Diagnostic and prognostic aspects of angina pectoris preceding myocardial infarction in long-term follow-up

AIM: To trace relations of premyocardial infarction (preMI) angina, myocardial reserves and clinical peculiarities within a year of outpatient follow-up. MATERIAL AND METHODS: Coronary and myocardial reserves were studied in 320 MI survivors using veloergometry, transesophageal pacing (TEP), 24-h ECG monitoring, echocardiography. Cardiac output reaction to TEP was assessed. RESULTS: Patients with preMI attacks of stable angina had coronary reserve 47.9% less than they had before MI while cardiac failure by NYHA criteria aggravated by 33.3%. Myocardial ischemia at bicycle exercise in these patients developed much later and its threshold rose by 34.2%. The degree of cardiac ejection fall in TEP in patients without angina before MI was 2.4 times greater than in patients without history of IHD. There were specific features of diastolic relaxation of the myocardium and variability of cardiac rhythm in the compared groups though the groups did not differ significantly by arrhythmia events and morphological characteristics of the scar zone. Survival showed a tendency to lowering of lethal outcome risk in the compared groups followed up since the observation month 6 without significant differences depending on the presence of preMI angina. CONCLUSION: PreMI angina contributes to formation of coronary and myocardial reserves which are better to assess at TEP and with analysis of hemodynamic reaction to induced rise in heart rate.     

The effect of intracoronary diltiazem on regional myocardial function and development of infarcts in porcine hearts

The effect of intracoronary (i.c.) pretreatment with diltiazem on regional myocardial function and the development of infarcts was investigated in regionally ischemic, reperfused porcine hearts. The left anterior descending coronary artery (LAD) was distally ligated in 16 pigs for 20-90 min followed by 24 h of reperfusion. Eight pigs were treated with increasing doses of i.c. diltiazem (0.375 mg/min, 0.75 mg/min, 1 mg/min) prior to ischemia. Eight pigs served as controls. Regional myocardial function was assessed by implanted ultrasonic crystals. Infarct size was determined as ratio of infarcted (tetrazolium stain) to ischemic myocardium (dye technique). I.c. diltiazem mainly depressed early systolic shortening (isovolumetric contraction) and lengthening during the first half of diastole. Pretreatment with this calcium antagonist significantly delayed the development of infarcts. In control experiments, a mean infarct size of 74% was found after 45-min ischemia. At that time no infarction was observed in the treated group, where infarcts started to evolve after 60-min ischemia. It is concluded that the favorable action of i.c. diltiazem can mainly be ascribed to a reduced myocardial oxygen consumption at the onset of ischemia.     

Quantification of the spectrum of changes in regional myocardial function during acute ischemia in closed chest pigs: an ultrasonic strain rate and strain study.

The objectives of this study were to define the spectrum of regional myocardial function changes during acute ischemia in closed chest animals by using newly developed ultrasonic strain rate and strain indexes derived from regional color Doppler myocardial imaging (CDMI) velocity data. Myocardial ischemia was induced in 18 pigs either with acute total 20-second occlusions (group 1, n = 12) or graded hypoperfusion (40 to 0 mL/min, group 2, n = 6) of the circumflex coronary artery. In addition, a dobutamine challenge (5 to 10 microg/kg per minute) was performed during sustained subtotal ischemia (10 mL/min) in group 2. CDMI acquisitions with parasternal views monitored the myocardial posterior wall function. Regional radial strain rate and strain (epsilon(r)) were measured for systole, isovolumic relaxation, early diastole, and atrial filling, respectively. During total and graded ischemia, epsilon(r) profiles were consistently modified, showing a delayed onset and a decrease in regional systolic thickening as well as increased postsystolic thickening. Radial strain rate and epsilon(r) indexes decreased consistently during systole and early diastole and increased during isovolumic relaxation. End-systolic epsilon(r) could differentiate total ischemia from severe hypoperfusion (10 mL/min), decreasing from 32% +/- 8% to 16% +/- 5% (versus 60% +/- 10% at baseline). During dobutamine infusion (10 microg/kg per minute), end-systolic epsilon(r) tended to decrease from 27% +/- 5% to 18% +/- 11%, whereas postsystolic thickening increased by 2-fold (P <.05). The combined analysis of regional deformation characteristics and global cardiac event timing derived from CDMI data can identify and quantify regional function changes induced by experimental acute ischemia in closed chest pigs. This would appear to be a potentially promising new noninvasive approach to the clinical evaluation of ischemia-induced changes in segmental myocardial function.     

兔可控性心肌缺血模型的建立

目的：建立兔可控性心肌缺血模型。方法：新西兰兔32只，开胸后将气囊梗阻器固定在冠状动脉左室支上，制作兔可控性心肌缺血模型；四肢安装肢体导联。术后7-10天监测兔心肌缺血前后心电图改变。结果：造模成功24只．气囊充气后1．5—2min观察到Ⅱ导联ST段抬高。结论：采用气囊梗阻器可以成功的制作兔可控性心肌缺血模型。     

CK技术判断顿抑心肌程度的实验研究

目的：本研究旨在评价彩色室壁动力分析（ＣｏｌｏｒＫｉｎｅｓｉｓ，简称ＣＫ）技术判断顿抑心肌程度的价值。建立８条犬心肌顿抑模型，根据冠状动脉结扎时间的不同将其分为两组。超声检查结果与核素心肌灌注显像和病理检查比较。发现（１）比较心肌顿抑节段３０和６０分钟时收缩期和舒张期心内膜ＣＫ彩色宽度，并分别与非缺血心肌节段心内膜ＣＫ宽度比较，差别均有显著性意义（ｐ均＜００１）。（２）比较冠状动脉结扎３０和６０分钟ＳＰＥＣＴ收缩和舒张期缺血心肌区内放射性计数与峰计数的比值，并分别与３０和６０分钟心肌顿抑节段收缩期和舒张期心内膜ＣＫ色带宽度进行比较，发现其高度相关（ｐ均＝０００１）。本研究表明ＣＫ的色带宽度可以反映短暂心肌缺血再灌注后心肌顿抑的程度，心肌缺血的时间越长心肌顿抑的程度越重，可能为预测心肌顿抑的持续时间提供依据     

Brain natriuretic peptide limits myocardial infarct size dependent of nitric oxide synthase in rats

BACKGROUND: Brain natriuretic peptide (BNP) has recently been shown to have a cardioprotective effect in animal models of myocardial ischemia-reperfusion (I-R) injury. We hypothesized that exogenous BNP limits myocardial infarction on nitric oxide synthase pathway. METHODS: A rat model of myocardial I-R injury was established by ligating the left descending coronary artery for 30 min and then reperfusing for 2 h. BNP was injected with different dose 5 min after the ligation and lasting for 145 min. The myocardial infarct size and the area at risk of ischemia were measured by staining with triphenyltetrazolium chloride (TTC) and Evans blue dye. To examine the role of nitric oxide synthase (NOS), expression of eNOS in the left ventricle was analyzed by western blotting. Nomega-nitro-L-arginine methyl ester (L-NAME; 30 ug/kg), or S-methylisothiourea (SMT; 3 ug/kg) was administrated before I-R with or without BNP. RESULTS: The control infarct-to-risk ratio was 45.1+/-1.72% (means+/-SE). BNP infused 5 min after ischemia limited infarct size in a dosage-dependent manner, with maximal protection observed at 0.01 ug/(kg min) (infarct-to-risk: 24.7+/-1.69%, P<0.01 vs. control), associated with a 10-fold increase of myocardial endothelial nitric oxide synthase above the control value. Protection afforded by BNP was abolished by L-NAME but not by SMT, suggesting the involvement of putative endothelial but not inducible nitric oxide synthase activation. CONCLUSIONS: We conclude that natriuretic peptide/NOS/NO signaling may constitute an important injury-limiting mechanism in myocardium.     

斑点追踪成像评价冠心病患者左心室舒张期形变及解旋运动

目的 观察应用斑点追踪成像(STI)技术评价冠心病患者左心室舒张期形变及解旋运动的价值.方法 随机选择临床拟诊为冠心病患者117例,根据冠状动脉造影或冠状动脉CTA结果分成心肌梗死组(60例)、心肌缺血组(31例)及对照组(26例).常规测量二尖瓣口舒张期血流速度(E、A)及二尖瓣后瓣环的运动速度(E'、A'),计算E/E'.运用STI技术测量左心室舒张期各方向应变率、解旋率.结果 与心肌缺血组、对照组相比,心肌梗死组E/E'增大,纵向、径向、圆周方向舒张早期及晚期应变率、解旋率减低(P＜0.001);与对照组比较,心肌缺血组仅解旋率、舒张早期纵向应变率、舒张早期与晚期圆周方向应变率减低,差异均有统计学意义(P均＜0.05).结论 STI技术能有效评价冠心病患者左心室舒张期各方向的形变及解旋运动;与常规超声参数相比较,左心室舒张期径向、圆周方向应变率及解旋率能更早地反映心肌缺血患者左心室舒张功能的减低.     

Determination of coronary-myocardial reserve by stress echocardiography in patients with programmed pacemaker

AIM: To study coronary-myocardial reserve in patients with a programmed pacemaker. MATERIALS AND METHODS: Stress-echocardiography was performed in 64 patients with coronary heart disease (CHD). The stress was induced by a gradual increase in the frequency of electrostimulation (ES) by 10 imp/min from initial 90 imp/min to threshold value which was defined as the frequency threshold of myocardial ischemia induction (FT). RESULTS: Registration of defects in local left ventricular contractility and cardiodynamics in frequent heart ES identified patients with predominant coronary and myocardial failure. Low FT (100-110 imp/min) indicates poor coronary reserve while a considerable rise of the end diastolic pressure in the left ventricle indicates limited myocardial reserve. Positive results of the test in isolated ventricular ES were obtained in 90.9%, in atrial ES in 72.7% of patients. CONCLUSION: As a highly informative and reproducible method, stress echocardiography can be employed for optimization of antianginal therapy in CHD patients with a pacemaker.     

超速起搏预处理对急性心肌梗死的延迟保护

目的　探讨超速心室起搏 (ventricularoverdrivepacing,VOP)预处理对急性心肌梗死的延迟保护作用 (delayedprotection ,DP)及可能机制。方法　 2 0只兔随机分为 4组 :(1)对照组 ,将电极导管送至右心室旷置 70min ,2 4h后结扎、冠状动脉左前降支造成缺血再灌注模型。 (2 )起搏组 ,缺血再灌注前 2 4h予VOP。 (3)放线菌素组 ,缺血再灌注前 2 4h静注放线菌素D阻滞热休克蛋白 (HSP)转录。 (4 )起搏 放线菌素组 ,延迟缺血再灌注前 2 4h予VOP并静脉注射放线菌素D ,缺血再灌注前后测定血流动力学变化 ,以TTC染色测量各组心肌梗死面积百分比 ,免疫组化染色间检测HSP70抗原 ,并观察心肌缺血再灌注后的组织学改变。结果　与对照组比较 ,起搏组心肌梗死面积减少 34 35 % (P <0 0 0 1) ,左心收缩和舒张功能均改善 ;心肌超微结构损伤减轻。其余组与对照组比较 ,在各项指标上差别无显著意义。HSP70免疫组化染色仅在起搏组心肌标本呈阳性。结论　多次VOP预处理对急性梗死心肌有明显的延迟保护作用 ,此作用与HSP70的表达密切相关。     

Silent myocardial ischemia in long-term ECG with various mani festations of coronary heart disease

Silent myocardial ischaemia seems to be of prognostic value in coronary artery disease. We examined 47 patients with coronary artery disease: 1. 20 patients with a history of myocardial infarction (MI), 2. 15 patients with chronic stable angina pectoris without a history of myocardial infarction (sAP), and 3. twelve patients with unstable angina with or without a history of myocardial infarction (uAP). Horizontal and downsloping ST-segment-depressions greater than or equal to 1 min and greater than or equal to 0.1 mV were defined as significant. There were 132 ST-segment-depressions, the relation between symptomatic and asymptomatic being 1:7.3, in MI 1:6.2, in sAP 1:5.3, in uAP 1:14. Heart rate increased before beginning of ST-segment-depression in 74% in MI, in 86% in sAP, but only in 38% in uAP. In sAP ST-segment-depressions were smaller (14% greater than 0.2 mV, none greater than 0.3 mV) than in patients with MI (42% greater than 0.2 mV, 12% greater than 0.3 mV) and uAP (25% greater than 0.2 mV, 9% greater than 0.3 mV). Mean duration of ST-segment-depression was 15.3 +/- 11.7 min in sAP (2 to 49 min), 28.5 +/- 35.6 min in MI (2 to 168 min), and 41.2 +/- 40 min in iAP (2 to 140 min). ST-segment-depressions in MI and sAP showed a circadian rhythm with a peak at midday and in the early evening and a small amount of ST-segment-depressions at night. In uAP ST-segment-depressions did not show that circadian variation. The number of ST-segment-depressions was higher in uAP than in MI and sAP.(ABSTRACT TRUNCATED AT 250 WORDS)     

Calcitonin gene-related peptide receptor antagonism does not affect the severity of myocardial ischemia during atrial pacing in dogs with coronary artery stenosis

Calcitonin gene-related peptide (CGRP) is a sensory neuropeptide that also has potent vasodilator activity. There are conflicting preclinical reports regarding the effect of CGRP receptor antagonism in the setting of myocardial ischemia. The present study was conducted in a canine model in which regional myocardial ischemia was reproducibly evoked by serial periods of atrial pacing (80 beats per min above baseline rate) in the presence of a 40% stenosis of the left anterior descending (LAD) coronary artery. Ischemia severity was quantitated by changes in unipolar epicardial electrograms (EG) recorded in the area of ischemia. In validation studies, the calcium entry blocker diltiazem reduced ischemia severity (before versus after treatment: DeltaEG, 1.92 +/- 0.23 versus 0.54 +/- 0.24 mV; p < 0.05) and tended to increase LAD flow (7.7 +/- 0.7 versus 9.4 +/- 1.4 ml/min; p = 0.10), whereas the coronary constrictor serotonin increased ischemia severity (before versus after treatment: DeltaEG, 2.11 +/- 0.44 versus 4.90 +/- 1.46 mV; p < 0.05) concomitant with a reduction in LAD flow (9.1 +/- 1.1 versus 5.4 +/- 1.5 ml/min; p < 0.05). A 30 microg/kg/min i.v. infusion test dose of the CGRP receptor antagonist CGRP((8-37)) was validated by demonstrating complete block of the depressor effects of exogenous i.v. 0.03 to 0.3 microg/kg CGRP. This dose of CGRP((8-37)), administered either intravenously or intra-atrially, had no effect on ischemia severity or paced LAD flow, indicating no intrinsic effect of CGRP receptor antagonism on the severity of acute myocardial ischemia. Likewise, the administration of a hemodynamically active dosing regimen of CGRP (0.03 microg/kg/min i.v.) had no effect on paced coronary flow or ischemia severity, suggesting no major role of CGRP in regulating ischemic blood flow.     

A clinical course of coronary heart disease after pacemaker implantation and optimization of the pacing regime

AIM: To study effects of pacemaker implantation on the course of coronary heart disease (CHD) with stable angina pectoris and choice of optimal regimen of pacing. MATERIAL AND METHODS: A total of 154 CHD patients with a pacemaker were examined. All the patients had angina of effort of functional class II-IV. RESULTS: The symptoms of the disease improved in 72 (46.8%) patients (group 1): the number of anginal attacks decreased, exercise tolerance increased, the dose of antianginal medicines went down. Pain attacks became more frequent, response to nitroglycerin changed in 30 (19.5%) patients of group 2. This was explained by 1.5-2-fold enhancement of heart rate by pacemaker raising myocardial oxygen consumption and psychocardial syndrome. In 52 (33.8%) patients of group 3 anginal attacks characteristics did not change. CONCLUSION: To optimize coronary reserve, frequency of electroimpulses must be reprogrammed to adjust to a functional class of angina and chronic cardiac failure as well as pacing regime. In particular, low coronary reserve demands optimal frequency of 55-65 imp/min while congenital cardiac failure--75-85 imp/min.     

Cardiac fibrinolytic capacity is markedly increased after brief periods of local myocardial ischemia, but declines following successive periods in anesthetized pigs

BACKGROUND: Fibrinolysis in blood is mainly reflected by the activities of tissue plasminogen activator (tPA) and of plasminogen activator inhibitor-1 (PAI-1). The effect of myocardial ischemia on their activities in the coronary circulation is, however, not established. OBJECTIVES: With an improved experimental model, we therefore examined the effect of a brief period of myocardial ischemia on their activities. Furthermore, the consequences of repeated periods of ischemia, mimicking the situations in patients with unstable angina, were investigated. METHODS: In six anesthetized pigs, we occluded the distal left anterior descending coronary artery (LAD) four times for 10 min with 40 min intervals and determined the activities of tPA and PAI-1 in arterial and coronary venous blood. By simultaneously recording LAD flow, we could estimate cardiac release of these factors at baseline conditions and during reperfusion. RESULTS: Neither net cardiac release of PAI-1 nor alterations in plasma PAI-1 levels were demonstrated during the experiment. However, a significant net release of tPA activity of 10.4 +/- 3.2 IU mL(-1) (P < 0.005) was recorded during baseline conditions. During reperfusion following the first period of ischemia, the cardiac release of tPA activity increased to a peak of 103 +/- 30-fold baseline release, but declined progressively after repeated periods of ischemia. After the fourth period, tPA release did not exceed an estimated baseline accumulation during ischemia and early reperfusion. CONCLUSIONS: In this porcine model, a substantial local increase in fibrinolytic capacity was observed after brief periods of ischemia, but declined subsequently by repeated periods of ischemia.     

速度向量成像技术评价犬心肌缺血与梗死状态下左心室节段性旋转特征

目的应用速度向量成像(VVI)技术评价心肌缺血及心肌梗死状态下犬心肌旋转运动特征。方法选用杂种犬12只,在超声实时引导下结扎前降支定量制备前降支轻度狭窄(狭窄率:50%～75%)与完全闭塞模型,应用VVI技术分析前降支结扎前、轻度狭窄与完全闭塞状态下左心室旋转特征的改变。结果 12只杂种犬成功制备前降支轻度狭窄与完全闭塞模型,应用VVI技术对缺血与梗死状态下心肌旋转运动分析结果显示:(1)前降支部分结扎状态下室间隔的旋转角度与圆周应变较正常显著降低(P<0.05);径向应变与应变率较正常差异有统计学意义(P<0.05);(2)前降支完全结扎状态下:前间隔、室间隔、前壁的旋转角度与旋转速度、圆周应变与圆周应变率较正常及部分结扎状态下均显著减低(P<0.05);径向应变与应变率较正常状态下显著降低(P<0.05),与部分结扎状态下比较,差异无统计学意义。结论 VVI技术可以无创、敏感地评价心脏旋转运动。前降支部分结扎状态下心脏的旋转在个别节段已经出现减低,前降支完全结扎后,旋转角度与旋转速度较结扎前、部分结扎后均显著降低,心脏旋转可以更加敏感的反映心脏收缩功能。     

Annexin V does not represent a diagnostic alternative to myoglobin for early detection of myocardial infarction

Annexin V is a calcium binding protein, which is widely present in various cells and tissues. Due to an early release reaction after myocardial injury the determination of annexin V might be useful for the rapid diagnosis of acute myocardial infarction. An enzyme-linked immunosorbent assay was used to measure annexin V in comparison to myoglobin in samples from healthy individuals, patients suffering from acute or chronic liver, renal, and pulmonary diseases as well as acute coronary syndromes and aortocoronary bypass surgery. Increased myoglobin and annexin V concentrations were observed 80 and 140 (maximum) minutes after myocardial ischemia induced by percutaneous transluminal coronary angioplasty. For the diagnosis of myocardial infarction annexin V (cutoff-level: 5.9 microg/L) showed a slightly higher sensitivity than myoglobin (annexin V: 74.5%; myoglobin: 59.6%), but specificity was much lower (annexin V: 39%; myoglobin: 82.5%). The area under the curve of a ROC analysis demonstrated that annexin V cannot be used as an early marker for the diagnosis of acute coronary syndromes. Increased annexin V levels are induced by several diseases, leading to a low specificity for the diagnosis of a myocardial injury.     

核素心肌灌注显像诊断无症状性心肌缺血价值

目的探讨核素心肌灌注显像诊断无症状性心肌缺血的临床应用价值。方法动态心电图或其他心电检测技术检测无症状性心肌梗死患者22例,均行核素心肌灌注显像与冠状动脉造影检查,并以冠状动脉造影结果为金标准,计算核素心肌灌注显像结果预测值。结果 22例患者中8例核素心肌灌注显像表现为不可逆性心肌缺血,14例表现为混合性心肌缺血,共检测出40个节段病变心肌。冠状动脉造影检出阳性血管45支(血管狭窄程度≥50%),其中28支狭窄程度>90%,15支狭窄程度>70%~90%,2支狭窄程度≤70%。核素心肌灌注显像阳性结果预测值为88.9%(40/45)。结论核素心肌灌注显像有助于无症状性心肌缺血诊断,并可用于评价心肌损害严重程度。     

Protection against myocardial dysfunction after a brief ischemic period in transgenic mice expressing inducible heat shock protein 70.

Brief ischemic periods lead to myocardial dysfunction without myocardial infarction. It has been shown that expression of inducible HSP70 in hearts of transgenic mice leads to decreased infarct size, but it remains unclear if HSP70 can also protect against myocardial dysfunction after brief ischemia. To investigate this question, we developed a mouse model in which regional myocardial function can be measured before and after a temporary ischemic event in vivo. In addition, myocardial function was determined after brief episodes of global ischemia in an isolated Langendorff heart. HSP70-positive mice and transgene negative littermates underwent 8 min of regional myocardial ischemia created by occlusion of the left descending coronary artery, followed by 60 min of reperfusion. This procedure did not result in a myocardial infarction. Regional epicardial strain was used as a sensitive indicator for changes in myocardial function after cardiac ischemia. Maximum principal strain was significantly greater in HSP70-positive mice with 88+/-6% of preischemic values vs. 58+/-6% in transgene-negative mice (P < 0.05). Similarly, in isolated Langendorff perfused hearts of HSP70-positive and transgene-negative littermates exposed to 10 min of global ischemia and 90 min of reperfusion, HSP70 transgenic hearts showed a better-preserved ventricular peak systolic pressure. Thus, we conclude that expression of HSP70 protects against postischemic myocardial dysfunction as shown by better preserved myocardial function.     

心肌缺血和有氧运动训练诱导VEGF表达时间规律的实验研究

摘要 目的：研究心肌缺血和有氧运动训练诱导血管内皮细胞生长因子（VEGF）表达的时间规律。方法：成功建模的健康成年巴马小型猪24只，体重23.7±4.0kg，随机分为对照组、缺血组和运动组。将可控性水囊梗阻器安装在猪冠状动脉钝缘支处，建立可控性猪心肌缺血模型。对照组不进行缺血刺激和有氧运动训练；缺血组进行单纯缺血刺激，2min/次，2次/d，持续缺血刺激8周；运动组除进行缺血刺激外，每天进行一次平板有氧运动训练，每次30min。每两周取动脉血，采用ELISA法检测血液VEGF。实验终点时采用Western Blot检测缺血区心肌VEGF。结果：缺血组第2周血液中VEGF的表达量明显高于实验前（P<0.05），随后进入平台期（P>0.05）。运动组中第2-4周血液中VEGF的表达量持续增高（P<0.05），随后达到平台期(P>0.05)。缺血区心肌VEGF表达和血液VEGF表达呈正相关（r=0.826，P<0.01）。结论：心肌缺血和有氧运动训练诱导的血液VEGF增高分别在第2周和第4周达到高峰，然后进入平台期。 关键词 心肌缺血;有氧运动;血管内皮细胞生长因子 中图分类号：R493,R541.4 文献标识码：A 文章编号：1001-1242(2008)-03-0193-05     

Inhibitors of bradykinin-inactivating enzymes decrease myocardial ischemia/reperfusion injury following 3 and 7 days of reperfusion

Inhibitors of bradykinin (BK)-inactivating enzymes protect from myocardial ischemia/reperfusion injury after short periods of reperfusion. However, protection after 2 to 3 h of reperfusion does not mean that myocardium remains viable for an extended time. Therefore, we examined the effects of inhibitors of angiotensin-converting enzyme (ramiprilat), EP24.11 (cFP-F-pAB), and EP24.15 (cFP-AAF-pAB) in a chronic model of myocardial ischemia/reperfusion injury. A left descending coronary artery was occluded for 30 min in anesthetized rabbits. Saline, ramiprilat, or endopeptidase inhibitors were given after 27 min of occlusion. The BK(2) receptor antagonist HOE140 was administered in certain experiments. After ischemia, the occlusion was released, and the animal allowed to recover for 3 or 7 days. Surgery was then repeated, and the heart removed for determination of infarct size. In separate experiments, the heart was removed after 2 h of reperfusion for determination of BK tissue levels. Ramiprilat and endopeptidase inhibitors reduced infarct size at 3 and 7 days. Combining inhibitors further reduced infarct size after 3 days. The protective effect of the endopeptidase inhibitors was blocked by HOE140. Infarct sizes at 7 days were larger than at 3 days. The additive effect of multiple inhibitors was absent at 7 days. Ramiprilat and cFP-F-pAB significantly increased tissue BK levels. We conclude that inhibition of BK-inactivating enzymes protects endogenous BK from degradation and provides long-lasting protection from myocardial ischemia/reperfusion injury. A single treatment at the time of reperfusion does not prevent extension of the infarction between 3 and 7 days.     

Association of transient myocardial ischemia with adverse in-hospital outcomes for angina patients treated in a telemetry unit or a coronary care unit.

BACKGROUND: Little is known about the frequency or consequences of transient myocardial ischemia in patients admitted to a telemetry unit for treatment of angina. OBJECTIVES: To compare the rate of transient myocardial ischemia in a group of patients with angina treated in a telemetry unit with the rate in a similar group treated in a coronary care unit and to determine if transient myocardial ischemia is associated with adverse in-hospital outcomes. METHODS: Continuous 12-lead electrocardiography was used to monitor changes in the ST segment in 186 patients in the coronary care unit (1994-1996) and 186 patients in the telemetry unit (1997-2000). Transient myocardial ischemia was defined as a change from baseline of 100 microV or more in the ST segment in 1 or more leads lasting 60 seconds or longer RESULTS: The rate of transient myocardial ischemia was 15% for patients in the telemetry unit and 19% for patients in the coronary care unit. Regardless of hospital unit, patients with transient myocardial ischemia were more likely than those without this complication to experience death or acute myocardial infarction after hospital admission. Most patients did not experience signs or symptoms during transient myocardial ischemia: 71% of patients in the telemetry unit versus 58% of patients in the coronary care unit (P =.28). CONCLUSIONS: Transient myocardial ischemia is common among patients with angina treated in a telemetry unit. ST-segment monitoring may be useful for detecting patients with ischemia who may benefit from more aggressive therapies aimed at abolishing ongoing ischemia.