低能量氦氖激光血管内照射对缺血再灌注心肌超微结构的影响

目的:探讨低能量氦氖激光血管内照射(ILIB)对缺血再灌注心肌组织超微结构的影响。方法:通过结扎冠状动脉阻断冠状动脉血流,复制家兔急性心肌缺血-再灌注损伤动物模型。将家兔随机分为4组:假手术组、心肌缺血30min组、缺血30min再灌注30min组、缺血30min再灌注30min+ILIB组。在透射电镜下观察各组心肌超微结构的变化。结果:假手术组心肌纤维呈阶段性收缩、间质水肿、线粒体轻度肿胀、间质可见闭塞的毛细血管;心肌缺血组心肌纤维排列紊乱、肌浆水肿、线粒体水肿、血管扩张、血管结构破坏、血管内可见白细胞镶嵌;缺血再灌注组心肌纤维排列相对整齐、线粒体水肿不明显、肌浆水肿较轻、心肌间质可见轻度毛细血管扩张淤血;缺血再灌注+ILIB组心肌纤维排列整齐、线粒体无肿胀、间质毛细血管内可见红细胞、无毛细血管内白细胞镶嵌现象、毛细血管管腔通畅、血管壁较完整。结论:IL-IB可使缺血再灌注心肌超微结构基本恢复正常,对心肌有保护作用。     

低能量氦氖激光血管内照射对缺血再灌注心肌超微结构的影响

目的：探讨低能量氦氖激光血管内照射（ILIB）对缺血再灌注心肌组织超微结构的影响。方法：通过结扎冠状动脉阻断冠状动脉血流，复制家兔急性心肌缺血-再灌注损伤动物模型。将家兔随机分为4组：假手术组、心肌缺血30min组、缺血30min再灌注30min组、缺血30min再灌注30min＋ILIB组。在透射电镜下观察各组心肌超微结构的变化。结果：假手术组心肌纤维呈阶段性收缩、间质水肿、线粒体轻度肿胀、间质可见闭塞的毛细血管；心肌缺血组心肌纤维排列紊乱、肌浆水肿、线粒体水肿、血管扩张、血管结构破坏、血管内可见白细胞镶嵌；缺血再灌注组心肌纤维排列相对整齐、线粒体水肿不明显、肌浆水肿较轻、心肌间质可见轻度毛细血管扩张淤血；缺血再灌注＋ILIB组心肌纤维排列整齐、线粒体无肿胀、间质毛细血管内可见红细胞、无毛细血管内白细胞镶嵌现象、毛细血管管腔通畅、血管壁较完整。结论：ILIB可使缺血再灌注心肌超微结构基本恢复正常，对心肌有保护作用。     

链脲佐菌素糖尿病大鼠的心肌病变

在40只链脲佐菌素糖尿病大鼠和40只正常对照鼠中,观察和比较不同病理时血糖、血脂、血浆果糖胺、左心室心肌酶含量、电镜下心肌改变、光镜下冠状动脉及其分枝的改变。在4周病程时,糖尿病大鼠心肌线粒体开始肿胀变性,8周时心肌酶含量明显降低,心肌病变显著,心肌排列不齐、断裂和心肌收缩带形成等。在11周病程中有持久性血糖过高和血脂过高,但未见冠状动脉及其分枝的病变。结果表明心肌病变系糖尿病特异性,作为糖尿病心脏病的一个重要独立组成部分而存在。     

超声心动图结合血清bFGF、MCP-1水平对无症状性心肌缺血冠脉病变程度的诊断价值

目的 探讨超声心动图结合血清碱性成纤维细胞生长因子(bFGF)、单核细胞趋化蛋白(MCP)-1水平对无症状性心肌缺血冠脉病变程度的诊断价值。方法 选取行冠状动脉造影检查(CAG)的127例无症状性心肌缺血患者，均行超声心动图及血清bFGF、MCP-1水平检测。根据罪犯血管冠状动脉造影(CAG)结果将患者分为轻度、中度与重度，对比不同冠脉病变程度患者超声心动图参数[左室收缩末期容积(LVESV)、左室舒张末期容积(LVEDV)、心肌收缩早期延迟时间、脉冲多普勒左室心肌做功指数(PW-Tei)、左室射血分数(LVEF)]及血清bFGF、MCP-1水平。采用受试者工作特征(ROC)曲线分析超声心动图各参数单项及联合对中重度患者的诊断价值，并分析超声心动图联合血清bFGF、MCP-1水平对中重度患者的诊断价值。结果 CAG检查结果显示，轻度狭窄34例、中度狭窄62例、重度狭窄31例；随着冠状动脉病变程度的加重，LVESV、LVEDV、心肌收缩早期延迟时间、PW-Tei及血清bFGF、MCP-1水平在轻度、中度、重度患者中依次升高，而LVEF依次降低，差异均有统计学意义(P<0.05);超...     

超声心动图心肌收缩早期延迟时间指标对判断冠状动脉狭窄程度的价值

目的:采用二维斑点追踪技术(2D-speckle tracking imaging, 2D-STI)中心肌的收缩早期延迟时间指标对判断冠状动脉(冠脉)狭窄程度的价值。方法:对185例可疑冠脉狭窄患者在冠脉造影前48 h进行超声心动图检查,测量心肌的收缩早期延迟时间、纵向应变(longitudinal strain, LS)、径向应变(radial strain, RS)及圆周应变(circumferential strain, CS)。根据冠脉造影结果分组:即冠脉无狭窄者为冠脉正常组(n=48),狭窄程度50%者为轻度狭窄组(n=37),50%≤狭窄程度70%者为中度狭窄组(n=55),70%≤狭窄程度100%者为重度狭窄组(n=45)。结果:与冠脉正常组比较,轻度狭窄组心肌的收缩早期延迟时间、纵向应变、径向应变及圆周应变无明显改变(P0.05),中度狭窄组心肌的收缩早期延迟时间延长,纵向应变减低(P0.05),重度狭窄组心肌的收缩早期延迟时间延长、纵向应变、径向应变及圆周应变均减低(P0.01)。ROC曲线显示,心肌的收缩早期延迟时间较纵向应变筛选冠脉中度、重度狭窄患者更佳。以收缩早期延迟时间为60.0 ms作为截断值时诊断价值最佳,敏感度为85.5%,特异度为74.1%,AUC=0.91。结论:中度以上的冠脉狭窄患者心肌的收缩早期时间明显延长,这一参数可准确识别不同程度冠状动脉狭窄患者。     

冠脉定量狭窄时犬心泵功能二维信息图的变化

对12条开胸狗冠状动脉前降支安放自制可调缩窄器,形成不同程度狭窄,获得左心室收缩压力（LVSP）和dp/dt等在临界狭窄时开始显著降低（P<0.05）。CO和SV在重度狭窄时分别降低了16％和20.6％（P均<0.01）。瞬时血流速率（dQ/dt）在轻度狭窄时降低7％,重度狭窄时降低19.4％（P<0.01）。二维信号环Q-dQ/dt面积在轻度狭窄时为对照组的89.47％（P<0.05）,在临界和重度狭窄时分别为对照组的80.87％和62.14％（P均<0.01）。提示冠脉不同程度的狭窄可导致心功能及收缩性不同程度受损。     

眼底动脉硬化对冠状动脉狭窄的预测价值分析

目的分析眼底动脉硬化对冠状动脉狭窄的预测价值。方法选取我院2016年7月~2017年4月收治的疑似冠心病患者90例作为研究对象。采取冠状动脉造影和无创眼底检查,对比检查结果进行分析,分析冠状动脉硬化危险因素。结果冠状动脉轻度狭窄有66.7%合并出现眼底动脉硬化,中度狭窄有63.3%合并出现眼底动脉硬化,重度狭窄有56.7%合并出现眼底动脉硬化。冠状动脉轻度狭窄患者出现轻度眼底动脉硬化有40%;冠状动脉中度狭窄患者出现轻度眼底动脉硬化有45%;冠状动脉重度狭窄患者出现轻度眼底动脉硬化有23.5%;冠状动脉轻度狭窄患者出现中重度眼底动脉硬化有60%;冠状动脉中度狭窄患者出现中重度眼底动脉硬化有52.6%;冠状动脉重度狭窄患者出现中重度眼底动脉硬化有76.5%。结论眼底动脉硬化应该与冠心病的严重程度成正相关,因此眼底动脉的硬化程度可以对冠状动脉狭窄程度进行预测,眼底检查作为冠状动脉狭窄的初步诊断方法,也是筛选冠状动脉疾病的方法,用于冠心病的早期诊断、治疗和预后有重要的意义。     

冠状动脉CT成像与冠状动脉造影的比较研究

目的 比较16层螺旋CT和冠状动脉造影对冠心病的诊断价值。方法 23例患者行16层螺旋CT冠状动脉成像(回顾性心电门控、0．42s螺旋扫描)，并与冠状动脉造影(CAG)对照。结果 在23例患者中，MSCT显示轻度狭窄13处，中度狭窄12处，重度狭窄8处。CAG发现轻度狭窄8处，中度狭窄9处，重度狭窄7处。结论 冠状动脉造影可能低估冠状动脉病变的严重程度，冠状动脉CT成像是对冠心病的早期诊断的有效补充。     

CT冠状动脉成像用于诊断无症状与有症状心肌缺血病人冠状动脉病变的差异

目的通过CT冠状动脉成像分析,比较无症状心肌缺血与有症状心肌缺血病人冠状动脉病变的差异。方法选取我院2014年11月—2015年11月收治的66例心肌缺血的病人,将无症状心肌缺血的33例病人设为对照组,有症状心肌缺血的33例病人设为观察组。两组均进行CT冠状动脉成像检查,比较两组出现动脉狭窄的发生率、狭窄程度及斑块出现的情况。结果 CT冠状动脉成像显示对照组动脉轻度狭窄15例(45.45%),中度狭窄5例(15.15%),重度狭窄1例(3.03%),完全闭塞0例;观察组动脉轻度狭窄5例(15.15%),中度狭窄12例(36.36%),重度狭窄6例(18.18%),完全闭塞4例(12.12%)。观察组动脉狭窄的总发生率(81.81%)与对照组(63.63%)无统计学无意义(P0.05);但对照组心肌缺血以轻度狭窄多发,观察组心肌缺血以中度以上者多发,且具有统计学意义(P0.05)。观察组动脉斑块的总发生率(84.84%)明显高于对照组(39.39%),具有统计学意义(P0.05)。结论无症状心肌缺血病人与有症状心肌缺血病人动脉狭窄的总发生率无明显差异,但有症状心肌缺血病人动脉狭窄的程度及出现斑块的数量要明显高于无症状心肌缺血病人。     

血清总胆红素与冠状动脉狭窄的相关性

目的 :探讨血清总胆红素水平与冠状动脉狭窄程度的关系。方法 :符合条件的冠状动脉造影患者 14 6例 ,根据狭窄程度分成 3组。正常组 :6 0例 ,血管狭窄程度 <10 %。轻度狭窄组 :16例 ,狭窄程度 10 %～ 4 9%。重度狭窄组 :70例 ,至少一支血管狭窄 >5 0 %。采空腹肘静脉血测定血清总胆红素水平并进行比较。结果 :正常组血清总胆红素显著高于轻度狭窄组及重度狭窄组 （P<0 .0 5 ） ,轻度狭窄组与重度狭窄组之间血清总胆红素水平差异无显著性。重度狭窄组中单支病变与两支病变、单支病变与三支病变的总胆红素水平有高度显著差异 （P<0 .0 1）。血清总胆红素水平越低者 ,冠状动脉狭窄程度越重。结论 :血清总胆红素水平与冠状动脉狭窄程度呈负相关。     

Study on reperfusion injury on sarcoplasmic reticulum in acute myocardial ischemia.

Reperfusion injury in early myocardial ischemia was studied in the dog with special reference to sarcoplasmic reticulum (SR) and contraction bands. Acute myocardial ischemia (I) was induced by occlusion of the left anterior descending coronary artery (LAD) for 10, 20 and 30 min followed by reperfusion for 15 min (R). Ca(++)-ATPase activity of SR in 10-min-R-Group was significantly reduced to 60% of control activity, but activity of 10-min-I-Group remained near the control level in subendomyocardium (Endo). ATPase activity in 30-min-I-Group diminished to 60% of control activity in Endo and it was similar for 30-min-R-Group. In ischemic myocardium, composition of major ATPase protein decreased significantly in 30-min-I-Group and similar reduction was observed in 20-min-R-Group in Endo. In morphology proportion of appearance of contraction bands in Endo was significantly increased in 20-min or longer-R-Groups. These results suggest that reperfusion injury is likely to occur when coronary artery is reflowed after 10 min of ischemia. This may be caused by increased intracellular Ca++ at a very early stage of reperfusion period, and reperfusion injury may be induced due to acceleration in the necrotic process of the membrane system in the myocytes during ischemia.     

Myocardial mechanical injury in acute ischemia: a pathophysiologic and histopathologic review

The recognition of histopathologic substrates of myocardial contractile damage in human acute ischemia is still very poor, notwithstanding the impressive advances in the inherent clinical diagnostic technology and concepts. The first and foremost inotropic abnormality ensuing ischemia, easily taken for atonic in origin, actually consists of a pathologic contracture of the injured myocardium, depending upon abrupt fall of ATP, and defective extrusion calcium pump with persistence of actomyosin rigor-complexes. In sustained ischemia, further membrane damage exposes the myocell to massive calcium intrusion, with eventual precipitation of it and cell death (reperfusion stone-heart). In case of transient, "hit and run" ischemia, the "stunned" myocardium undergoes prolonged contractile abnormalities. In keeping with fundamentals in pathophysiology of contraction, ischemic myofibrils in human hyperacute infarct, showed spare I bands, accounting for contracture and followed by loss of the regular cross-striation register; then, groups of adjacent sarcomeres were seen to join into true "contraction" bands, with Z lines impinging upon A bands and obliterating the I bands. Coagulative denaturation of contractile proteins follows, presenting as irregular, amorphous degeneration stripes astride irreversibly damaged myocells. As such, these cells can be passively overstretched by the nearby functioning muscle. In turn, the fixed waviness of viable, acutely ischemic myocardium was thought to configure, histologically, the loss of ATP-dependent "plasticity" of myofilaments, in a state of contracture. The "relaxant effect" of inotropic-chronotropic-positive catecholamines, favoring diastole, has been also pointed out. The present microscopic findings are cogent to clinicopathologic problems of coronary ischemia-reperfusion, and sudden death from cardiogenic shock.     

Coronary slow flow phenomenon: description of three cases evaluated with myocardial perfusion scintigraphy.

The coronary slow flow phenomenon (CSFP) is an angiographic finding characterized by delayed opacification of the epicardial coronary arteries in the absence of significant stenosis, spasm, dissection or thrombus. Although this poorly understood phenomenon received little attention, patients with CSFP at coronary angiography often suffer from recurrent episodes of chest pain, sometimes occurring during an acute coronary syndrome. We describe 3 cases of patients with CSFP who complained of recurrent chest pain; in one of them an episode of chest pain was so severe as to bring the patient to the emergency department. Indeed, in all our 3 cases myocardial ischemia was evaluated on the basis of a positive myocardial scintigraphy result. In conclusion, it is suggested that CSFP may be an acute and recurrent perturbation of microvascular function with an often severe impairment of quality of life. Myocardial perfusion scintigraphy might help for an accurate assessment of myocardial ischemia in such patients.     

急性心肌梗死超急期J波综合征的临床特征

目的总结急性心肌梗死超急期J波综合征患者的临床特征。方法收集55例选择性冠状动脉造影诊断的急性心肌梗死超急期患者,观察其心电图的演变过程,统计分析J波综合征与冠状动脉病变以及室性心律失常发生之间的关系。结果急性心肌梗死超急期J波综合征患者16例,其中严重右冠状动脉狭窄10例,发生室性心律失常11例,急性心肌梗死超急期J波综合征患者的右冠状动脉狭窄发生率高(P<0.05),室性心律失常的发生率明显高于无J波综合征的患者(P<0.05)。结论急性心肌梗死超急期J波综合征多见于右冠状动脉受累的患者,易致室性心律失常。     

Two-dimensional echocardiography in experimental coronary stenosis. II. Relationship between systolic wall thinning and regional myocardial perfusion in severe coronary stenosis

To determine if there is a quantitative relationship between systolic contraction abnormalities (demonstrated by two-dimensional echocardiography) and reduced myocardial perfusion in a setting of moderate and severe coronary stenosis, we created 70% or 90% reduction in circumflex coronary artery diameter in open-chest dogs. Transient ischemia was induced by superimposing increased myocardial oxygen requirements (i.v. isoproterenol, aortic constriction) in the presence of the stenosis or by decreased coronary perfusion (lowering arterial pressure with i.v. nitroprusside, nitroglycerin, or hemorrhage). Acute systolic wall thinning show by two-dimensional echocardiography or by implanted myocardial sonomicrometers was taken as functional evidence of myocardial ischemia. Myocardial perfusion was determined by radiolabeled microspheres when wall thinning was apparent. Systolic wall thinning could not be induced by these interventions when the degree of coronary stenosis was only 70%. Systolic wall thinning occurred only when increased myocardial oxygen requirements or decreased aortic pressure were superimposed on 90% coronary stenosis. Under these conditions, myocardial perfusion was reduced to 28 +/- 27 ml/100 g/min (mean +/- SD), 15--25% of control. Aortic diastolic pressure was a major determinant of ischemia in that contraction abnormalities produced by a 90% stenosis and vasodilators or hemorrhage could be acutely reversed by superimposing acute aortic constriction, which elevated arterial pressure; myocardial perfusion increased correspondingly. Thus, the demonstration of transient systolic wall thinning by two-dimensional echocardiography during a stressful intervention indicated that severe coronary stenosis was present, and that the perfusion of the acutely dyskinetic myocardial area was 25% of control or less.     

Impending acute myocardial infarction during severe exercise associated with a myocardial bridge.

A young man had an impending acute myocardial infarction while playing soccer. Chest pain and anterior ST-segment elevation lasted 3 hours despite anti-ischemic medication, including streptokinase thrombolysis. An electrocardiogram recorded after the symptoms had passed was normal. There was a minimal increase in cardiac enzyme levels, and a pyrophosphate scan and echocardiogram were normal. Coronary cineangiography showed normal coronary arteries except for systolic compression of the left anterior descending coronary artery. An exercise stress test, while the patient was on atenolol, showed absence of myocardial ischemia. This impending acute myocardial infarction could have been caused by an acute thrombus with lysis prior to catheterization or by a deep muscle bridge that kinked or twisted the coronary artery due to myocardial forceful muscular contraction during the sympathetic stimulation of exercise. In conclusion, an impending acute myocardial infarction may occur in young patients having myocardial bridges, and a beta-blocker must be administered, especially when this condition appears during severe exercise.     

Angina pectoris and acute myocardial infarction due to "slow-flow phenomenon" in nonatherosclerotic coronary arteries: a case report

A 51 year-old White woman with angina pectoris and nonatheromatous coronary artery disease is presented. Cardiac catheterization demonstrated a "slow-flow phenomenon" in the left coronary artery accompanied by severe angina pectoris and anterolateral ST-segment elevation and culminating in an acute nontransmural myocardial infarction. At repeat coronary arteriography, ergonovine maleate provocation proved negative. This patient is unique, since the previously documented 6 cases with this coronary cineangiographic response did not exhibit angina pectoris or ECG evidence of myocardial ischemia during the "slow-flow phenomenon," and none was complicated by an acute myocardial infarction. Various aspects of the pathophysiology of angina pectoris in this patient, including the recently described "reduced vasodilator reserve" concept, are briefly outlined.     

Plasma interleukin-18 concentration: a novel marker of myocardial ischemia rather than necrosis in humans

OBJECTIVE: Myocardial ischemia contributes to cytokine expression in the myocardium in animals; therefore, plasma interleukin-18 concentration may be a good marker of myocardial ischemia/injury in patients with possible acute coronary syndrome. We sought to determine whether increases in plasma interleukin-18 concentrations might be indicative of myocardial ischemia in patients with acute coronary syndrome. METHODS: Plasma interleukin-18 concentrations were assessed in 27 acute coronary syndrome patients in whom creatine kinase activity was within normal range on admission, in addition to 10 controls. Myocardial infarction was retrospectively evidenced in 15 of the 27 patients. All patients with acute coronary syndrome were treated by emergent coronary interventions just after admission. Blood sampling was done immediately after admission to determine plasma IL-18 concentration and biochemical markers of myocardial infarction. RESULTS: An increase in plasma interleukin-18 concentration was observed in acute coronary syndrome patients on admission, regardless of the retrospective evidence of myocardial necrosis. Plasma interleukin-18 elevation preceded creatine kinase-MB elevation in myocardial infarction patients. Plasma interleukin-18 concentrations on admission did not correlate with peak creatine kinase-MB (r=0.38, P=n.s.) or with left ventricular ejection fraction (r=-0.14, P=n.s.). CONCLUSIONS: Plasma interleukin-18 concentration elevates quickly after severe myocardial ischemic event regardless of evolving myocardial necrosis. Thus, plasma interleukin-18 concentration may be a good and early marker to identify whether the symptom is due to myocardial ischemia, and therefore, may be used in deciding the therapeutic strategy in individual patients with possible acute coronary syndrome.     

Myocardial perfusion-contraction matching. Implications for coronary heart disease and hibernation

Experimental studies demonstrate that short-term regional perfusion-contraction matching, in which the energy demands of regional myocardial contraction are reduced to match the diminished myocardial substrate supply, occurs during states of low coronary blood flow under resting conditions and during exercise-induced ischemia. This phenomenon is rapidly reversible and appears to occur in several clinical settings. Sustained perfusion-contraction matching is observed in states of partial experimental ischemia of intermediate duration lasting several hours. This condition might be called short-term hibernation and resembles clinical conditions such as unstable angina pectoris or myocardial infarction with some residual perfusion in which the contractile defect can be improved by reperfusion provided the ischemia is not severe enough to cause transmural necrosis. Such experimental and clinical observations may or may not relate to the setting of regional dysfunction at rest in patients with chronic coronary heart disease, in whom manifestations of acute ischemia may be absent but improvement of wall motion abnormalities occurs after CABG or balloon angioplasty. This condition may constitute the hypothetical state of chronic myocardial hibernation, for which tentative evidence exists from metabolic and perfusion studies using PET. Whether such a condition of prolonged perfusion-contraction matching might be associated with adaptive processes that could allow its persistence for long periods without manifest ischemia remains to be investigated.     

Echocardiography in experimentally-induced myocardial ischemia

Using an experimental canine model, we have employed echocardiography to study segmental dyskinesis produced by acute coronary occlusion. Characteristic alterations in posterior wall and septal motion occur after acute coronary ligation; these resemble clinical abnormalities described in acute and old myocardial infarction. The degree of dyskinesis produced is directly related to the severity of the perfusion deficit. Coronary reperfusion had variable effects on dyskinesis; most animals showed improvement but in some the myocardial contraction abnormalities became more severe. A variety of interventions were undertaken during ischemia. The elevated level of arterial pressure induced by the administration of methoxamine increased ventricular diameter and presumably oxygen requirements, and was deleterious to ischemic wall motion whereas the administration of norepinephrine reduced ventricular diameter and improved function. Intra-aortic balloon counterpulsation had little effect on either ischemic motion or perfusion. These experimental studies generally support conclusions drawn from clinical echocardiograms about the relationship of abnormalities of wall motion to coronary artery lesions and myocardial ischemia, and suggest further clinical uses for echocardiography in coronary disease.