冠脉造影正常的急性心肌梗死1例

急性心肌梗死(AMI)绝大多数是在冠状动脉粥样硬化的基础上发生,但也可发生在冠脉造影正常或轻度病变的冠状动脉,本文报道1例外科小手术后出现AMI而冠脉造影正常的病人.     

冠脉造影正常的急性心肌梗死1例

急性心肌梗死 (AMI)绝大多数是在冠状动脉粥样硬化的基础上发生 ,但也可发生在冠脉造影正常或轻度病变的冠状动脉 ,本文报道 1例外科小手术后出现AMI而冠脉造影正常的病人 .1　资料患者 ,男 ,5 0岁 ,干部 .因左食指受伤外科治疗 ,术后出现胸骨下段闷痛 ,疼痛剧烈持续不能缓解 ,伴大汗 ,含服硝酸甘油不能缓解 ,心电图示急性心肌损伤 ,STⅡⅢ 、αVF、V2 ～V6 弓背抬高 ,心肌酶迅速升高 .既往有甲亢病史十余年 ,吸烟 .体查 :BP110 /6 8mmHg ,神清 ,双侧甲状腺Ⅰ度肿大无血管杂音 ,双肺 (- ) ,心界不大 ,心音低钝 ,心率 82次 /分 ,律齐 ,…     

冠脉微循环障碍的研究进展

冠脉微循环（Coronary Microvascular）是指心脏中由微动脉（＜300μm）、毛细血管（平均8μm）和微静脉（＜500μm）构成的微循环系统,当冠脉微循环系统受到一种或多种不良因素影响出现异常后即发生冠脉微循环障碍,也有学者将后者称为冠脉微血管功能不全（Coronary Microvascular Dysfunction,CMVD）。近年来随着介入治疗的广泛开展,冠脉微循环障碍的各种类型在临床上均屡见不鲜,包括冠心病或急性心肌梗死患者通过冠脉支架植入术或冠脉旁路移植术使血管再通后出现的无复流现象;     

阿托伐他汀对急性心肌梗死大鼠内皮微颗粒及心肌细胞凋亡的影响

目的:探讨阿托伐他汀(atorvastatin,AT)对大鼠急性心肌梗死早期内皮微颗粒(endothial microparticles,EMP)及心肌细胞凋亡的影响。方法:将24只雄性SD大鼠随机分为假手术组(sham组)、心肌梗死组(MI组)和阿托伐他汀心肌梗死组(MI+AT组),每组8只。采用冠状动脉结扎制作急性心肌梗死大鼠模型。分别在造模后2 h和24 h采外周血检测肌酸激酶同工酶(creatine kinase-MB,CK-MB)、心肌肌钙蛋白T(cardiac troponin T,c Tn T)和EMP,其中循环EMP用流式细胞术检测。通过TUNEL检测心肌细胞凋亡情况。结果:造模后2 h,MI组大鼠的CK-MB表达水平较sham组大鼠显著升高(P0.05);MI组及MI+AT组大鼠EMP表达水平及心肌细胞凋亡率上升,显著高于sham组(P0.05)。造模后24 h,MI组大鼠EMP表达水平显著高于sham组(P0.05);MI+AT组大鼠CK-MB、c Tn T、EMP表达水平及心肌细胞凋亡率较MI组显著降低(P0.05)。此外,MI组大鼠的CKMB表达水平在造模后24 h较造模后2 h显著升高(P0.05);MI+AT大鼠CK-MB、c Tn T和EMP表达水平在造模后24 h较2 h显著下降(P0.05)。结论:AT可降低大鼠急性心肌梗死时的EMP水平和心肌细胞凋亡率,提示AT对内皮功能有保护作用。     

冠脉介入治疗对冠心病急性心肌梗死患者 心肌损伤及心室重塑的影响

目的 观察冠脉介入治疗对冠心病急性心肌梗死患者心肌损伤及心室重塑的影响。方法 选取我院自2017年9月~12月收治的64例冠心病急性心肌梗死患者作为观察对象,随机分为研究组33例和对照组31例。对照组给予吸氧、镇静、对症治疗,并给予氯吡格雷+阿司匹林口服,研究组在此基础上进行冠脉介入治疗,对比两组CK、CK-MB、BNP及LVEF、LFESV、LVEDV变化情况。结果 在治疗3 d、7 d后,研究组BNP水平均低于对照组,差异有统计学意义（P＜0.05）。研究组CK峰值、CK-MB峰值与对照组比较,差异无统计学意义（P＞0.05）,但研究组CK峰值、CK-MB峰值出现时间均短于对照组,差异有统计学意义（P＜0.05）。治疗7 d后,两组患者LVEF均升高,LFESV、LVEDV均降低,且研究组LVEF高于对照组,LFESV、LVEDV低于对照组,差异均有统计学意义（P＜0.05）。结论 冠脉介入治疗冠心病急性心肌梗死患者可降低患者BNP水平,改善患者心肌损伤,促进心室重塑,具有较高的应用价值。     

微颗粒与急性冠脉综合征

Coronary heart disease (CHD) is an important cause of death in the world. Among them, acute coronary syndrome (ACS) is a type of CHD that has a high mortality rate. Microparticles (MPs) are tiny particles formed in the process of cell activation and apoptosis, carrying specific markers of their mother cells. There is more and more evidence that MPs derived from endothelial cells, platelets, white blood cells and other cells are closely related to the formation of ACS. Through a variety of pathways, they take part in endothelial cell damage, vascular dysfunction, plaque erosion and rupture, and thrombosis. The findings of MPs enrich our knowledge about ACS, and may provide a new approach to the treatment of ACS.     

冠脉痉挛致急性下壁、右室、正后壁心肌梗死1例

<正>急性心肌梗死(AMI)罪犯血管多为具有一定狭窄程度病变的冠状动脉血管,多由不稳定斑块破裂和继发血栓形成引起冠脉血流完全中断所致。正常冠脉较少发生急性心肌梗死。本文就我院2012年3月收治的1例冠脉痉挛引起的急性心肌梗死报道分析如下。1资料与方法1.1临床资料患者,男,57岁,因间断性胸痛2个月,劳累后加重10 h入院,既往高血压病史5年,平时规律服药,血压控制尚可。入院     

择期经皮冠脉介入术对急性心肌梗死心肌微循环的作用

目的应用心肌声学造影(MCE)评价急性心肌梗死(AMI)患者择期经皮冠脉介入术(PCI)前后的心肌微循环。方法选择20例AMI患者,在择期PCI治疗前、后分别应用声诺维(SonoVue)静脉注射,行间歇触发、二次谐波MCE检查,应用声学密度分析软件(AD)定量测定心肌微循环内造影剂的声学峰值强度(PI)、曲线下面积(AUC)。结果治疗前梗死相关节段的PI、AUC明显低于正常灌注节段(P<0.001);择期PCI治疗后梗死节段的PI、AUC仍明显低于正常节段(P<0.001),但较PCI前明显升高(P<0.001),校正后的PIr、AUCr亦明显升高(P<0.001);而正常灌注节段的PI、AUC在PCI前后无明显变化(P>0.05)。结论MCE可定量评定AMI患者的心肌微循环;择期PCI可改善AMI患者梗死节段的微循环。     

冠脉微循环观察与中医望诊

<正>中医对心血管疾病的望诊以舌诊和面部望诊为主。过去由于方法学的限制,冠脉微循环观察相对困难,随着心血管影像学技术的快速发展,使评价冠脉微循环功能、结构状态成为可能,并为临床中医望诊提供了极有价值的平台和广阔前景。     

冠脉介入治疗后心肌梗死区灌注程度及存活对左室重构及功能的影响

评价冠脉介入治疗（PCI）后核素显像心肌梗死区灌注程度及存活对左室重构及功能的影响。选取20例急性前壁心肌梗死患者,男18例,女2例。梗死后20h内,梗死相关血管已接受冠状动脉介入治疗,冠脉血流正常。所有患者PCI术后10天内接受静息状态下双核素心肌显像（心肌灌注及心肌代谢显像）。根据基线梗死区灌注减低程度和心肌有无存活,分为两组,通过超声心动观察不同组患者12个月后左室舒张末直径（LVEDD）及左室收缩功能（LVEF）的变化,观察梗死区心肌存活状态及灌注情况对于左室重构的影响,间接反映其对自身心肌干细胞修复功能的影响。结果表明,梗死心肌有存活的患者（n=10）与无存活组（n=10）相比,两组12个月后LVEDD都无明显变化。梗死心肌有存活的患者LVEF有所改善,43.6±7.83 vs.46.79±12.68,无存活组LVEF轻度下降,39.10±8.71 vs.37.70±7.57,P〉0.05。梗死区灌注减低程度不同的两组患者PCI术后12个月,LVEDD都无明显变化。LAD PER%〈50%组（n=9）LVEF值有所改善,39.89±10.19%vs.42.22±13.54%,但变化不具有显著性,P〉0.05;LAD PER%〉50%组（n=11）LVEF值无改善,并可见轻度下降,42.55±6.86%vs.41.20±8.32%。LAD PER%〈50%且同时梗死区有存活心肌的患者（n=5）LVEF改善明显,上升了4.8%,与LAD PER%〉50%且同时梗死区无存活心肌的患者（n=6）相比具有统计学意义,P=0.029。结论：急性前壁心肌梗死并行PCI治疗的患者,心肌灌注程度不同与梗死区心肌是否有存活都对患者的左室重构改善无明显影响,但心肌灌注程度较好的患者和有心肌存活的患者左室收缩功能都有轻度改善;尤其值得注意的是,在心肌灌注程度较好,并且有存活心肌存在的情况下,心功能改善明显。而相对梗死区灌注差且无心肌存活的患者,12个月后,心功能减低,左室重构更加明显。     

睾酮对大鼠心肌梗塞后心肌肥大的影响

本文应用立体形态定量技术,观察睾酮(T)对心肌梗塞后心肌肥大的影响。实验分为:假手术组(S组)、心肌梗塞组(MI组)。心肌梗塞后睾酮治疗组(MIT组)。结果证明,与S组相比,MI及MIT组大鼠心肌细胞核密度明显减少,尤其以MIT组变化显著,MIT组平均核长度明显增加;MI组的 dp/dt max明显降低,T值延长,MIT组的上两指标无显著差异。MI后血浆T总浓度与平均每核心肌细胞体积呈显著正相关关系。提示:睾酮确实促进了MI后心肌肥大,从而促进了心功能的恢复。     

Chronic lymphocytic leukemia involving the coronary arteries with accompanying acute myocardial infarction

An 83-year-old man with chronic lymphocytic leukemia (CLL) for 10 years presented with dyspnea and hypotension. Blood investigations and electrocardiogram were consistent with acute myocardial infarction. The patient deteriorated quickly and died shortly thereafter. At autopsy, there was severe atherosclerosis of the coronary arteries and an inferolateral left ventricular wall myocardial infarct. Microscopy showed that CLL involved the nodes, liver, spleen, bowel, and kidneys. The coronary artery walls were infiltrated with leukemia cells invading the tunica media and the atheromatous plaque. Infiltration of the coronary arteries by CLL is not common and the possible role in coronary syndromes is discussed.     

当归对大鼠心肌梗死后心肌纤维化的影响及机制

目的： 观察转化生长因子-β1(TGF-β₁)、巨噬细胞在心肌梗死后心肌纤维化发生发展过程中的变化及当归的治疗作用，探讨心肌梗死后心肌纤维化的发生及当归的干预机制。 方法： 结扎SD大鼠冠脉前降支复制心肌梗死模型，随机分为假手术（sham）组、心肌梗死（MI）组和心肌梗死当归（MI+angelica）组。术后24 h开始给药，MI+angelica组腹腔注射当归（20 mL·kg^-1·d^-1，相当于生药10 g·kg^-1·d^-1），sham组和MI组腹腔注射等量生理盐水。于术后1、2、4周记录左室血流动力学改变，检测非梗死区心肌胶原含量、TGF-β₁及巨噬细胞的变化。 结果： ① MI组和MI+angelica组非梗死区心肌TGF-β₁及巨噬细胞阳性表达显著高于sham组（P<0.01），以1周的阳性表达为最高，但MI+angelica组低于MI组（P<0.01）；② 术后各时点MI组心功能受损，于术后2周和4周心肌胶原含量明显高于sham组（P<0.01）；术后4周MI+angelica组心功能损害轻于MI组，心肌胶原含量低于MI组（P< 0.01）。 结论： 当归通过抑制巨噬细胞在非梗死区的浸润、下调TGF-β₁的表达，阻断促纤维化发生的环节，减轻心肌梗死后非梗死区反应性胶原的过度沉积，防治心肌梗死后心肌纤维化，改善心脏功能。     

Alterations in vasomotor control of coronary resistance vessels in remodelled myocardium of swine with a recent myocardial infarction

The mechanism underlying the progressive deterioration of left ventricular (LV) dysfunction after myocardial infarction (MI) towards overt heart failure remains incompletely understood, but may involve impairments in coronary blood flow regulation within remodelled myocardium leading to intermittent myocardial ischemia. Blood flow to the remodelled myocardium is hampered as the coronary vasculature does not grow commensurate with the increase in LV mass and because extravascular compression of the coronary vasculature is increased. In addition to these factors, an increase in coronary vasomotor tone, secondary to neurohumoral activation and endothelial dysfunction, could also contribute to the impaired myocardial oxygen supply. Consequently, we explored, in a series of studies, the alterations in regulation of coronary resistance vessel tone in remodelled myocardium of swine with a 2 to 3-week-old MI. These studies indicate that myocardial oxygen balance is perturbed in remodelled myocardium, thereby forcing the myocardium to increase its oxygen extraction. These perturbations do not appear to be the result of blunted β-adrenergic or endothelial NO-mediated coronary vasodilator influences, and are opposed by an increased vasodilator influence through opening of K_ATP channels. Unexpectedly, we observed that despite increased circulating levels of noradrenaline, angiotensin II and endothelin-1, α-adrenergic tone remained negligible, while the coronary vasoconstrictor influences of endogenous endothelin and angiotensin II were virtually abolished. We conclude that, early after MI, perturbations in myocardial oxygen balance are observed in remodelled myocardium. However, adaptive alterations in coronary resistance vessel control, consisting of increased vasodilator influences in conjunction with blunted vasoconstrictor influences, act to minimize the impairments of myocardial oxygen balance.     

大鼠实验性左室心肌梗塞对右室收缩性能的影响

对左室心肌梗塞(MI)是否会直接影响右室功能,至今尚有争议。本实验观察大鼠左室MI时右室dp/dt max的改变及其与左室dp/dt max和梗塞范围(IS)间的关系。结果发现冠脉结扎后1天,在左室dp/dt max显著降低的同时,右室dp/dt max也显著降低,且与左室dp/dt max呈显著的直线正相关,而与IS呈显著的直线负相关。在冠脉结扎后3天时,左室dp/dt max有显著恢复,但仍低于对照水平,而右室dp/dt max已恢复正常,且与左室的dp/dt max和IS间不再具有显著的直线相关关系。由此证明;在大鼠左室MI早期,右室收缩性能可受到直接影响,影响的程度与IS及左室收缩性能降低的程度相关;但当左室收缩性能恢复到一定程度时,这种影响消失。     

氟伐他汀对大鼠心肌梗死后心室重塑的影响

目的:探讨羟甲基戊二酰辅酶A还原酶抑制剂氟伐他汀对SD大鼠心肌梗死后心室重塑的过程及心功能的影响。方法:SD大鼠冠状动脉前降支结扎形成心肌梗死,24h后存活的大鼠随机分成心肌梗死(AMI)对照组和氟伐他汀治疗组,治疗组予以氟伐他汀20mg·kg^-1·d^-1灌胃给药,对照组予以蒸馏水灌胃;另设假手术组。8周后进行心脏超声、血液动力学检测判定心脏功能和进行心脏形态学分析;同时检测血浆总胆固醇(Tch)、肌酐(Cr)、天冬氨酸氨基转移酶(AST),NO₂^-/NO₃^-、谷胱甘肽过氧化物酶(glutathioneperioxidase,GSH-PX)以及血浆、心肌脂质过氧化物(LPO)水平。结果:氟伐他汀组血浆Tch水平与AMI组比较没有显著性差异,平均主动脉压和心率差别无显著性,显著降低了左室舒张末压和减少了肺相对重量(P＜0.05);减少了右室相对重量、左室后壁厚度、肺相对重量和心肌纤维化(P＜0.05,P<0.01);降低了血浆和心肌的LPO的水平,抑制NO₂^-/NO₃^-的过度表达,增加了GSH-PX的表达(P＜0.05);血浆Cr和AST水平无显著差别(P＞0.05)。结论:氟伐他汀改善大鼠AMI后心室重塑,相对延缓心力衰竭的进展;氟伐他汀抗氧化机制可能参与这个过程。     

芪苈强心对心肌梗死后大鼠心肌细胞凋亡的影响

目的: 探讨芪苈强心对心肌梗死大鼠心肌细胞凋亡的影响。方法: 结扎冠脉前降支制作大鼠心肌梗死模型,随机分为假手术组(sham, n=5)、心肌梗死组(MI, n=16)和芪苈强心组(4 g·kg^-1·d^-1, n=15),28 d后检测心肌梗死面积,TUNEL法检测心肌细胞凋亡指数(AI),免疫组化法检测Fas蛋白表达,Western blotting检测黄嘌呤氧化酶(XO)和caspase-3蛋白表达,比色法测定XO和清除活性氧活性。结果: MI组非梗死区心肌细胞AI升高,Fas、XO和caspase-3蛋白表达增强,XO活性增加,清除活性氧活性降低(P<0.01)。芪苈强心组与MI组比较,非梗死区心肌细胞AI降低,Fas和caspase-3蛋白表达减少,XO活性降低,清除活性氧活性升高(P<0.01),但梗死面积和XO蛋白表达在两组间无显著差异(P>0.05)。结论: 芪苈强心能够抑制非梗死区心肌细胞凋亡,其作用机制可能与减少活性氧簇生成及降低Fas和caspase-3的表达有关。     

吡格列酮对心肌梗死大鼠心肌能量代谢及血流动力学的影响

目的: 探讨吡格列酮对心肌梗死后大鼠心肌能量代谢及血流动力学的影响。方法: 采用开胸结扎冠状动脉左前降支建立心肌梗死模型,取术后72 h存活的20只大鼠随机分为手术组(MI组,n=10)和吡格列酮干预组(P组,n=10,吡格列酮3 mg·kg^-1·d ^-1灌胃8周),另设假手术组(SH组,n=10)。分别喂养8周后用Western blotting法测定大鼠心肌组织中过氧化物酶体增殖物激活受体γ(PPARγ)的蛋白表达水平。用生物组织氧耗测量仪测定线粒体氧化呼吸活性,高效液相层析法(HPLC)法测量线粒体内腺苷酸含量;氚标记二磷酸腺苷(-ADP)掺入法检测线粒体膜腺苷酸转运体(ANT)转运活性,经颈动脉插管测定血流动力学参数,并计算心室重塑指标。结果: 与SH组比较,MI组PPARγ的蛋白表达水平明显下调(P<0.01),线粒体内高能磷酸盐含量、呼吸活性和ANT转运活性明显降低(P<0.01),血流动力学指标紊乱(P<0.01); 与MI组比较,吡格列酮8周干预升高PPARγ的蛋白表达水平,改善心梗后心衰大鼠线粒体呼吸活性及ANT转运活性,增加线粒体内高能磷酸盐含量(P<0.01),但血流动力学指标改善不显著。结论: 心肌梗死后心力衰竭过程中,吡格列酮干预活化PPARγ,升高PPARγ蛋白的表达,可改善心力衰竭大鼠心肌能量代谢;但对血流动力学指标改善不显著。     

Pathological evaluation of coronary lesions in cases of cardiac rupture during acute myocardial infarction: An autopsy study of 148 out-of-hospital sudden death cases

We pathologically evaluated coronary artery lesions of left ventricular ruptures during acute myocardial infarctions (148 sudden out-of-hospital death cases; 93 men and 55 women; age range 42–94 years; mean age 68.9 years; 143 atherosclerotic and 5 non-atherosclerotic lesions). Among the 143 hearts with atherosclerotic coronary lesions, three-vessel disease was most frequent, and plaque rupture or erosion and occlusive thrombus were identified in most cases. Ages of the main component of the occlusive thrombus in the culprit coronary artery corresponded histopathologically to those of myocardial infarction. One of the most outstanding features in this pathological study is that acute thrombus in the culprit coronary artery was identified morphologically in most of the cases with advanced myocardial infarction (3 or more days). On the other hand, in cases of fresh myocardial infarction, a preceding mural non-occlusive organizing thrombus was observed mostly underneath the main component of the thrombus. It is suggested that, in most cases, cardiac rupture during acute myocardial infarction occurs at the time of a new ischemic event caused by a new thrombotic coronary lesion.     

Effect of isometric exercise on catecholamines in the coronary circulation

Summary Arterial and coronary sinus blood levels of catecholamines, adenosine 3, 5-cyclic monophosphate (c-AMP) and lactate were measured during isometric exercise in fourteen patients. In no patient did lactate production occur. Mean resting total catecholamine levels both arterial (0.53±0.07 ng/ml; 2.94±0.38 nmol/l) and coronary sinus (0.4±0.08 ng/ml; 2.22±0.44 nmol/l), did not change significantly on exercise. Coronary sinus c-AMP levels fell on exercise from 11.5±0.8 nmol/l (resting) to 9.9±0.8 nmol/l (exercise) (P<0.01) with an arterial-coronary sinus difference of 1.2 nmol/l (P<0.01) on exercise.Our findings suggest that isometric exercise does not normally result in excessive cardiac symphathetic activity.