微电极阵列芯片技术在抑郁大鼠胸1～5脊髓与心脏组织场电位变化的应用

目的 用微电极阵列芯片技术(MEA)研究慢性应激抑郁大鼠模型的胸1～5脊髓和心脏局部组织的场电位变化.方法 SD大鼠20只,随机分为抑郁组(n=10)和对照组(n=10).用Cronli方法建立慢件轻度不可预见性应激抑郁模型,观察模型的心功能、心律失常发生、大鼠胸1～5脊髓、心房及心室肌组织局部的场电位时程(FAPD)变化规律和HE、Massion染色、电镜检查心脏病理和结构的变化.结果 抑郁组大鼠在慢性应激3周后,体表心电图P波从(25.43±3.38)ms增加到(35.09±7.92)ms,QT间期从(81.93±16.35)ms增加到(114.64±35.08)ms(P＜0.01),并出现房性早搏(n=2)、室性早搏(n=3).抑郁组慢性应激后胸1～5脊髓神经FAPD延长和频率适应性降低[500 mV刺激时,FAPD为(144.25±32.63)ms,1000 mV刺激时为(152.38±30.86)ms,P＞0.05];抑郁组心房肌组织FAPD为(83.14±4.61)ms,FAPD离散度(FAPDd)为(628.25±90.01)ms,显著长于对照组FAPD(45.76±3.66)ms及FAPDd(348.67±69.42)ms(P＜0.05).抑郁组大鼠心肌细胞体积增大,排列较紊乱,间质炎性细胞浸润和心肌细胞问质胶原纤维增生.结论 慢性应激抑郁出现胸1～5脊髓FAPD延长和房性及室性心律失常,其病理基础为心肌细胞炎性浸润和心肌纤维化,电生理变化基础为心房组织FAPD延长和FADPd增加.提示交感通路激活和电传导异常介导了慢性应激抑郁时心律失常的发生.     

β受体阻滞剂对心力衰竭大鼠模型心肌纤维化的影响

目的 探讨不同β受体阻滞剂对心力衰竭大鼠模型心肌纤维化的影响.方法 取Sprague-Dawley雄性大鼠,采用结扎前降支方法建立慢性心力衰竭模型.将存活动物随机分组为心力衰竭组(n=9)、卡维地洛组(n=10)、美托洛尔组a=8),并建立假手术模型(n=10),观察各试验组动物的血液动力学变化,进行心肌纤维化的相关指标测定.结果 与心力衰竭组[(4.7±2.5)mm Hg,1 mm Hg=0.133 kPa]比较,美托洛尔组[(3.9±3.0)mm Hg]、卡维地洛组[(4.0±2.6)mm Hg]心肌梗死后左心室舒张末压水平显著低,美托洛尔、卡维地洛改善左心室±dp/dt(P＜0.05).心力衰竭组羟脯氨酸水平[(4.9±2.6)mg/g]明显高于假手术组[(2.5±1.0)mg/g]及卡维地洛组[(2.8±1.8)mg/g],P＜0.05.卡维地洛组羟脯氨酸水平明显低于美托洛尔组[(4.6±2.3)mg/g],P＜0.05.心力衰竭组心肌间质胶原容积百分数、血管周围胶原面积/冠状动脉腔横断面积(PCVA/VLCA)明显高于假手术组及卡维地洛组(P＜0.05).卡维地洛组PCVA/VLCA(3.9±1.2)明显低于美托洛尔组(5.1±1.7),P＜0.05.结论 卡维地洛组胶原含量低于美托洛尔组,提示卡维地洛较美托洛尔有更强的抑制心肌梗死后心肌纤维化的作用.     

阻断神经元型Nav1.8通道对心脏交感神经节活性和心室电生理性质的影响

目的探讨阻断神经元型Nav1.8通道对正常犬心脏交感神经节活性和心室电生理性质的影响。方法16只健康成年犬(16~18kg)随机分为实验组(n=8)和对照组(n=8)。分离左侧心脏交感神经节,实验组向神经节内注射20mmol/L的Nav1.8通道特异性阻断剂(A-803467)0.1 ml,对照组向神经节内注射等体积的二甲基亚枫。在基础状态和药物注射60min后,分别记录左侧心脏交感神经节活性,并测定心室有效不应期(ERP)和动作电位时程(APD)。结果实验组在干预后心脏交感神经节的放电频率[(45±6)次/分vs(83±7)次/分,P0.05]和幅度[(0.03±0.01)mV vs(0.05±0.01)mV,P0.05]均显著降低,心室各部位ERP和APD_(90)显著延长,ERP离散度[(13±5)ms vs(21±4)ms,P0.05]和APD_(90)离散度[(22±10)ms vs(38±14)ms,P0.05]显著降低。而对照组以上指标无显著性改变(P0.05)。结论阻断Nav1.8通道可显著降低心脏交感神经节活性,提高心室电生理稳定性。阻断Nav1.8通道可能具有抑制室性心律失常的作用。     

过表达肌浆网钙ATP酶治疗实验性慢性缺血性心力衰竭

目的 研究肌浆网钙ATP酶2a(SERCA2a)基因过表达对慢性缺血性心力衰竭(心衰)心功能及心肌内质网应激(ERS)相关凋亡的影响.方法采用ameroid环束扎小型猪前降支制备慢性缺血性心衰模型.开胸心肌内注射重组腺相关病毒以过表达SERCA2a或对照报告基因绿色荧光蛋白.60 d后检测血流动力学、SERCA2a的表达和活性、心肌凋亡及ERS标志蛋白-分子伴侣GRp78、凋亡蛋白caspase-12的表达.结果基因转导后60 d,与心衰对照及报告基因组相比,转基因组SERCA2a蛋白表达和活性显著增高,心功能参数改善,心肌凋亡指数降低,伴GRP78和活化caspase12表达下降.结论过表达SERCA2a可改善慢性缺血性心衰的心脏功能,其机制可能涉及减轻ERS相关的心肌细胞凋亡.

Abstract：

Objective Chronic myocardial ischemia (CMI) has become the most importat cause of heart failure (HF) all over the world. The aim of the current study was to investigate the effects of Sarcoendoplasmic reticulum calcium ATPaee 2a (SERCA2a) gene transfer on cardiac function and endoplasmic reticulum stress (ERS) associated myocardial apoptosis in a minipig HF animal model induced by CMI. Methods HF was induced in minipigs by implantation of ameroid constrictor in the initial segment of left anterior descending (LAD) branch of coronary artery. After confirmation of myocardial perfusion defects and cardiac function impairment by myocardial perfusion imaging and echocardiography, animals were divided into 4 groups (n =4 each): HF group, HF + enhanced green fluorescent protein (EGFP) group,HF + SERCA2a group, and shamed animals as control group. A total amount of 1×1012 v.g. Of rAAV1EGFP or rAAV1-SERCA2a were injected intramyocardially to each animal of HF + EGFP and HF +SERCA2a groups. Sixty days after gene transfer, protein level and activity of SERCA2a were examined,cardiac functions and changes of serum inflammatory and neuro-hormonal factors were determined. Apoptotic index of the ischemic myocardium, protein levels of ER stress marker glucose regulated protein 78 ( GRP 78) and ER stress specific apoptotic marker caspase-12 were also assayed. Results At the study end,echocardiographic and hemodynamic measurements indicated a significant improvement of both cardiac systolic and diastolic function in HF + SERCA2a group compared with HF/HF + EGFP groups [LVEF (60.2±8.6)%vs (44.2±7.1)% and (46.8±6.7)%, Ev/Ay 1.28±0.24 vs 0.77 ±0.17 and 0.80±0.21, +dp/dtmax(2713.9 ±434.0) mm Hg/s ( 1 mm Hg =0.133 kPa) vs (1892.3 ±434.2) mm Hg/s and (1931.2±397.4)mm Hg/s, -dp/dtmax (1422.1±334.4) mm Hg/s vs (848.3±308.3) mm Hg/s and (849.5±278.3)mm Hg/s, P＜0.05], along with increase in both SERCA2a protein level (1.13±0.26 vs 0.73 ±0.17 and 0.64±0.18, P＜0.05) and activity [(16.2±5.5) IU/ml vs (7.9±3.1) IU/ml and (7.5 ±2.8)IU/ml, P ＜0.05] compared with HF/HF + EGFP groups. Serum concentrations of inflammatory factor tumor necrotic factor α [(382.3±114.4) ng/L vs (732.3±201.4) ng/L and (689.8±192 5) ng/L, P＜0. 05], neural-hormonal factors brain natriuretic peptide [(142.6±45.3) ng/L vs (422.3±113.6) ng/L and(393.7 ±103.3)ng/L, P＜0.01], endothelin-1 [(111.4 ±37.5)ng/L vs (193.5 ±54.3)ng/L and (201.0±72.1)ng/L,P＜0.05] and angiotensin Ⅱ[(189.7±65.2)μg/L vs (538.3 ± 135.2) μg/L and ( 525.5±144.1)μg/L, P＜0.01] were also significantly decreased in HF + SERCA2a group compared with HF/HF + EGFP groups. The apoptotic index [(12.71±4.11)% vs(23.22±7.23) % and (24.31±6.38)%, P＜0.05], protein levels of GRP78 (1.27±0.33 vs 3.23±1.14 and 4.18±1.13, P＜0.05)and protein level ratios of cleaved caspase-12 to total caspase-12[(4.62±1.93)% vs (9.71±2.70)% and (10.14±2.81)%, P＜0.05] were also significantly reduced in the ischemic myocardium of HF+SERCA2a group compared with the HF/HF + EGFP groups. Conclusion Overexpression of SERCA2a significantly improved cardiac systolic and diastolic function in this HF model partly through attenuation of ER stress related myocardial apoptosis, suggesting its therapeutic potential for CM1 related heart failure.     

胺碘酮慢性作用对兔心室肌细胞L型钙通道电流和跨壁动作电位相关性研究

目的 从单个心室肌细胞L型钙通道电流时间常数(τ)和组织块跨壁动作电位复极90%时程(APD90),探讨胺碘酮慢性作用抗心律失常的可能细胞电生理机制.方法 健康兔口服胺碘酮80 mg·kg-1·d-1共4周,记录离体兔带血管心室肌组织块跨膜心室肌细胞动作电位后分离心室肌细胞,记录单细胞L型钙通道电流τ,比较对照组、胺碘酮组及索他洛尔组干预下τ与APD90比值(τ/APD90)变化.结果 对照组τ为(98±8)ms(n=10)、APD90为(220±10)ms(n=5)、τ/APD90为0.44±0.03.与对照组相比,胺碘酮组τ明显延长[为(164±8)ms,n=8,P＜0.05],APD90亦明显延长[为(321±12)ms,n=5,P＜0.05],τ/APD90较对照组增加(分别为0.51±0.03与0.44±0.03,P＜0.05).索他洛尔(3×10-5mmoL/L)组与对照组相比,τ明显延长[为(128±7)ms,n=8,P＜0.05],但因APD90延长较著[为(405±13)ms,n=4,P＜0.01],使τ/APD90较对照组明显减少(分别为0.32±0.05与0.44±0.03,P＜0.05).索他洛尔+胺碘酮组的τ为(150±12)ms、APD90为(355±11)ms(n=4),与索他洛尔组比较,τ/APD90增加(为0.44±0.02,P＜0.05),与对照组相比,差异无统计学意义(P＞0.05).结论 心室肌细胞膜L型钙通道电流的τ/APD90大小与胺碘酮慢性作用相关,这为胺碘酮慢性作用的安全性提供了一种可能解释.     

D-半乳糖诱导心肌细胞非酶糖基化对钙调节蛋白的影响

目的 研究D-半乳糖诱导衰老的心肌细胞中的非酶糖基化反应,及其对心肌细胞内钙调节蛋白水平的影响. 方法 实验用5 g/L D-半乳糖干预培养心肌细胞建立衰老模型.显微镜下观察心肌细胞的形态和搏动情况.以β-半乳糖苷酶染色观察细胞衰老,ELISA法检测心肌细胞晚期糖基化终产物(AGEs)的含量,采用western blot检测肌浆网Ca2+-ATP酶(SERCA,心脏主要是SERCA2a)及受磷蛋白(PLN)的含量. 结果 D-半乳糖诱导的心肌细胞内β-半乳糖苷酶染色阳性率显著高于正常对照组[(75.6±4.9)%和(17.15±2.9)%,P＜0.01)];细胞内AGEs较正常对照组明显增高[(702.58±32.16)pg/ml和(93.22±26.14)pg/ml,P＜0.01];SERCA2a含量明显下降与正常对照组比值为0.39±0.05(P＜0.01);PLN含量明显下降与正常对照组比值为0.27±0.03(P＜0.01);同时伴有心肌细胞形态和搏动的异常. 结论 D-半乳糖可通过心肌细胞的非酶糖基化诱导的心肌细胞老化,同时降低心肌细胞内的SERCA2a、PLN蛋白含量,影响心肌细胞的舒缩活动.     

褪黑素对糖尿病大鼠线粒体保护机制的研究

目的 探讨褪黑素(melatonin,MT)对链脲佐菌素(streptozotocin,STZ)诱导的糖尿病大鼠线粒体功能的影响及其机制.方法 STZ诱导糖尿病大鼠模型,将糖尿病大鼠随机分为糖尿病组和褪黑素干预组(褪黑素组),并以正常组作对照.干预8周后,观察各组大鼠心脏、肝脏及肾脏线粒体膜电位和肿胀度的变化,并通过免疫组化法分析线粒体外膜上的电压依赖性阴离子通道(voltage-dependent anion channel,VDAC)蛋白的表达.结果 (1)与糖尿病组比较,褪黑素组心脏、肝脏、肾脏膜电位均明显升高,分别为[(553.6±193.5)mV对(311.4±133.7)mV,P＜0.05]、[(745.7±115.8)mV对(358.9±158.7)mV,P＜0.05]、[(951.6±246.1)mV对(425.8±177.9)mV,P＜0.05];(2)与糖尿病组比较,褪黑素组心脏、肝脏、肾脏肿胀度趋势明显增强;(3)与糖尿病组比较,褪黑素组心脏、肝脏、肾脏VDAC表达均明显增加,分别为(76.93±8.263对58.59±7.62,P＜0.05)、(50.69±6.33对40.11±6.30,P＜0.05)、(77.86±8.59对61.44±12.86,P＜0.05).结论 褪黑素保护糖尿病大鼠心脏、肝脏及肾脏线粒体功能,初步推测可能与上调线粒体VDAC蛋白的表达有关.     

比索洛尔对心力衰竭大鼠心肌肌浆网钙三磷酸腺苷酶2a活性的影响

目的观察比索洛尔对心力衰竭大鼠心肌肌浆网钙三磷酸腺苷酶2a(SERCA2a)活性的影响。方法采用阿霉素腹腔注射法建立大鼠心力衰竭模型,随机分为假手术组、模型组和比索洛尔组,分别以蒸馏水或比索洛尔连续灌胃35d。心脏超声检测大鼠心功能指标,酶联免疫吸附试验(ELISA)检测血浆脑钠尿肽水平,实时定量聚合酶链反应检测心肌miR-25-3p表达水平,Western blot检测心肌SERCA2a和受磷蛋白表达水平,定磷法测定心肌SERCA2a活性。结果与假手术组比较,模型组大鼠心输出量、左心室短轴缩短率(FS)、左心室射血分数(LVEF)、心肌SERCA2a和受磷蛋白表达水平、SERCA2a与受磷蛋白比值和SERCA2a活性降低[SERCA2a活性(0.029±0.025)比(0.088±0.062)U/mg pro;P0.01],血浆脑钠尿肽和心肌miR-25-3p表达水平升高。与模型组比较,比索洛尔组大鼠心输出量、FS、LVEF、心肌SERCA2a和受磷蛋白表达水平、SERCA2a与受磷蛋白比值和SERCA2a活性升高[SERCA2a活性(0.072±0.063)比(0.029±0.025)U/mg pro;P0.05],血浆脑钠尿肽和心肌miR-25-3p表达水平降低。结论比索洛尔可以改善心力衰竭大鼠心功能,下调心肌miR-25-3p表达水平,提高SERCA2a与受磷蛋白比值,增强SERCA2a活性。     

磁共振成像对猪不同心脏状态下经冠状动脉干细胞移植后体内再分布的评价

目的 探讨磁共振成像在停跳与不停跳两种心脏状态下,对猪心肌梗死模型经冠状动脉注射骨髓间充质干细胞后全身各主要脏器干细胞早期再分布中的应用价值.方法 用带球囊导管经股动脉选择性插管至雌猪左冠状动脉前降支,在第二对角支的近端将球囊扩张90 min建立急性心肌梗死模型.模型建立后7 d,随机分为4组,分别为不停跳心脏细胞移植组(不停跳组,n=6)与对照组(n=6),停跳心脏细胞移植组(停跳组,n=6)与对照组(n=6).超顺磁氧化铁颗粒(SPIO)标记的干细胞移植3 d后,行磁共振T2*WI示踪检查.取动物心、肝、脾、肺、肾脏的标本,用实时定量聚合酶链反应检测雄性细胞特异性的SRY基因,切片进行普鲁士蓝染色,观察细胞在体内的分布和形态.结果 除肾脏外,心、脾、肝中干细胞移植组T2*值较对照组差异均有统计学意义,但移植组在不同心脏状态下不停跳组与停跳组心肌T2*值差异无统计学意义[(-7.81±2.03)ms比(-6.56±1.72)ms,P＞0.05],而不停跳组脾脏及肝脏的T2*值明显低于停跳组[脾脏:(-16.72±2.83)ms比(-22.18±3.98)ms,P＜0.01,肝脏:(-2.40±0.44)ms比(-5.32±3.40)ms,P＜0.05],在肾脏中两组差异无统计学意义.SRY基因在不停跳组及停跳组的脾脏及肝脏的表达差异有统计学意义,病理学检查见移植细胞呈普鲁士蓝染色阳性.结论 干细胞SPIO标记后,磁共振成像可以作为方便而有效的手段在移植早期活体示踪干细胞,评价其在体内的分布情况.经冠状动脉途径注射骨髓间充质干细胞后,许多细胞流向心脏以外的器官,尤其是脾脏.心脏停跳与不停跳状态下经冠状动脉注射骨髓间充质干细胞对干细胞在心脏的滞留无明显差别.     

糖尿病兔心房电机械功能受损与心房颤动的关系

目的 应用组织多普勒超声心动图(DTE)评价四氧嘧啶诱导的糖尿病兔心房电机械功能,同时观察心房病理、电生理改变及心房颤动(房颤)易感性的变化.方法 应用四氧嘧啶诱导成功糖尿病兔共8只,健康对照组8只,饲养8周,应用DTE测定心电图P波开始至心房各节段速度曲线上舒张晚期a'波开始的时间间期(Pastart)及心电图P波开始至DTE速度曲线上舒张晚期a＇波峰值处的时间间期( Papeak);建立Langendorff灌流的离体兔心脏模型,测量心房间传导时间(IACT)、心房各点有效不应期(AERP)、AERP的离散度(AERPD)、应用短阵快速刺激观察房颤诱发情况,应用天狼猩红染色评价左心房纤维化情况.结果 与对照组比较,糖尿病组兔左心房前后径明显增大[(6.8±0.6)mm对(8.3±0.6)mm,P＜0.01],室间隔增厚[(1.9±0.2)mm对(3.0±0.5) mm,P＜0.01];左心房侧壁Pastart及右心房Pastart延长[分别为(40.5±12.9) ms对(60.4±20.4) ms,P＜0.05;(59.8±20.1)ms对(83.0±11.0)ms,P＜0.05)];IACT延长[(37.6±8.9) ms对(27.7±2.1) ms,P＜0.01)],房颤诱发率升高(6/8对1/8,P＜0.05);病理检查提示糖尿病组左心房心肌间质明显纤维化.两组房间隔处Pastart,左心房后壁Pastart及Papeak均与IACT显著相关.结论 糖尿病兔心房电机械功能受损,与心房肌纤维化、心房间电传导延迟有关,可能是糖尿病发生房颤的机制之一.     

Anaerobic myocardial abscess following myocardial infarction

An anaerobic myocardial abscess due to Bacteroides fragilis developed in a 60-year-old man when he had an acute myocardial infarction while recuperating from surgery for a paracolonic abscess. Anaerobic bacteremia is a common event and may lead to infection in areas of low oxygen tension far removed from the original portal of entry.     

曲尼司特对心肌梗死后心肌间质纤维化的影响

目的探讨曲尼司特对兔心肌梗死后心肌间质纤维化干预作用。方法结扎左前降支制作兔心肌梗死模型,分实验组和对照组。3周后经胃管分别给予曲尼司特及安慰剂1月,心脏彩超评价心功能并检测血清转化生长因子（transform ing growth factor,TGF-β1）,I、III型胶原浓度及组织羟脯胺酸含量。结果实验组治疗前后心功能、心腔内径、室壁厚度明显改善,血清TGF-β1,I、III型胶原浓度及羟脯胺酸含量较对照组明显下降。结论曲尼司特可有效拮抗心肌梗死后心肌间质纤维化,预防心室重构。     

Transient myocardial ischaemia after acute myocardial infarction

The prevalence and characteristics of transient myocardial ischaemia were studied in 203 patients with recent acute myocardial infarction by both early (6.4 days) and late (38 days) ambulatory monitoring of the ST segment. Transient ST segment depression was much commoner during late (32% patients) than early (14%) monitoring. Most transient ischaemia (greater than 85% episodes) was silent and 80% of patients had only silent episodes. During late monitoring painful ST depression was accompanied by greater ST depression and tended to occur at a higher heart rate. Late transient ischaemia showed a diurnal distribution, occurred at a higher initial heart rate, and was more often accompanied by a further increase in heart rate than early ischaemia. Thus in the first 2 months after myocardial infarction transient ischaemia became increasingly common and more closely associated with increased myocardial oxygen demand. Because transient ischaemic episodes during early and late ambulatory monitoring have dissimilar characteristics they may also have different pathophysiologies and prognostic implications.     

Assessment of myocardial viability using myocardial contrast echocardiography

Myocardial contrast echocardiography (MCE) is a technique that uses microbubbles as a tracer during simultaneous ultrasound of the heart. The microbubbles can be used to provide quantitative information regarding the adequacy of myocardial blood flow (MBF), as well as the spatial extent of microvascular integrity. In acute myocardial infarction, MCE can identify the presence of collateral flow within the risk area, and can therefore predict preservation of myocardial viability and ultimate infarct size even prior to reperfusion. After reperfusion, the extent of microvascular no-reflow can be determined, and has significant implications for recovery of left ventricular function. In chronic ischemic heart disease, MCE has also been shown to successfully differentiate viable from necrotic myocardium. This technique can accurately predict recovery of function after revascularization. More importantly, MCE can be used to identify viable segments that may help to prevent infarct expansion and remodeling, and thus improve patient outcomes.     

Assessment of myocardial viability with myocardial contrast echocardiography

The application of noninvasive imaging techniques to assess myocardial viability has become an important part of routine management of patients with acute myocardial infarction and chronic coronary artery disease. Information regarding the presence and extent of viability may help identify patients likely to benefit from revascularization or therapy directed at attenuating left ventricular remodeling. Myocardial contrast echocardiography (MCE) is capable of defining the presence and extent of viability by providing an accurate assessment of microvascular integrity needed to maintain myocellular viability. It is especially suited for the spatial assessment of perfusion, even when myocardial blood flow is reduced substantially in the presence of severe epicardial stenoses or in a bed dependent on collateral perfusion. The routine use of MCE to evaluate viability in patients with acute and chronic coronary artery disease is now feasible with the advent of new imaging technologies and microbubble agents capable of myocardial opacification from venous injections. The utility of this technique for determining treatment strategies has not been established but is forthcoming.     

Emergency myocardial revascularization in acute evolving myocardial infarct

Immediate coronary artery bypass for acute evolving myocardial infarction could be the elective therapy if provided on useful time, because myocardial salvage can be achieved by early reperfusion. Thirty eight patients had emergency coronary artery by-pass graft for acute evolving myocardial infarction during the early phase: 35 were male, the mean age was 51 years (34 to 74). The mean interval between the onset of symptoms and surgery in this series of patients was two hours and a half. This interval seems to be also the time limit in our experience to get a partial or complete recovery of ischemic area. Four patients died in hospital, but they were in severe cardiogenic shock before emergency surgery. Twenty nine cases were free of symptoms at a mean follow-up of 18 months (6 to 36) and two suffered for residual angina. Three patients died after discharge few months later: two during redo emergency vein grafts operations, one in deep left ventricular failure, while he was waiting for heart transplant. All these patients operated on as emergency developed acute myocardial infarction during their stay in hospital waiting for catheter study, surgical operation or during percutaneous transluminal coronary angioplasty. Saphenous vein grafts, were used in twenty nine patients, left internal mammary artery in nine cases, single in four and associated to saphenous vein in five, with an average number of anastomoses of 2.6 (1 to 6) for patient. ECG was found to be normal in 76% of the patients operated on within two hours and a half from the beginning of symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)     

Silent myocardial ischemia after acute myocardial infarction.

Silent ischemia after myocardial infarction has definite prognostic significance but should be interpreted within the context of other prognostic indicators. The rationale for therapeutic intervention is based on the prognostic implications of silent ischemia and the potentially deleterious effect of repeated episodes of ischemia on the integrity of the left ventricle. We measured parameters of ischemia in 20 patients who showed asymptomatic ischemic ST-T changes on exercise testing in the early phase after myocardial infarction. After diltiazem administration, a reduction of exercise-induced ST-T depression from 2.3 +/- 0.8 to 0.7 +/- 0.6 mm (p less than 0.01) occurred, and regional wall-motion score at exercise, determined by radionuclide angiography, improved significantly (p less than 0.02). These and other observations warrant further studies in which the duration, severity and frequency of the ischemic episodes should be quantified and correlated with prognosis after myocardial infarction.