橙皮苷对糖尿病大鼠心泵功能和心率变异性的影响

目的:研究橙皮苷对链佐星(STZ)诱发的糖尿病大鼠心泵功能和心率变异性(HRV)的影响并初步探讨其作用机制。方法:30只大鼠随机分为对照组(n=6)、糖尿病组(n=12)和橙皮苷治疗组(n=12)。运用Langerdorff灌流糖尿病鼠离体心脏HRV功率谱分析等方法,观察橙皮苷对糖尿病大鼠的心脏收缩力、冠状动脉(冠脉)流量、心电图QRS波及HRV的影响。结果:橙皮苷10×10-6 mol/L可增加离体大鼠心脏冠脉流量106.0%,并使心肌收缩力增加87.3%,QRS波宽缩短33.3%。糖尿病鼠的心率加快,窦性RR间期的标准差(SDNN)减小,交感神经、迷走神经紧张性低频/高频比(LF/HF)增大,而橙皮苷处理后,心率、SDNN和LF/HF值均有所恢复。结论:橙皮苷可改善STZ诱发糖尿病大鼠的冠脉循环和心泵功能,并逆转由糖尿病引起的HRV变化。     

左西孟旦对心力衰竭大鼠离体心脏的保护作用及机制研究

目的观察左西孟旦对心力衰竭大鼠离体心脏功能的影响,并探讨其作用机制。方法采用腹主动脉缩窄法制作大鼠心衰模型,使用Langendorff离体心脏灌流实验方法,观察左西孟旦对心力衰竭大鼠离体心脏功能的影响,运用不同阻断剂干预后,观察左西孟旦作用的变化。结果左西孟旦可增强心力衰竭大鼠离体心脏功能,其心率减慢,LVSP-LVDP升高,+dP/Dt_(max)升高,-dP/Dt_(max)降低,L-NAME、Gli预处理后,左西孟旦对心力衰竭心脏功能的作用减弱。结论左西孟旦可以明显改善心力衰竭大鼠离体心脏功能,其作用可能与NO的合成、KATP通道开放有关。     

丙泊酚对心肌肥厚大鼠离体心脏功能的保护作用

目的观察丙泊酚(propofol)对心肌肥厚大鼠离体心脏功能的影响,并探讨其作用机制。方法采用Langendorff心脏灌流实验方法,观察Propofol对心肌肥厚大鼠离体心脏功能的影响。观察不同阻断剂对Propofol作用的影响。结果 Propofol可增强心肌肥厚大鼠离体心脏心功能,心率减慢,主动脉收缩压(LVSP-LVDP)升高,左室压最大上升速率(+dp/dt_(max))升高,左室压最大下降速率(-dp/dt_(max))降低,吲哚美辛预处理后,Propofol对心脏功能的影响减弱。结论 Propofol可以明显改善心肌肥厚大鼠离体心脏功能,其作用可能与前列环素(PGI_2)的合成有关。     

羟基红花黄色素通过RhoA/ROCK通路保护大鼠心肌再灌注损伤的机制研究

目的:研究羟基红花黄色素A对大鼠离体缺血心脏再灌注的保护作用,探讨其与Rho/ROCK信号通路的作用。方法:36只大鼠被随机分为7组,采用离体心脏灌流模型,给予缺血预处理及药物灌流,比较各组心率、冠状动脉流量,测定左心室内压,TTC心肌染色评估梗死范围,Western blot检测心肌组织内ROCK1、ROCK2活性以及Caspase-3的表达。结果:治疗组大鼠心脏缺血再灌注损伤减轻,心肌梗死面积减少,ROCK1、ROCK2活性以及Caspase-3的表达减低。结论:羟基红花黄色素A能够减轻大鼠心脏缺血再灌注损伤,同时减少心肌梗死面积,其作用机制可能与其抑制RhoA/ROCK信号通路,减少Caspase-3的表达有关。     

扎考必利对大鼠离体心脏心功能及心律的影响

目的 观察扎考比利对大鼠离体心脏心功能和心律的影响.方法应用Langendorff离体心脏灌流装置,以不同浓度(1 μmol/L、3 μmol/L、10 μmol/L、30 μmol/L)灌流大鼠心脏,观察药物对离体心脏心功能指标及Ⅱ导心电图的变化.结果 扎考比利对大鼠离体心脏心功能及心律无明显影响.结论与西沙必利相比,扎考比利对心脏收缩功能及舒张功能均无明显作用,是一种相对安全的药物.     

ATP敏感性钾通道开放剂克罗卡林、JTV和KRN对大鼠冠状动脉流量及心功能的影响

目的本研究拟对ATP敏感性钾通道、(KATP通道)开放剂克罗卡林、JTV506、KRN2391用Langendorff及双冠状动脉分别灌流大鼠离体心肌缺血模型,系统地研究KATP通道开放剂对冠状动脉扩张及心功能的影响.方法用Langendorff大鼠心肌缺血模型,将健康雄性Wistar大鼠用戊巴比妥钠进行腹腔麻醉后,经主动脉逆行插管悬挂于Langendorff装置上,剪去左心耳,将充水导管球囊插入左心室,记录心电、灌流压、左心室压力及灌流量.结果KATP通道开放剂克罗卡林、JTV和KRN对大鼠冠状动脉流量的影响,观察期间对照组及溶剂组灌流量均无明显改变,而克罗卡林、JTV和KRN在达1μM浓度后明显增加灌流量,说明其有明显的扩冠作用.KATP通道开放剂克罗卡林、JTV和KRN对大鼠心功能的影响实验中各组左室舒张末压均未见改变(1.1kPa),对照组及溶济组左室收缩压亦无明显变化,而当克罗卡林和JTV浓度达10μM时,KRN达20μM浓度时可明显降低收缩压.结论KATP通道开放剂克罗卡林、JTV和KRN可明显增加冠状动脉流量,较高浓度时可明显降低左室收缩压.     

线粒体膜钾通道阻断剂在硫化氢对大鼠心功能调节的意义

目的 观察线粒体膜KATP通道特异性阻断剂5-羟基葵酸盐(5-hydroxydecanoate,5-HD)对硫化氢(H2S)灌流的大鼠离体心脏心功能的影响,以探讨线粒体膜KATP通道阻断剂在H2S调节心功能过程中的意义.方法 应用Langendorff灌流大鼠离体心脏,用生理浓度NaHS(100 μmol/L)持续灌流20 min,测最心率、左室内压差(△LVP=左室收缩压-左室舒张压)、左室内压变化速率(±dp、dtmax)、冠状动脉流量等指标,分别应用非特异性KATP通道阻断剂格列苯脲、线粒体膜KATP通道阻断剂5-HD预灌流,后给予生理剂量NaHS灌流,观察其是否可以阻断H2S的心功能效应.结果 生理剂量NaHS持续灌流20 min内,可以显著抑制±dp/dtmax及ALVP(P<0.05),而对心率、冠状动脉流量几乎没有影响.非特异性KATP通道阻断剂格列苯脲及线粒体膜KATP通道阻断剂5-HD均可以大部分阻断生理剂量NaHS对心功能的抑制效应.结论 内源性H2S可以通过开放线粒体膜KATP通道,产生对心肌的负性肌力调节作用.     

缺血后适应对糖尿病大鼠再灌注心肌的保护作用及其与P-Akt的关系

目的:探讨缺血后适应对糖尿病大鼠离体心脏缺血再灌注损伤的影响及其信号机制。方法:2W龄健康SD大鼠60只,雌雄不拘,体质量250～300g,随机分为6组:1.空白对照组(N组);2.缺血再灌注组(IR组);3.缺血后适应组(Post组);4.糖尿病大鼠后适应组(Dpost组);5.糖尿病大鼠缺血再灌注组(DIR组);6.糖尿病大鼠空白组(DN组)。观测心脏冠状动脉灌流量、心肌梗死范围、免疫印迹(western blot)对P-Akt的测定、电镜下观察心肌和线粒体的改变。结果:缺血后适应组(Post组DPost组)较缺血再灌注组(IR组DIR组)冠状动脉流量明显增加,心肌梗死范围明显减少,P-Akt的表达明显增强,心肌纤维和线粒体的完整程度明显较好。结论:缺血后处理在糖尿病大鼠离体心脏具有显著的保护作用,这一作用可能与Akt激活有关。     

天麻素在铁诱导的大鼠离体心肌损伤中的保护作用

目的观察天麻素在铁诱导的大鼠离体心肌损伤中的保护作用。方法应用Langendorff离体心脏灌流系统,灌注Fe-HQ建立铁诱导的离体心肌损伤模型。SD大鼠随机分成4组:正常组、Fe-HQ组、天麻素(0.1、0.025 mmol/L)组。观察天麻素对心率(HR)、左室收缩压(LVSP)、dp/dt max、冠脉流量(CF)的影响;测定冠脉流出液中的乳酸脱氢酶(LDH)及肌酸激酶(CK)的含量和心肌中丙二醛(MDA)的浓度;观察心肌组织的超微结构。结果天麻素能抑制铁诱导的心肌的HR、LVSP、dp/dt max、CF的下降;降低冠脉流出液中LDH和CK的含量及心肌中MDA的浓度。结论天麻素可改善铁诱导的心肌收缩功能和脂质过氧化,对铁诱导的大鼠离体心肌损伤有显著的保护作用。     

冠心灵对冠脉血流量、心肌收缩力和心电活动的影响

目的 :研究中药复方制剂冠心灵的心血管作用并初步探讨其作用机制。方法 :运用细胞内微电极技术、L angendorff离体心脏灌流和心率变异性功率谱分析等方法 ,研究冠心灵对心肌细胞动作电位的影响 ;观察其对冠脉血流量和心肌收缩力的作用 ;分析冠心灵对冠心病患者心率变异性的影响。结果 :冠心灵增强 Ca2 +跨膜内流 ;增加冠脉血流量和心肌收缩力 ;改善因缺血导致冠脉流量和心肌收缩力的下降 ;功率谱分析显示心迷走交感对心率的调控作用比升高。结论 :冠心灵有改善心肌缺血的作用。     

Different effects of a high-cholesterol diet on ischemic cardiac dysfunction and remodeling induced by coronary stenosis and coronary occlusion

OBJECTIVES: The aim of the study was to assess whether and how the high-cholesterol diet (HCD)-related worsening of heart failure differs between coronary stenosis (CS)-induced myocardial ischemia and coronary occlusion-induced myocardial infarction (MI). BACKGROUND: An HCD, a risk factor for coronary artery disease, also worsens ischemic heart failure. Although accelerated coronary plaque formation may be a cause of this, other mechanism(s), such as its effects through the coronary microcirculation, remain to be clarified. METHODS: In rats fed a normal chow diet or HCD, CS or MI was created surgically, and we assessed left ventricular (LV) function by echocardiography and myocardial inflammation by histopathology. In the CS groups, CS severity by histopathology, myocardial perfusion by microspheres, myocardial protein kinase C (PKC) translocation by Western blotting, and myocardial endothelial nitric oxide (NO) function were also investigated by the in vitro myocardial oxygen consumption method. RESULTS: Coronary stenosis impaired myocardial endothelial NO function and reduced coronary flow reserve, evoking myocardial ischemia, as shown by PKC- activation, myocardial inflammation, fibrosis, cardiac dysfunction, and remodeling. By itself, HCD greatly augmented such CS-induced myocardial abnormalities without modulating the CS severity. Such detrimental effects of HCD were ameliorated by supplying a cofactor of endothelial NO synthase-tetrahydrobiopterin. In contrast, MI-induced heart failure was not aggravated by HCD. CONCLUSIONS: The CS-induced ischemic myocardium seems to be more susceptible to the pro-inflammatory effect of HCD than infarcted myocardium, leading to aggravation of LV dysfunction and remodeling via modification of the coronary circulation downstream of the epicardial CS site, partly through impairment of endothelial NO.     

急性ST段抬高型心肌梗死直接PCI术后ST段回落的临床研究

目的：通过观察急性ST段抬高型心肌梗塞（STEMI）直接经皮冠状动脉介入治疗（PCI）术后,梗塞相关动脉（IRA）达心肌梗塞溶栓（TIMI）血流3级患者心电图ST段回落程度,探讨ST段回落与心肌损伤及心脏收缩功能的关系。方法：选择在发病12h内接受直接PCI治疗后TIMI血流达到3级的STEMI患者115例,PCI术前、术后行心电图检查,观察ST段回落情况,术前、后测定患者肌酸激酶（CK）、肌酸激酶同工酶（CK-MB）及肌钙蛋白T（cTnT）,术后测定左室射血分数（LVEF）;按照ST段回落幅度（∑STR）不同,患者被分为两组：A组：∑STR〈50%,21例,为心肌灌注不良组,B组：∑STD≥50%,94例,为心肌灌注良好组;分析两组患者ST段回落程度与CK、CK-MB、cTnT及LVEF的关系。结果：（1）两组患者IRA部位、病变血管支数,PCI治疗前TIMI血流分级、cTnT水平,发病到PCI时间等差异均无显著性（P〉0.05）;（2）两组患者术前、后CK、CK-MB水平差异无显著性（P〉0.05）;（3）术后A组cTnT水平明显高于B组[（1.30±0.43）μg/L∶（1.0±0.45）μg/L,P〈0.05];（4）术后A组LVEF明显低于B组[（44.13±4.83）%∶（47.93±5.23）%,P〈0.05]。结论：急性ST段抬高型心肌梗塞直接PCI术后,TIMI血流达到3级,ST段回落良好的患者,心肌组织水平灌注程度较好,心肌损伤程度轻,左心收缩功能较好。     

Improvement by propranolol of regional myocardial dysfunction and abnormal coronary flow pattern in conscious dogs with coronary narrowing

The effects of propranolol on regional myocardial function and the pattern of coronary blood flow velocity were studied during partial coronary arterial constriction in conscious resting dogs. Miniature ultrasonic crystals were implanted subendocardially in the left ventricle for measurement of segment length in control and ischemic areas. Coronary blood flow was limited by inflation of an hydraulic-cuff around the left circumflex coronary artery to produce stable hypofunction in the ischemic segment. With coronary stenosis, which reduced mean flow by an average of 31 percent of the control value, the heart rate increased by 17 beats from 78 ± 4 beats/min (mean ± standard error of the mean) and the flow pattern changed from a dominant diastotic to a dominant systolic pattern (peak velocity ratio of systole to diastole, 0.35 ± 0.06 to 1.06 ± 0.09) without change in left ventricular systolic pressure. After administration of propranolol (0.5 mg/kg Intravenously), heart rate decreased to 72 ± 4 from 95 ± 4 beats/min and contraction in the Ischemic segment increased markedly, as did left ventricular wall thickening. Simultaneously, coronary flow returned to a normal velocity pattern. These favorable effects were only partially diminished by cardiac pacing to increase the heart rate to that before treatment with propranolol. This study provides evidence for a substantial beneficial effect of propranolol when myocardial dysfunction results from transient coronary arterial stenosis, and it suggests several mechanisms that may be operative under these conditions.     

Blood flow velocity in the carotid artery as a measure of myocardial contractility.

An attempt was made to derive a useful noninvasive index to evalute a change in myocardial contractile state using transcutaneous Doppler flow-velocity curve from the carotid artery. In 5 mongrel dogs and in 43 patients with various heart disease, Doppler flow velocity curves were obtained from the ascending aorta intravascularly using a Doppler catheter and/or from carotid artery transcutaneously using a Doppler probe. The first derivative of left ventricular pressure (dp/dt) and electrocardiogram (ECG) were recorded simultaneously. The following 3 indices were measured from the Doppler flow-velocity curves: (1) macimum acceleration of blood flow (dv/dt), (2) time from onset of ejection to peak flow (time-to-peak), (3) time interval between the beginning of Q wave of ECG to the peak of Doppler flow velocity curve (ECG Q-Doppler peak).Among these 3 indices, only ECG Q-Doppler peak demonstrated a significant correlation between the values measured intravascularly and transcutaneously. Also, only ECG Q-Doppler peak showed significant correlation with maximum of dp/dt (max dp/dt). Since ECG Q-Doppler peak showed correlation with heart rate, the difference between observed and predicted ECG Q-Doppler peak (delta ECG Q-Doppler peak) was calculated to exclude the effect of heart rate. Predicted value of ECG Q-Doppler peak was calculated from the regression equation between heart rate and ECG Q-Doppler peak in the separate experiments. There was significant correlation between delta ECG Q-Doppler peak and max dp/dt. In 15 patients with coronary artery disease and in 16 healthy subjects, delta ECG Q-Doppler peak and the other noninvasive method (systolic time intervals) were measured. Delta ECG Q-Doppler peak showed better result in the separation of 2 groups than by systolic timeintervals. It was concluded that delta ECG Q-Doppler peak is a useful index to evaluate the myocardial contractile state since this index is readily obtained noninvasively.     

Antiphospholipid syndrome and antiphospholipid antibodies as a risk factors of ischaemic heart disease and myocardial infarction in patients with systemic lupus erythematosus

Ischemic heart disease and myocardial infarction in patients with SLE--are usually secondary to early coronary atherosclerosis. Estimation if antiphospholipid syndrome and antiphospholipid antibodies are the risk factor for myocardial infarction and ischemic heart disease in patients with TRU. We examined 129 patients with SLE (114 women and 15 men). All the patients underwent comprehensive physical examination. ECG, ultrasound heart examinations were performed. They were followed by heart scintygraphic examination if indicated. Routine biochemical and hematological laboratory tests were performed including fasting glucose level, concentration of homocysteine, uric acid and lipids. Wide range of immunological essays were performed, testing for antinuclear antibodies (ANA), extractable nuclear antigen antibodies (ENA), antiphospholipid antibodies (anticardiolipin antibodies--aCL, lupus anticoagulant--LA, antiprothrombine antibodies aPT, anti-beta2glicoprotein-I antibodies), anti-dsDNA antibodies, anti-nucleosome antibodies, antihistone antibodies, antineutrophil cytoplasmic antibodies (ANCA) and antiendothelial antibodies (AECA). Statistical analysis was performed with chi2 Yates, chi2 Pearson and R rang Spearman tests. Multivariate regression analysis was also done. Ischemic heart disease was found in 20 (15.5%) SLE patients, myocardial infarctions were diagnosed in 9 (6.97%). Ischemic heart disease and myocardial infarction were significantly related to presence of secondary antiphospholipid syndrome (SAPS), OR: 4.21, p = 0.008 and OR: 12.8; p = 0.02 respectively). They were also related to high activity of SLE, OR: 7.18; p = 0.012 and OR: 27.3; p = 0.006 respectively. Ischemic heart disease was significantly more common in older patients (52.75 years versus 42.15 years; p = 0.0008) and in patients with hypertension (p < 0.05). Impaired glucose tolerance (OR: 8.44; p = 0.03), presence of aCL IgG (OR; 2.93; p = 0.05) and p-ANCA anti-MPO (OR: 6.08; p = 0.036) were found to be risk factors of ischemic heart disease. Myocardial infarction was significantly associated with high uric acid level (OR: 5.01; p = 0.052) and impaired glucose tolerance (OR: 7.42; p = 0.047) and with presence of the following antibodies: aCL IgG and/or aCL IgM (OR: 5.61; p = 0.039), ANCA in the indirect immunofluorescence essay (OR: 5.78; p = 0.035), anti-MPO antibodies (OR: 6.58; p = 0.051) and AECA (OR: 11.10; p = 0.026). Presence of antiphospholipid antibodies and SAPS are significant risk factors of ischemic heart disease and myocardial infarction in SLE patients. The risk factors of ischemic heart disease and myocardial infarction in SLE patients significantly differ from the ones in general population.     

12导联同步动态心电图在冠心病心肌缺血诊断中的应用

目的探讨12导联同步动态心电图（DCG）在冠心病心肌缺血诊断中的价值,进一步推广在基层医院中的应用。方法选取本院就诊中疑诊为冠心病的250例作为研究对象,同时行12导联和3导联同步DCG24h监测,收集相关信息,进行统计学分析。结果 12导联同步DCG对心肌缺血诊断的阳性率明显高于3导联者,两者之间有显著差异（P〈0.05）;12导联同步DCG对下壁、侧壁心肌缺血的诊断优于3导联同步记录。结论 12导联描记在冠心病心肌缺血诊断上明显优于3导联记录,可以减少冠心病的漏诊率。     

Comparison of Holter electrocardiography and thallium 201 scintigraphy in the detection of myocardial ischemia

OBJECTIVE OF THE STUDY: To compare ischemic changes (I) detected by Holter ECG (H ECG) to the myocardial perfusion defects found in 201 TI myocardial perfusion scintigraphy. DESIGN: 201 TI exercise test was made during the performance of a 24 hours H ECG. The validation of ST segment changes detected by H ECG during the exercise test was made on basis of reversible myocardial perfusion defects (RPD) detected on 201 TL and a relation between ST segment changes detected during the remaining 24 hours recording period and 201 TI (TI) RPD was established. SETTING: The patients (pt) included in the study have come from Cardiology and Heart Surgery Clinics of a Central teaching hospital. MATERIAL AND METHODS: 20 pt with a high coronary artery disease prevalence have been submitted to a two lead (V5 and aVF) 24 hour H ECG during which they have performed a symptom limited bicycle exercise test followed by an injection of 201 TI with acquisition 5 minutes later. Ischemic episodes detected on H ECG were quantified and their relation with heart rate and symptoms was established. As far as 201 TI studies are concerned the fixed and reversible perfusion defects as well as their location were evaluated. RESULTS: 1. H ECG: 6 pt (30%) presented ST changes on H ECG during the exercise test and a total of 9 pt (45%) had ST changes during exercise and during the remaining period of H ECG. 2. TI: 19 pt presented perfusion defects images (fixed in 7, reversible in 14, both kinds of defects in 7). 3. H ECG validation: H ECG during exercise presented I in 6 out of 14 pt with RPD on TI (sensitivity = 43%). Six of these 8 pt, with negative H and positive TI, had a chronic myocardial infarction. All the 6 pt with negative TI had negative H ECG (specificity = 100%). 4. H ECG TI comparison: 7 (50%) of the 14 pt with RPD had ST changes on 24 hrs H ECG. Seven of 11 pt with negative H ECG had RPD in TI. Two pt with negative TI had positive H ECG. These 2 pt had during H ECG a higher heart rate (HR) than the HR recorded during the exercise test. CONCLUSIONS: 1. In pt with known CAD, TI has a high sensitivity and specificity to show perfusion defects. 2. Considering TI as gold standard, H ECG showed to be a useful method to detect I in the studied population (sens. = 43%; spec. = 100%). 3. H ECG revealed to be an important diagnostic tool in detecting additional I episodes beyond the ones recorded during TI exercise test.     

犬冠状动脉脂肪栓塞引起慢/无血流模型的建立

目的:建立犬冠状动脉脂肪栓塞动物模型,为介入性无复流发生过程中脂肪栓塞的作用提供理论依据。方法:杂种犬20只,施行左室造影及冠状动脉造影,记录血流动力学参数,脂肪栓子注入后,造成犬优势动脉无复流,观察造影结果。同步监测体表心电图,并监测其后组织学及超微结构的改变。结果:建模中共有17只犬成活,其中15只犬达到冠状动脉造影无复流动物模型的标准,即(TIMI)血流≤Ⅱ级,校正的TIMI血流记帧法(CTFC)≥36.2帧,建模成功率75%。慢/无血流模型建立成功后,心率增快,血压下降,左室收缩末压显著降低(P0.05)。实验过程中,体表心电图出现急性心肌损伤及再灌注的心电图衍变规律。结论:选择性冠状动脉内注入脂肪栓子建立的慢/无血流犬模型是成功的。     

冠状动脉慢血流患者的腺苷负荷心肌灌注显像研究

目的:评价腺苷负荷心肌灌注单光子发射计算机断层扫描(SPECT)在诊断冠状动脉慢血流(CSF)中的临床价值。方法:根据冠状动脉造影(CAG)结果不同,分为CSF组、正常血流(NCF)组和CAG阳性组。使用校正的TIMI血流分级方法评价冠状动脉血流速度。3组均行CAG、静息心电图(ECG)、腺苷负荷ECG、静息及腺苷负荷SPECT检查,评价其心肌血流灌注情况。结果:CSF组腺苷负荷SPECT诊断心肌缺血阳性率(84%),明显高于平静ECG(20%)及腺苷负荷ECG(52%)。CSF组在腺苷负荷SPECT中显示心肌缺血的范围和程度高于NCF组,低于CAG阳性组。结论:CSF与心肌缺血关系密切,腺苷负荷SPECT可以作为检测CSF者心肌缺血的一种有效的无创性检查方法。     

Transient ischemia in angina pectoris: frequent silent events with everyday activities

To help characterize episodes of transient myocardial ischemia, 80 patients with chronic stable angina and evidence of obstructive coronary disease were studied by ambulatory electrocardiographic (ECG) monitoring outside the hospital to detect both symptomatic and asymptomatic episodes of ST-segment depression. In addition, patients were tested on an outpatient basis by means of positron emission tomography to assess regional coronary blood flow under different conditions. All patients showed ECG evidence of transient ischemia, with or without symptoms, while active outside the hospital. In-hospital testing showed that symptomatic and asymptomatic disturbances in regional coronary blood flow occurred with normal everyday activities and were not caused by physical exertion involving marked increases in heart rate and blood pressure. Most of these provocations were followed by a decrease in coronary blood flow in a poststenotic segment of myocardium and, like the ischemic events monitored out of hospital, the majority were silent. Many of these features characterizing the activity of ischemic heart disease may not be apparent from a patient's anginal history or results of hospital diagnostic testing.