动脉前降支的方法建立大鼠AMI模型.建模后,尿激酶原组大鼠每天经尾静脉注射2.5 mg/kg尿激酶原,Sham组和AM...     

心大静脉闭塞对心脏起搏阈值的影响

目的探讨心大静脉闭塞对心脏起搏阈值的短期与长期影响.方法24头家猪采用经皮放置金属弹簧圈,建立心大静脉闭塞动物模型,分别测定闭塞前和闭塞后1 h、1～3周右心室心尖部、左心室游离壁、左心室间隔部以及左心室心尖部起搏阈值;4头家猪用经皮经腔冠状动脉成形术球囊阻塞心大静脉建立心大静脉阻塞模型,测定阻塞前和阻塞后5、15、25、35、45、60 min心大静脉内起搏阈值.结果心大静脉闭塞后,左心室间隔部、心尖部起搏阈值明显升高(均P＜0.01),左心室游离壁起搏阈值无明显变化.心大静脉阻塞60 min内,局部起搏阈值差异无统计学意义(均P＞0.05).结论心大静脉闭塞可导致邻近部位心肌起搏阈值升高,但心大静脉内局部起搏阈值在阻塞后1 h内无明显变化.     

Prognostic significance of peripheral monocytosis after reperfused acute myocardial infarction:a possible role for left ventricular remodeling.

OBJECTIVES: The aim of this study was to determine the significance of peripheral monocytosis in clinical outcome after reperfused acute myocardial infarction (AMI), especially relating to post-infarct left ventricular (LV) remodeling. BACKGROUND: Peripheral monocytosis occurs two to three days after AMI, reflecting infiltration of monocytes and macrophages into the necrotic myocardium. However, the prognostic significance of peripheral monocytosis after AMI remains to be determined. METHODS: A total of 149 patients with first Q-wave AMI were studied. White blood cell (WBC) count, percentage of monocytes and serum C-reactive protein level were measured every 24 h for four days after the onset of AMI. We assessed association between peripheral monocytosis and prognosis including pump failure, LV aneurysm and long-term outcome after AMI. RESULTS: Patients with pump failure (p < 0.0001) or LV aneurysm (p = 0.005) had higher peak monocyte counts than those without these complications. Predischarge left ventriculography revealed that peak monocyte count was positively correlated with LV end-diastolic volume (p = 0.024) and negatively correlated with ejection fraction (p = 0.023). Multivariate analyses showed that peak monocyte count > or = 900/mm(3) was an independent determinant of pump failure (relative risk [RR] 9.83, p < 0.0001), LV aneurysm (RR 4.78, p = 0.046) and cardiac events (RR 6.30, p < 0.0001), including readmission for heart failure, recurrent myocardial infarction and cardiac deaths, including sudden deaths. CONCLUSIONS: Peripheral monocytosis is associated with LV dysfunction and LV aneurysm, suggesting a possible role of monocytes in the development of LV remodeling after reperfused AMI.     

经皮穿刺心外膜电-解剖标测及射频消融心肌梗死后室性心动过速的实验研究

目的探讨经心外膜途径在电-解剖标测系统指导下行射频消融治疗心肌梗死后室性心动过速的可行性和安全性。方法成年中华小型猪共7只,采用经皮穿刺的方法将球囊置于左前降支中下部,封堵150 min建立心肌梗死模型。3～5周后将心肌梗死模型猪,行电生理检查诱发室性心动过速。经胸穿刺进入心包腔,采用电-解剖标测系统在窦性心律下进行心外膜电压标测和线性消融。射频消融后再次行电生理检查,不能再诱发室性心动过速为消融成功。结果存活的心肌梗死模型的猪7只,3～5周后行电生理检查,共诱发出单形性室性心动过速共8种,7种表现为右束支阻滞图形,1种表现为左束支阻滞图形,室性心动过速(VT)周长平均在(338±66)ms。1只猪同时诱发心室颤动,电除颤转复窦性心律。7只猪心包穿刺均成功,完成心外膜电压标测,沿瘢痕区到二尖瓣环或正常心肌区逐点进行线性消融。射频消融后再次行电生理检查,6只猪不能再诱发室性心动过速。结论经胸穿刺进入心包腔行心外膜标测和消融治疗心肌梗死后室速的方法是安全可行的,心外膜标测消融心肌梗死后室速的方法可以作为心内膜消融的一种有效补充方法。     

女性急性心肌梗死静脉溶栓后ST段再抬高对预后的影响

目的 探讨女性急性心肌梗死（AMI）静脉溶栓成功后ST段延迟性再抬高对预后的影响。方法入选发病6h之内行溶栓治疗成功的女性AMI患者106例,根据溶栓12h后ST段是否再抬高分为ST段再抬高观察组（观察组,n=38）和ST段未再抬高对照组（对照组,n=68）。监测两组患者CK-MB峰值及峰值时间,溶栓后1周、2周、1月、3月、6月时复查心电图、动态心电图及心脏超声,6月内每月复查6min步行试验,比较两组上述指标差异。结果观察组年龄,合并高血压、糖尿病、高脂血症、肥胖者比例以及CK-MB峰值均显著高于对照组（P均〈0.05）,CK-MB峰值时间较对照组前移程度小（P〈0.05）,恶性心律失常、心力衰竭、室壁瘤发生率及死亡率均显著高于对照组（P〈0.05）,左室射血分数和6min步行实验值均低于对照组（P〈0.05）。结论女性急性心肌梗死溶栓成功后延迟性ST段再抬高者恶性心律失常、心力衰竭、室壁瘤、死亡发生率高,预后相对差。     

ST-segment depression in lead aVR predicts predischarge left ventricular dysfunction in patients with reperfused anterior acute myocardial infarction with anterolateral ST-segment elevation.

BACKGROUND: Patients with an anterolateral acute myocardial infarction (AMI) have a worse prognosis, and those with additional inferolateral wall involvement might be higher risk because of more extensive area at risk. Lead -aVR obtained by inversion of images in lead aVR has been reported to provide useful information for inferolateral lesion. METHODS: We examined the relation between ST-segment deviation in lead aVR on admission electrocardiogram (ECG) and left ventricular function in 105 patients with an anterolateral AMI undergoing successful reperfusion < or = 6 hours after onset. Patients were classified according to ST-segment deviation in lead aVR on admission ECG: group A, 23 patients with ST elevation of > or = 0.5 mm; group B, 47 patients without ST deviation; and group C, 35 patients with ST depression of > or = 0.5 mm. RESULTS: There were no differences among the 3 groups in age, sex, or site of the culprit lesion. In groups A, B, and C, the peak creatine kinase level was 3661 +/- 1428, 4440 +/- 1889, and 6959 +/- 2712 mU/mL, and the left ventricular ejection fraction (LVEF) measured by predischarge left ventriculography was 54% +/- 9%, 48% +/- 7%, and 37% +/- 9%, respectively(P < .01). During hospitalization, congestive heart failure occurred more frequently in group C than in groups A or B (P < .05). ST-segment depression in lead aVR had a higher predictive accuracy than other ECG findings in identifying patients with predischarge LVEF < or = 35%. CONCLUSIONS: We conclude that in patients with an anterolateral AMI, ST-segment depression in lead aVR on admission ECG is useful for predicting larger infarct and left ventricular dysfunction despite successful reperfusion.