Prevalence of normal coronary angiography in the acute phase of suspected ST-elevation myocardial
中医“治未病”理念在脂肪肝防治中的体现
总第22卷256期2020年12月大众科技Popular Science&TechnologyVol.22No.12December2020中医“治未病"理念在脂肪肝防治中的体现刘谢盛庆寿(广西中医药大学，广西南宁530001)【摘要】中医"治未病”是预防医学的重要组成部分，其理念涵盖了未病先防、既病防变、瘻后防复三个层面。
脂肪性肝病是我国最常见慢性肝病，文章将中医"治未病”理念贯穿脂肪肝的防治始末，对脂肪肝早防御、早发现、早治疗，从而降低治疗成本，提高治疗效率，为临床实践提供新思路。
【关键词】治未病；脂肪肝；防治【中图分类号】R575【文献标识码】A【文章编号】1008-1151(2020)12-0092-03 Embodiment of the Concept of"Preventive Treatment of Disease"of TraditionalChinese Medicine in the Prevention and Treatment of Fatty Liver Abstract:"Preventive treatment of disease**in traditional Chinese medicine is an important part of preventive medicine.Its concept covers three aspects:prevention before disease,prevention of b oth diseases,prevention and recovery after treatment.IF a tty liver disease is the most common chronic liver disease in China.In this paper,the concept of"preventive treatment of disease*'in traditional Chinese medicine runs through the prevention and treatment of fatty liver,so as to prevent,detect and treat fatty liver early,and so as to reduce the treatment cost and improve the treatment efficiency,and provide new ideas for clinical practice.Key words:preventive treatment of disease;fatty liver;prevention引言脂肪性肝病(Fatty Liver Disease,FLD)是由多种病因引起的肝细胞内脂肪堆积过多闪、肝细胞变性、炎性渗出、甚至肝细胞坏死的肝脏病理性表现。
医学论文写作英语：Glamour of Grammar
It can work as grammatical connectors.
e.g.: If dysphagia is present, the radiologist
should… In the presence of dysphagia but a normal
barium swallow endoscopy is indicated.
cf.：
Immunohistochemical analysis of paraffin embedded specimens of eight colon tumours and normal colon mucosa in rats treated with AOM was performed.
English for Writing Medical Research Papers
Glamour of Grammar
I. Nominalization
Definition
Nominalization refers to the use of nouns in place of adjectives, verbs or even clauses.
aggressive immunosuppressive marrow ablative treatment of the recipient.
Fronting is preferred. In EMP and other EST articles, more information is put into the subject. This way of building up the subject is called fronting, which can catch the reader’s attention. e.g.:
铁死亡在心血管疾病中的调节途径及作用
syndromes in patients with angiographically normal or nearnormal(non-obstructive)coronary arteries[J].T rends in CardiovascularMedicine,2018,28(8):541-551.[16]SCALONE G,NICCOLI G,CREA F.Editor's Choice-pathophysiology,diagnosis and management of MINOCA:anupdate[J].European Heart Journal Acute Cardiovascular Care,2019,8(1):54-62.[17]RIEBER J,HUBER A,ERHARD I,et al.Cardiac magneticresonance perfusion imaging for the functional assessment ofcoronary artery disease:a comparison with coronary angiographyand fractional flow reserve[J].European Heart Journal,2006,27(12):1465-1471.[18]PEDRIZZETTI G,CLAUS P,KILNER P J,et al.Principles ofcardiovascular magnetic resonance feature tracking andechocardiographic speckle tracking for informed clinical use[J].Journal of Cardiovascular Magnetic Resonance,2016,18(1):1-12.[19]刘敏.心脏磁共振成像技术临床应用及进展[J].中华老年心脑血管病杂志,2021,23(5):449-451.[20]ZOU Q A,ZHENG T A,ZHOU S L,et al.Quantitative evaluation ofmyocardial strain after myocardial infarction with cardiovascularmagnetic resonance tissue-tracking imaging[J].InternationalHeart Journal,2020,61(3):429-436.[21]李坤成,张振.心脏MR特征追踪技术进展及其临床应用[J].中国医学影像技术,2022,38(1):1-5.[22]CARBERRY J,CARRICK D,HAIG C,et al.Persistence of infarctzone T2hyperintensity at6months after acute ST-segment-elevation myocardial infarction:Incidence,pathophysiology,andprognostic implications[J].Circ Cardiovasc Imaging,2017,10(12):e006586-e006586.[23]SONG L S,MA X H,ZHAO X X,et al.Validation of black blood lategadolinium enhancement(LGE)for evaluation of myocardialinfarction in patients with or without pathological Q-wave onelectrocardiogram(ECG)[J].Cardiovascular Diagnosis andTherapy,2020,10(2):124-134.[24]REINSTADLER S J,STIERMAIER T,LIEBETRAU J,et al.Prognostic significance of remote myocardium alterationsassessed by quantitative noncontrast T1mapping in ST-segmentelevation myocardial infarction[J].JACC:CardiovascularImaging,2018,11(3):411-419.[25]KIM R J,ALBERT T S,WIBLE J H,et al.Performance of delayed-enhancement magnetic resonance imaging with gadoversetamidecontrast for the detection and assessment of myocardialinfarction:an international,multicenter,double-blinded,randomizedtrial[J].Circulation,2008,117(5):629-637.[26]万俊义,赵世华.心脏磁共振钆对比剂延迟强化的临床意义及判断预后的价值[J].中国医学影像技术,2012,28(8):1600-1603. [27]VICENTE-IBARRA N,FELIU E,BERTOMEU-MARTÍNEZ V,et al.Role ofcardiovascular magnetic resonance in the prognosis of patientswith myocardial infarction with non-obstructive coronary arteries[J].Cardiovasc Magn Reson,2021,23(1):83.(收稿日期:2022-08-29)(本文编辑邹丽)铁死亡在心血管疾病中的调节途径及作用王世远,李虹摘要阐述铁死亡的调节途径及其在心血管疾病(CVD)中的作用㊂CVD是我国乃至世界人口死亡和影响生活质量的主要原因,目前,经典的细胞死亡不能完全解释CVD的发生㊁发展,铁死亡的发现进一步补充了CVD发生的可能原因,同时,自噬在铁死亡中发挥着重要作用㊂关键词铁死亡;心血管疾病;自噬;综述d o i:10.12102/j.i s s n.1672-1349.2023.15.016心血管疾病(cardiovascular disease,CVD)是指一组包括心脏病㊁血管病㊁心力衰竭㊁心律失常㊁心脏瓣膜病㊁心肌病㊁心内膜炎等的循环系统疾病㊂CVD的预防㊁治疗㊁预后成为世界范围内生命健康的重要问题㊂细胞死亡在CVD的发生中至关重要㊂一般情况下,心肌细胞和血管细胞死于调节性细胞死亡(RCD),而非意外细胞死亡(ACD),铁死亡(ferroptosis)作为RCD中的新成员,补充了CVD的发生,且自噬在其中发挥重要作用㊂了解铁死亡的调节途径及其在CVD 中的作用,为CVD病人获取更大收益㊂1铁及铁死亡铁是一种微量元素,成人体内含有3~5g的总铁,其中2/3以血红蛋白和肌红蛋白的形式存在,近1/3储存在蛋白中即铁蛋白,而细胞外铁仅占全身铁的0.1%作者单位山西医科大学第二医院(太原030001)通讯作者李虹,E-mail:**********************引用信息王世远,李虹.铁死亡在心血管疾病中的调节途径及作用[J].中西医结合心脑血管病杂志,2023,21(15):2799-2802.左右㊂在机体内,补充铁流失的途径主要有两种,一是在脾脏和其他器官巨噬细胞的作用下,吞噬衰老或损伤的红细胞,释放其中的铁到循环中用于合成血红素[1];二是通过饮食摄入铁[2]㊂铁是参与多种生物过程的必需矿物质元素,如血红素合成㊁DNA合成㊁蛋白质合成㊁催化反应㊁细胞呼吸㊁整体代谢等[3-5]㊂机体铁稳态主要依靠铁调素(hepcidin,阻止细胞铁外流作用)-膜铁转运蛋白(FPN)轴来调节[1]㊂CVD的发生与铁的过载或缺乏密切相关㊂目前,细胞死亡可分为ACD和RCD两种形式[6]㊂RCD主要包括:细胞凋亡(apoptosis)㊁自噬(autophagy)㊁坏死性凋亡(necroptosis)㊁细胞焦亡㊁依赖性细胞死亡(parthanatos)㊁内源性细胞死亡(entosis)㊁溶酶体依赖性细胞死亡(lysosome-dependent cell death,LDCD)㊁氧中毒(oxeiptosis)等形式[7]㊂2012年,Dixon等[8]提出一种新型细胞死亡形式,其特点为非凋亡性㊁铁依赖性的,即铁死亡㊂铁死亡作为RCD新的一员,其线粒体具有致密紧凑㊁嵴缺失㊁膜浓缩及外膜破裂的特点[9]㊂其发生过程中,过载铁在细胞内积聚产生活性氧(ROS),氧化多不饱和脂肪酸,造成细胞膜结构的破坏,最终导致细胞死亡[8]㊂研究表明,铁死亡参与CVD㊁神经退行性疾病㊁肿瘤㊁脑卒中㊁中毒性损伤等多种疾病的发生㊂2铁死亡与自噬自噬是生物体内细胞重要的代谢过程,将衰老或损伤的蛋白质㊁细胞器分解成氨基酸和脂肪酸,可进入循环再次被利用和供应能量,以便维持内环境稳态[10]㊂细胞自噬主要分为以下几个过程:初始自体吞噬泡的形成㊁中间自体吞噬泡的形成㊁降解自体吞噬泡的形成[11]㊂按照溶酶体转运方式和生理功能,自噬主要分为巨自噬㊁微自噬㊁分子伴侣介导的自噬[12]㊂已有研究表明,选择性自噬如铁蛋白吞噬㊁脂肪吞噬㊁时钟吞噬㊁分子伴侣介导的自噬等在铁死亡过程中不可或缺[13];自噬的调节因子如Beclin1㊁核因子E2相关因子2(nuclear factor erythroid derived2-like2, Nrf2)㊁信号转导和转录激活因子3(signal transducer and activator of transcription3,STAT3)㊁p53在铁死亡中发挥着重要的调节作用[14]㊂在生物体内,自噬作用的缺乏或过度均会导致不同程度的RCD[15-16]㊂3铁死亡的调节途径3.1铁代谢细胞内的铁稳态取决于铁的吸收㊁利用㊁储存和排泄之间的动态平衡㊂铁具有活跃的氧化还原能力和不成对的电子特点,成为铁死亡重要的基础因素㊂在正常生物机体内,分泌的胃酸将食物中的Fe3+还原为Fe2+,在十二指肠和空肠上段被吸收㊂在芬顿(Fenton)和类芬顿反应中,Fe2+和过氧化氢(H2O2)反应产生大量羟基自由基和脂质过氧化物,最终导致铁死亡[17]㊂血红素加氧酶1(Hmox1)可将血红素降解生成Fe2+,使游离铁水平增加,进一步导致铁死亡的发生[18-19]㊂在铁蛋白吞噬中,核受体共激活因子4 (NCOA4)将铁蛋白转化为细胞内铁的自噬,并产生游离铁[20-22]㊂研究发现,转录因子BTB结构域和CNC 同源物1(BACH1)是铁代谢的调节剂,在铁死亡中发挥一定作用[23]㊂还有研究发现,由铁蛋白应激诱导的Prominin2可抑制铁蛋白细胞的死亡[24]㊂3.2脂质过氧化多不饱和脂肪酸(PUFAs)是构成细胞膜的重要成分,对维持细胞膜的功能起到重要作用,而PUFAs与自由基相互作用发生的脂质过氧化正是铁死亡的主要原因[25]㊂在长链脂酰辅酶A合成酶4(ACSL4)的催化作用下,PUFAs中的花生四烯酸(AA)和肾上腺酸(AdA)分别合成相应的脂酰辅酶AA-CoA和AdA-CoA,参与膜磷脂的合成,其产物在溶血卵磷脂酰基转移酶3 (LPCAT3)的催化作用下,发生酯化反应生成磷脂酰乙醇胺PE-AA和PE-AdA,再被脂氧合酶(LOXs)或细胞色素P450氧化还原酶(POR)氧化成脂质过氧化产物PE-AA-OOH和PE-AdA-OOH[26]㊂正常情况下,这些有害物质可被谷胱甘肽过氧化物酶4(glutathione peroxidase4,GPX4)还原成没有毒性的脂醇;相反,当机体GPX4处于低水平,其抗氧化作用降低,过氧化物产物会过度积累,引起铁死亡的发生[27-29]㊂3.3Xc-谷胱甘肽(GSH)-GPX4途径GSH具有重要的抗氧化和清除自由基的作用,在谷氨酸-半胱氨酸连接酶(GCL)和谷胱甘肽合酶(GSS)的催化作用下,产生谷氨酸㊁半胱氨酸和甘氨酸㊂GSH有两种形式,还原形式(GSH)和氧化二硫化物形式(GSSG),在自由基等条件刺激下,GPX4发挥其抗氧化或催化脂质氢过氧化物的还原作用,将GSH 转化为GSSG,并将脂质过氧化物(L-OOHs)还原为其相应的脂质醇(L-OHs),限制了脂质过氧化在膜中的扩散,从而减少铁死亡的发生[9,30-32]㊂System Xc-是一种胱氨酸/谷氨酸逆向转运蛋白,可促进胱氨酸和谷氨酸在质膜上的交换,合成GSH[33]㊂相关研究表明,当抑制System Xc-时,可进一步抑制GPX4的抗氧化作用,最终发生铁死亡[34]㊂3.4铁死亡抑制蛋白1(FSP1)-辅酶Q10(CoQ10)-NAD(P)H途径FSP1-CoQ10-NAD(P)H途径是一种与Xc-GSH-GPX4通路协同作用的独立系统,其可独立清除过多的脂质过氧化物,抑制铁死亡的发生[35-36]㊂NADPH是除GSH之外的另一种抗氧化化合物,可通过减少脂质ROS来抑制铁死亡;FSP1是一种氧化还原酶,在NAD(P)H作用下,将泛醌(亦称辅酶Q10,CoQ10)还原为泛醇(CoQH2),CoQH2可通过捕获脂质过氧自由基,抑制脂质过氧化和铁死亡的发生[37]㊂CoQH2是甲羟戊酸途径产生的CoQ10还原形式,抑制甲羟戊酸途径可能会减少CoQ10生成量,进而导致铁死亡[38]㊂3.5三磷酸鸟苷环水解酶1(GCH1)-四氢生物蝶呤(BH4)-二氢叶酸还原酶(DHFR)途径GCH1-BH4-DHFR通路是一种独立于Xc-GSH-GPX4途径的通路,在敲除GPX4诱导铁死亡的模型中,GCH1发挥其保护作用,对其他形式的细胞死亡具有选择性[39]㊂GCH1既是BH4的起始酶,又是限速酶,调节着BH4的含量,DHFR可调节BH4的生成[40]㊂BH4是一种内源性自由基捕获抗氧化剂,通过捕获脂质衍生的过氧自由基阻断脂质过氧化,保护脂质膜免受自身氧化[40]㊂因此,可以得出GCH1-BH4-DHFR通路可通过阻断脂质过氧化抑制铁死亡㊂3.6线粒体线粒体的独有特点 电压依赖性阴离子通道(VDAC)是位于线粒体外膜的蛋白质,当这些蛋白细胞越多,发生铁死亡的敏感性就越高[41]㊂线粒体同样参与着铁死亡的发生,其机制还包括胱氨酸饥饿㊁谷氨酰胺分解,升高膜电位和亚铁含量,促进芬顿反应和脂质过氧化发生,最终造成铁死亡[42-43]㊂4铁死亡与心血管疾病4.1动脉粥样硬化(atherosclerosis,AS)AS是一种以脂质代谢异常为特征的病理过程,主要由脂质沉积㊁内皮细胞损伤㊁氧化应激㊁血管平滑肌细胞(VSMC)增殖㊁巨噬细胞转化㊁炎症和免疫功能障碍等引起[44-45]㊂研究表明,抑制铁死亡可通过减轻脂质过氧化和内皮功能障碍缓解AS,在体内,铁死亡抑制剂Fer-1可减轻高脂饮食的ApoE-/-小鼠诱导的AS 和脂质过氧化;体外细胞实验研究表明,Fer-1可改善氧化型低密度脂蛋白(ox-LDL)诱导的铁死亡和内皮功能障碍[46]㊂4.2心肌梗死(myocardial infarction,MI)MI在全世界具有非常高的致死率㊂研究表明,在MI小鼠模型中,MI部位的铁蛋白重链1(FTH1)水平下降,引起游离铁水平升高和氧化应激发生,促进心肌细胞铁死亡,导致心肌细胞死亡和MI发生[47]㊂有研究表明,与正常组织相比,MI组织中GPX4蛋白的数量减少,引起铁死亡,最终导致MI的发生[48]㊂4.3缺血/再灌注损伤(I/R)I/R通常是指急性心肌梗死血管再通最严重的并发症[49]㊂尤其在再灌注阶段,会产生大量的ROS和自由基,引起心肌细胞损伤坏死和铁死亡[50-51]㊂铁死亡抑制剂Liproxstatin-1(Lip-1),通过降低线粒体上的电压依赖性阴离子通道1(VDAC1)㊁ROS水平和增加GPX4水平保护心肌免受I/R损伤[52-53]㊂由此得出,铁死亡可引起I/R损伤[54]㊂4.4心力衰竭(heart failure,HF)HF是大多数CVD的终末阶段,心脏发生重塑由代偿变为失代偿,出现心肌肥厚和纤维化,最终导致心脏功能的下降[55]㊂已有研究表明,在HF中Toll样受体4(TLR4)和NADPH氧化酶4(NOX4)明显上调,而当敲除TLR4和NOX4时可显著抑制自噬和铁死亡,并对抗心脏重塑和改善心脏功能,为治疗HF提供了基础[56]㊂4.5心肌病阿霉素(DOX)是一种常用的第二代蒽环类抗癌药物,具有很强的心肌毒性,最终导致心肌病㊂有研究表明,在DOX小鼠模型中,Nrf2通过增加血红素加氧酶1(heme oxygenase1,Hmox1)的含量,降解血红素,释放游离铁引起铁过载,导致心肌细胞铁死亡[57];而铁死亡抑制剂Fer-1在该模型中能减轻DOX所致心肌病[57]㊂铁死亡可能在糖尿病心肌病(diabetic cardiomyopathy,DCM)中存在一定作用,但目前机制尚不清楚㊂5小结铁死亡作为一种新的调节性细胞死亡形式出现,参与着CVD的发生㊂本研究一方面从铁代谢㊁脂质过氧化㊁Xc-GSH-GPX4途径㊁FSP1-CoQ10-NAD(P)H 途径㊁GCH1-BH4-DHFR通路㊁线粒体来阐明铁死亡的发生,为阻止铁死亡进而引起心血管疾病提供了研究基础;但其他调节途径机制目前尚未明确,例如能量应激(energy stress)㊁热休克蛋白(HSP)等,可成为进一步的研究点㊂另一方面主要阐明了铁死亡在AS㊁MI㊁I/R损伤㊁HF㊁DOX所致心肌病中的作用,为治疗CVD 提供了新的思路㊂参考文献:[1]PAPANIKOLAOU G,PANTOPOULOS K.Systemic iron homeostasis anderythropoiesis[J].IUBMB Life,2017,69(6):399-413.[2]GREEN R,CHARLTON R,SEFTEL H,et al.Body iron excretion inman:a collaborative study[J].The American Journal of Medicine,1968,45(3):336-353.[3]KOBAYASHI M,SUHARA T,BABA Y,et al.Pathological roles ofiron in cardiovascular disease[J].Current Drug Targets,2018,19(9):1068-1076.[4]ABBASPOUR N,HURRELL R,KELISHADI R.Review on iron andits importance for human health[J].Journal of Research inMedical Sciences,2014,19(2):164-174.[5]ALI M K,KIM R Y,BROWN A C,et al.Critical role for ironaccumulation in the pathogenesis of fibrotic lung disease[J].TheJournal of Pathology,2020,251(1):49-62.[6]TANG D L,KANG R,VANDEN BERGHE T,et al.The molecularmachinery of regulated cell death[J].Cell 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独刺鱼际穴治疗支气管哮喘急性发作验案
Advances in Clinical Medicine 临床医学进展, 2023, 13(10), 15435-15439Published Online October 2023 in Hans. https:///journal/acmhttps:///10.12677/acm.2023.13102158独刺鱼际穴治疗支气管哮喘急性发作验案葛楠1，李俐2*1福建中医药大学针灸学院，福建福州2福建中医药大学附属第二人民医院针灸科，福建福州收稿日期：2023年8月28日；录用日期：2023年9月21日；发布日期：2023年10月8日摘要近年来支气管哮喘的全球患病率、死亡率呈上升趋势，而支气管扩张剂等哮喘防治药物易产生免疫抑制、产生耐药性、增加呼吸道感染风险之弊端，使得哮喘的治疗陷入两难。
故探寻支气管哮喘急性发作期时低毒副作用且高效的治疗方法意义重大。
本文通过介绍独刺鱼际穴治疗支气管哮喘急性发作验案2则，阐释独刺鱼际穴对于哮喘急性发作时的临床效能，该法疗效显著、不良反应少，远期随访疗效佳，以期对临床诊疗哮喘有所裨益。
关键词鱼际穴，支气管哮喘，验案Treatment of Acute Attack of BronchialAsthma by Acupuncture Onlyat the Yuji PointNan Ge1, Li Li2*1School of Acupuncture and Moxibustion, Fujian University of Traditional Chinese Medicine, Fuzhou Fujian2Department of Acupuncture and Moxibustion, The Second Affiliated People’s Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou FujianReceived: Aug. 28th, 2023; accepted: Sep. 21st, 2023; published: Oct. 8th, 2023AbstractIn recent years, the global prevalence and mortality of bronchial asthma are on the rise. Howev-er, anti-asthma drugs such as bronchodilator asthma are prone to produce immunosuppression,*通讯作者。
血清内脂素、脂联素和C-反应蛋白与冠状动脉病变的相关性
血清内脂素、脂联素和C-反应蛋白与冠状动脉病变的相关性焦路阳;袁彬;袁晓梅;孙浩杰;袁宇【期刊名称】《新乡医学院学报》【年(卷),期】2012(029)008【摘要】目的探讨血清内脂素(Visfantin)、脂联素(APN)和C-反应蛋白(CRP)与冠状动脉病变的关系.方法 70例经冠状动脉造影确诊的冠状动脉粥样硬化性心脏病(冠心病)患者作为观察组,并根据血管病变情况分为单支病变组、双支病变组、多支病变组,另选20例健康体检者作为对照组,采用酶联免疫吸附试验测定血清Visfantin、APN、CRP水平,比较不同程度病变者血清Visfantin、APN、CRP的差异及其与冠状动脉病变的相关性.结果观察组血清Visfantin、CRP水平均显著高于对照组(P＜0.01),APN水平显著于低于对照组(P＜0.01).双支病变组和多支病变组血清CRP、Visfantin水平及Gensini积分均明显高于单支病变组(P＜0.05)；多支病变组血清Visfantin、CRP水平及Gensini积分显著高于双支病变组(P＜0.05).双支病变组和多支病变组的APN水平均低于单支病变组(P＜0.05),但双支病变组和多支病变组比较差异无统计学意义(P＞0.05).血清Visfantin与CRP(r=0.929,P＜0.001)、Gensini 积分(r=0.777,P＜0.001)呈正相关,与APN(r=-0.351,P＜0.001)呈负相关；APN与CRP(r=-0.873,P＜0.001)、Gensini积分(r=-0.740,P＜0.001)呈负相关；CRP与Gensini积分呈正相关(r=0.692,P＜0.001).结论血清Visfantin、APN、CRP均可能是冠心病的危险因素,对评估冠状动脉病变程度有重要价值.%Objective To discuss the relationships of serum visfatin,adiponectin(APN) and C-reactive protein(CRP) with coronary artery disease. Methods Seventy patients with coronary heart disease who wereconfirmed by coronary angiogra-phy were selected as observation group, and according to the number of vascular lesion, the patients were divided into three subgroup:single-vessel disease group,double-vessel disease group and muti-vessel disease group. In addition,20 healthy people were selected as control group. Serum visfatin, APN and CRP levels were measured by enzyme-linked immunosorbent assay. The differences of them in different severity of coronary artery disease patients and the the relationships of serum visfatin, APN and CRP with coronary artery disease were analyzed. Results Compared with the control group,serum visfatin and CRP levels were significantly increased (P<0.01) ,APN level was significantly decreased in observation group(P <0.01). Serum visfatin, CRP levels and Gensini points in double or multi-vessel disease group were significantly higher than in single-vessel disease group(P <0. 05) ;and the indexes in multi-vessel disease group were significantly higher than in double-vessel disease group (P<0.05). Serum APN level in double or multi-vessel disease group was higher than single-vessel disease group(P <0. 05). However, there was no significant difference in serum APN between double-vessel disease group and multi-vessel disease group (P>0. 05). Multiple correlation analysis showed that serum visfatin level was positively correlated with the serum level of CRP (r = 0. 929, P < 0. 001) and Genisini points ( r = 0. 777, P < 0. 001 ) , negatively correlated with the serum level of APN ( r = -0. 351 ,P <0. 001). Serum APN level was negatively correlated with the serum level of CRP (r = - 0. 873 ,P <0. 001) and Genisini points ( r = - 0. 740, P < 0. 001) . Serum CRP level waspositively correlated with Genisini points ( r = 0. 692, P < 0. 001) . Conclusion Visfatin, APN and CRP levels may be risk factors for coronary heart disease. They all have significant value to evaluate degree of coronary artery disease.【总页数】3页(P600-602)【作者】焦路阳;袁彬;袁晓梅;孙浩杰;袁宇【作者单位】新乡医学院第一附属医院检验科,河南卫辉 453100;新乡医学院第一附属医院神经内二科,河南卫辉 453100;新乡医学院第一附属医院呼吸内科,河南卫辉 453100;新乡医学院第一附属医院核医学科,河南卫辉 453100;新乡医学院第一附属医院心血管内二科,河南卫辉 453100【正文语种】中文【中图分类】R543.3【相关文献】1.血清内脂素、脂联素和C-反应蛋白在2型糖尿病肾病发生发展中作用的研究 [J], 毕进2.冠状动脉病变程度及Gemini积分与血清脂联素和高敏C反应蛋白的相关性 [J], 杨萌;王显良;王荦楠;蔡瑞艳3.血清C-反应蛋白(CRP)、内脂素、脂联素在2型糖尿病肾病不同时期的变化 [J], 潘苗;张黎;张晓虹;梁蕴谊4.血清内脂素、超敏C反应蛋白与冠状动脉病变的相关性分析 [J], 何全利;刘伟5.血清脂联素和超敏C反应蛋白水平与冠心病患者冠状动脉病变不稳定性及狭窄程度的相关性分析 [J], 杨美霞;李凌;刘刚琼因版权原因，仅展示原文概要，查看原文内容请购买。
The metabolic syndrome—a new worldwide definition
The metabolic syndrome (visceral obesity, dyslipidaemia, hyperglycaemia, and hypertension), has become one of the major public-health challenges worldwide.1There has been growing interest in this constellation of closely related cardiovascular risk factors. Although the association of several of these risk factors has been known for more than 80years,2the clustering received scant attention until 1988 when Reaven described syndrome X: insulin resistance, hyperglycaemia, hypertension, low HDL-cholesterol, and raised VLDL-triglycerides.3Surpris-ingly, he omitted obesity, now seen by many as an essential component, especially visceral obesity.1Various names were subsequently proposed, the most popular being metabolic syndrome.1The cause of the syndrome remains obscure. Reaven proposed that insulin resistance played a causative role,3 but this remains uncertain. Lemieux et al suggested visceral obesity and the hypertriglyceridaemic waist phenotype as a central component,4but this too has been contested. Several different factors are probably involved, many related to changes in lifestyle.1The ultimate importance of metabolic syndrome is that it helps identify individuals at high risk of both type 2 diabetes and cardiovascular disease (CVD). Several expert groups have therefore attempted to produce diagnostic criteria. The first attempt was by a WHO diabetes group in 1999, which proposed a definition that could be modified as more information became available.5The criteria had insulin resistance or its surrogates, impaired glucose tolerance or diabetes, as essential components, together with at least two of: raised blood pressure, hyper-triglyceridaemia and/or low HDL-cholesterol, obesity (as measured by waist/hip ratio or body-mass index), and microalbuminuria. The European Group for the Study of Insulin Resistance6then produced a modification of the WHO criteria excluding people with diabetes and requiring hyperinsulinaemia to be present. Waist circumference was the measure of obesity, with different cutoffs for the other variables.A fresh approach came from the US National Cholesterol Education Program: Adult Treatment Panel III in 2001, with a focus on cardiovascular disease risk.7The specific remit was to facilitate clinical diagnosis of high-risk individuals. It was less glucocentric than the definition from WHO and the European Group for the Study of Insulin Resistance, requiring the presence of any three of five components: central obesity, raised blood pressure, raised triglycerides, low HDL-cholesterol, and fasting hyperglycaemia.The different definitions inevitably led to substantial confusion and absence of comparability between studies. One difficulty has been that the conceptual framework used to underpin the metabolic syndrome (and hence drive definitions) has not been agreed on. Opinions have varied as to whether the metabolic syndrome should be defined to mainly indicate insulin resistance, the metabolic consequences of obesity, risk for CVD, or simply a collection of statistically related factors. Prevalence figures for the syndrome have been similar in any given population regardless of which definition is used, but different individuals are identified.8What matters, of course, is which produces the best prediction of subsequent diabetes and CVD. Thus Adult Treatment Panel III was superior to WHO in the San Antonio Study, but WHO gave better prediction of CVD in Finnish men.9,10 Another problem with the WHO and the Adult Treatment Panel definitions has been their applicability to different ethnic groups, especially as relates to obesity cutoffs.11For example, the risk of type 2 diabetes is apparent at much lower levels of adiposity in Asian populations than in European populations.12With current metabolic syndrome definitions, particularly Adult Treatment Panel III, suspiciously low prevalence figures in Asian populations resulted,12 suggesting the need for ethnic-specific cutoffs, at least for obesity.The International Diabetes Federation (IDF) felt there was a strong need for one practical definition that would be useful in any country for the identification of people at high risk of CVD, but also diabetes. This definition would also allow comparative long-term studies, which could then be used, if necessary, to refine the definition on the basis of solid endpoints. As a result, an IDF consensus group met in 2004, with representatives from the organisations that had generated the previous definitions and members from all IDF regions. Their recommenda-tions are now available.13There was consensus that the components identified by Adult Treatment Panel III were a sensible starting point. It was also agreed that diabetes and insulin resistance had been overemphasised as core measurements in the earlierThe metabolic syndrome—a new worldwide definitiondefinitions. Measurement of insulin resistance was deemed impractical, although it is clear that several metabolic syndrome components, especially waist circumference and triglycerides, are highly correlated with insulin sensitivity.4Central obesity, as assessed by waist circumference, was agreed as essential (panel), because of the strength of the evidence linking waist circumference with cardiovascular disease and the other metabolic syndrome components,and the likelihood that central obesity is an early step in the aetiological cascade leading to full metabolic syndrome. The waist circumference cutoff selected was the same as that used by European Group for the Study of Insulin Resistance, and lower than the main Adult Treatment Panel III recommendations, because most available data suggest an increase in other cardiovascular disease risk factors in Europids (white people of European origin, regardless of where they live in the world) when the waist circumference rises above 94 cm in men and 80cm in women.1Ethnic-specific waist circumference cutoffs have been incorporated into the definition (table),and have been based on available data linking waist circumference to other components of the metabolic syndrome in different populations.12,14,15The levels of the other variables were as described by Adult Treatment Panel III, except that the most recent diagnostic level from the American Diabetes Association for impaired fasting glucose (5·6 mmol/L [100 mg/dL]) was used.16Although this new definition will still miss substantial numbers of people with impaired glucose tolerance (because an oral glucose-tolerance test is not required), it retains the simplicity of the instrument.The consensus group also recommended additional criteria that should be part of further research into metabolic syndrome, including: tomographic assessment of visceral adiposity and liver fat, biomarkers of adipose tissue (adiponectin, leptin), apolipoprotein B, LDL particle size, formal measurement of insulin resistance and an oral glucose-tolerance test, endothelial dysfunction, urinary albumin, inflammatory markers (C-reactive protein,tumour necrosis factor ␣, interleukin 6), and thrombotic markers (plasminogen activator inhibitor type 1,fibrinogen). These factors should be combined with assessment of CVD outcome and development of diabetes so better predictors can be developed.Researchers and clinicians should use the new criteria for the identification of high-risk individuals and for research studies. Preventive measures are obviously needed in the people identified. Mounting evidence suggests that lifestyle modification with weight loss and increased physical activity will be beneficial, although specific studies in metabolic syndrome are needed. TherePanel:International Diabetes Federation: metabolic syndrome definitionCentral obesityWaist circumference*—ethnicity specific (see table 1)Plus any two:Raised triglyceridesϾ150 mg/dL (1·7 mmol/L)Specific treatment for this lipid abnormality Reduced HDL-cholesterolϽ40 mg/dL (1·03 mmol/L) in men Ͻ50 mg/dL (1·29 mmol/L) in womenSpecific treatment for this lipid abnormality Raised blood pressure Systolic у130 mm Hg Diastolic у85 mm HgTreatment of previously diagnosed hypertension Raised fasting plasma glucose†Fasting plasma glucose у100 mg/dL (5·6 mmol/L)Previously diagnosed type 2 diabetesIf above 5·6 mmol/L or 100 mg/dL, oral glucose tolerance test is strongly recommended,but is not necessary to define presence of syndrome*If body-mass index is over 30 kg/m 2, central obesity can be assumed and waist circumference does not need to be measured. †In clinical practice, impaired glucose tolerance is also acceptable, but all reports of prevalence of metabolic syndrome should use only fasting plasma glucose and presence of previously diagnosed diabetes to define hyperglycaemia. Prevalences also incorporating 2-h glucose results can be added as supplementary findings.are suggestions from the Finnish Diabetes Prevention Study that individuals with metabolic syndrome show less development of diabetes with lifestyle advice.17In many people, however, pharmacological intervention will be needed. There is no specific treatment for the metabolic syndrome so individual abnormalities will have to be attended to.Again, long-term studies will help establish whether existing or newer agents, such as agonists for the peroxisome-proliferator-activated ␣/␥receptors or cannabinoid-1 receptor blockers,18could be of specific benefit.Recently, the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD) have published a provocative discussion paper on the syndrome.19They raise several interesting questions, based on a critique of the earlier WHO and Adult Treatment Panel III criteria: 1) is it indeed a syndrome, particularly as the precise cause is unknown, 2) does it serve a useful purpose, and 3) is it labelling (and medicalising) people unnecessarily? Additionally, it has been suggested in an editorial that recognition of the metabolic syndrome has been largely driven by industry to create new markets.20A major part of the ADA/EASD19stance is based on pure semantics, but the IDF (and the cardiovascular community) feel strongly that this clustering of closely related risk factors for CVD and type 2 diabetes is indeed a very good basis for calling this a syndrome. Many examples exist of conditions being given a name even when the precise underlying cause or causes, are unknown (eg, type 2 diabetes). The IDF feels that it serves a useful purpose to focus on people, in both the community and clinical settings, who are at high risk of developing CVD and type 2 diabetes, particularly using the new IDF criteria proposed above.Indeed, the ADA has just reinvented and redefined the condition of “prediabetes” for people who only have a 50% chance of developing diabetes.20We also emphasise most strongly in our longer article13that treatment must be focused on lifestyle change—and on the individual components if the former fails. This is a far cry from a condition claimed to be invented by industry.21The metabolic syndrome concept has been around for over 80years.1The burgeoning epidemic of type 2 diabetes and CVD worldwide, particularly in the developing world seem adequate reasons for identifying and treating people with the syndrome.We would stress that the new IDF criteria are not the final word, but hopefully will help identify people at increased risk, and through further research will lead to more accurate predictive indices.*K George M M Alberti, Paul Zimmet, Jonathan Shaw, for the IDF Epidemiology Task Force Consensus Group Department of Endocrinology and Metabolism, St Marys Hospital, London W2 1NY, UK (KGMMA); and International Diabetes Institute, Melbourne, Victoria, Australia (PZ, JS)George.Alberti@The International Diabetes Federation Consensus Group was supported by an unrestricted educational grant from AstraZeneca. KGMMA receives consultancy fees from AstraZeneca, GlaxoSmithKline, Novartis, and Servier. PZ has received consultancy fees from Novartis, GlaxoSmithKline, Bristol Myer Squibb, Bayer AG, Abbott, and Merck, and has received payment for speaking from E Merck, Sanofi-Aventis, AstraZeneca, Kissei, and Fournier. JS has received consultant fees from Merck, Eli Lilly, and Novo Nordisk.1Eckel RH, Grundy SM, Zimmet PZ. The metabolic syndrome. Lancet2005;365: 1415–28.2Kylin E. Studien ueber das Hypertonie-Hyperglyka “mie-Hyperurika”miesyndrom. Zentralblatt fuer Innere Medizin1923; 44: 105–27.3Reaven G. Role of insulin resistance in human disease. Diabetes1988; 37: 1595–607.4Lemieux I, Pascot A, Couillard C, et al. Hypertriglyceridemic waist: a marker of the atherogenic metabolic triad (hyperinsulinemia; hyperapolipoprotein B; small, dense LDL) in men? Circulation2000; 102: 179–84.5Alberti K, Zimmet P. Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification ofdiabetes mellitus provisional report of a WHO consultation. Diabet Med1998; 15: 539–53.6Balkau B, Charles MA. Comment on the provisional report from the WHO consultation. European Group for the Study of Insulin Resistance (EGIR).Diabet Med1999; 16: 442–43.7Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, AndTreatment of High Blood Cholesterol In Adults (Adult Treatment Panel III).JAMA2001; 285: 2486–97.8Cameron AJ, Shaw JE, Zimmet PZ. The metabolic syndrome: prevalence in worldwide populations. Endocrinol Metab Clin North Am 2004; 33: 351–76. 9Stern MP, Williams K, Gonzalez-Villalpando C, Hunt KJ, Haffner SM. Does the metabolic syndrome improve identification of individuals at risk oftype 2 diabetes and/or cardiovascular disease? Diabetes Care2004; 27:2676–81.10Lakka HM, Laaksonen DE, Lakka TA, et al. The metabolic syndrome and total and cardiovascular disease mortality in middle-aged men.JAMA2002; 288: 2709–16.11WHO expert consultation. Appropriate body-mass index for Asian populations and its implications for policy and intervention strategies.Lancet2004; 363: 157–63.12Tan CE, Ma S, Wai D, Chew SK, Tai ES. Can we apply the National Cholesterol Education Program Adult Treatment Panel definition of themetabolic syndrome to Asians? Diabetes Care2004; 27: 1182–86.13International Diabetes Federation. The IDF consensus worldwide definition of the metabolic syndrome. April 14, 2005:/webdata/ docs/Metac_syndrome_def.pdf (accessed June 10, 2005).14Snehalatha C, Viswanathan V, Ramachandran A. Cutoff values for normal anthropometric variables in asian Indian adults. Diabetes Care2003; 26:1380–84.15Examination Committee of Criteria for ‘Obesity Disease’ in Japan; Japan Society for the Study of Obesity.New criteria for ‘obesity disease’ in Japan.Circ J2002; 66: 987–92.16Genuth S, Alberti KG, Bennett P, et al. Follow-up report on the diagnosis of diabetes mellitus. Diabetes Care2003; 26: 3160–67.17Lindstrom J, Louheranta A, Mannelin M, for the Finnish Diabetes Prevention Study Group. The Finnish Diabetes Prevention Study (DPS):lifestyle intervention and 3-year results on diet and physical activity.Diabetes Care2003; 26: 3230–36.18Van Gaal LF, Rissanen AM, Scheen AJ, for the RIO-Europe Study Group.Effects of the cannabinoid-1 receptor blocker rimonabant on weight reduction and cardiovascular risk factors in overweight patients: 1-year experience from the RIO-Europe study. Lancet 2005; 365: 1389–97.19Kahn R, Buse J, Ferrannini E, Stern M. The metabolic syndrome: time for a critical appraisal: joint statement from the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care2005; 28:2289-304. [Also Diabetologia 2005; published online Aug 4.DOI:10.1007/s00125-005-1876-2]20Zimmet P, Shaw J, Alberti KG. Preventing type 2 diabetes and the dysmetabolic syndrome in the real world: a realistic view. Diabet Med 2003; 20:693–702.21Gale EAM. Editorial: the myth of the metabolic syndrome. Diabetologia 2005; 10: 1873–75.Last year I joined the research advisory board of the drug company GlaxoSmithKline and get paid for that work. I was asked to write this article by The Lancet and my fee for writing will be diverted to a charity. You need to know these things before you read on.A ward round can reveal that many patients are taking ten or more drugs. A scan of a newspaper identified no fewer than six stories suggesting therapeutic breakthroughs. Therapeutic interventions, central to the practice of medicine, have spilled over into daily news—ranging from the adoption of fluoxetine as a drug for well-being in the 1990s to the pursuit of cardiovascular disease prevention resulting in 2003 for calls for a “polypill” for the entire population.1Yet despite this enthusiasm for drugs from doctors and patients,paradoxically the reputation of the drug industry is at an all time low—the industry is often portrayed as aiming for profit above all else. And it is not just the moral highgrounders who are voicing concern. Read this, fromthe business section of a major newspaper: “most drug failures are a by-product of the way the industry is structured: it develops drugs as fast as possible and employs an army of salesmen to sell like crazy before the patent expires. It ignores the fact that the side-effects of a drug are often not known until it has been taken by hundreds of thousands of patients.”2If this picture is correct, is industry alone to blame or are the medical profession and academia complicit in helping industry pursue profit above all else? This question is the theme of a report by Carl Elliott.3Let us get one thing straight: the drug industry works within a system that demands it makes a profit to satisfy shareholders. Indeed it has a fiduciary duty to do so. The best way to make a lot of money is to invent a drug that produces a dramatically beneficial clinical effect, is far more effective than any existing options, and has few unwanted effects. Unfortunately most drugs fall short of this ideal. Does this stop doctors from prescribing them,or patients’ groups from demanding availability for all?Clearly not. Even if we consider novel drugs rather than me-too products, recent examples provide some insights:the interferons for multiple sclerosis, drugs for dementia,and the inhibitors of cyclo-oxygenase 2 (COX-2).Interferon was potentially an exciting scientific advance and seemed to produce detectable biological effects in patients with multiple sclerosis. However, you needed an MRI to detect the change and the extent to which structural changes translated into clinical benefit,and improvement in quality of life, was unclear. In 2000,the UK National Institute for Clinical Excellence 4released an early statement that “on the basis of a very careful consideration of the evidence their [the interferons]modest clinical benefit appears to be outweighed by their very high cost”. The outcry was immediate, loud, and successful. Doctors, nurses, carers, and a patients’ group lobbied Government and the drug was made available within the UK National Health Service (NHS), albeit withDeveloping an open relationship with the drug industryPublished online July 7, 2005DOI:10.1016/S0140-6736(05)66835-3See Correspondencepage 1077See Department of Errorpage 1078。
_Q波_的鉴别与诊断
对于不够标准的又该怎样诊断呢 ? 没有 局限性的电静止 、纤维化或其他成分代 等位性 Q波 ,导致误诊 。至今 ,常规心电
出现 Q 波的又没有症状 、有了症状而没 替心肌 、室间隔肥厚及自主神经或间接 图是临床上应用最广的一项无创性检查
有 Q 波等无 Q 波的 M I呢 ? 因此 ,在传 刺激等有关 [3 ] ,但不是 M I导致的病理性 技术 ,是诊断 M I心律失常的重要手段之
(ACS)的提出与应用 ,心电图作为无创 波都恢复正常 。那么此时与心电图的正 说 ,坏死性变化是不能恢复的 ,但在某些
的 M I判断与排除是快捷 、方便 、实用 ,具 常变异 ,或称位置性 Q 波如何区分 ? 非 急性心肌缺血情况下 ,确可发现一些暂
有其他检查不可替代的重要作用 。ACS M I疾病所导致的 Q波及等位性 Q波 ,人 时性 Q波 。当严重缺血使得细胞内大量
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于坏死 ,一旦恢复血供 ,有可能又恢复除 联 R波的递增不良 ,即 V1 ～V5 导联的 R 位置的改变 。位置性 Q 波不属于病理性 极性能 。这便是可逆 Q波出现的原因 。 波振幅丢失了逐渐增高的趋势 ;胸导联 Q波 ,其不是因 M I或其他器质性疾病引
不够诊断为传统病理 Q 波的条件 , 皮病 、淀粉样变性 、原发性或转移性心脏 现及必要的心脏超声 、头胸导联心电图
或者心电ห้องสมุดไป่ตู้上根本没有出现 Q 波 ,系部 肿瘤 、肥厚性心肌病 、左心室肥厚 、右心 等无创性检查 ,进一步还可做冠状动脉
分 M I的梗死面积小 ,心电图上没有出现 室肥厚 、肺气肿 、肺源性心脏病 、大量心 造影等有创性检查 。作为临床心电图检
冠状动脉周围脂肪组织与动脉粥样硬化的关系生物学到影像学进展
•综述"冠状动脉周围脂肪组织与动脉粥样硬化的关系：生物学到影像学进展韩婷婷,穆癑,洪叶,黄明刚【摘要$近年来，冠状动脉周围脂肪组织(PCAT)已经成为心血管疾病中具有独特生物学意义的诊断指标之一。
在生理解剖中PCAT是最接近血管壁的脂肪组织，它通过旁分泌途径及滋养血管分泌机制形成的促炎信号，调节血管周围炎症及血管重构，从而影响冠状动脉粥样硬化发展的进程。
动脉粥样硬化形成是心脑血管疾病发生的病理学基础。
因此，PCAT无论数量还是质量都是决定心脏代谢风险的关键因素，在心血管诊断与治疗方面具有重要的临床意义。
本文就PCAT在冠状动脉粥样硬化斑块形成及演变过程中所发生的生物学行为及影像学研究现状与进展进行综述。
【关键词$冠状动脉周围脂肪组织；病理生理；动脉粥样硬化；易损斑块；体层摄影术，X线计算机:PET【中图分类号$R543.3；R814.42【文献标志码】DOI：10.13609/ki.10000313.2021.05.022据相关统计显示&1',随着国民经济水平的提高，人们生活质量的改善，心血管疾病已成为我国城乡居民死亡的首要原因，且死亡呈年轻化趋势。
动脉粥样硬化斑块是导致心血管疾病的病理学基础，其中易损斑块的破裂、血栓形成是引发心血管疾病甚至主要不良心血管事件(major adverse cardiovascular events, MACE)的重要因素，因此早期检测出易损斑块并给予及时有效的临床干预，可大大降低MACE的发生。
冠状动脉周围脂肪组织(pericoronary adipose tissue,PCAT)是指冠状动脉三大主要分支血管外膜周围的脂肪组织，属于心外膜脂肪(epicardial adipose tissue,EAT)的组成部分。
PCAT由多种细胞类型组成，被认为是一种代谢活跃的内分泌器官，通过旁分泌及滋养血管分泌机制形成的促炎信号影响冠状动脉粥样硬化发展的进程，在心血管疾病的发病机制中起着至关重要的影响作用。
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P Widimsky MD DrSc FESC1, B Stellova MD1, L Groch MD2, M Aschermann MD DrSc FESC1, M Branny MD3, M Zelizko MD CSc4, J Stasek MD PhD1, P Formanek MD5; on behalf of the PRAGUE Study Group Investigators P Widimsky, B Stellova, L Groch, et al; on behalf of the PRAGUE Study Grouቤተ መጻሕፍቲ ባይዱ Investigators. Prevalence of normal coronary angiography in the acute phase of suspected ST-elevation myocardial infarction: Experience from the PRAGUE studies. Can J Cardiol 2006;22(13):1147-1152.
La prévalence de coronarographies normales pendant la phase aiguë d’une présomption d’infarctus du myocarde avec surélévation du segment ST : L’expérience des études PRAGUE
CLINICAL STUDIES
Prevalence of normal coronary angiography in the acute phase of suspected ST-elevation myocardial infarction: Experience from the PRAGUE studies
BACKGROUND: Acute ST-elevation myocardial infarction in patients with normal coronary arteries has previously been described, but coronary angiography in these patients was performed after the acute phase of the infarction. It is possible that these patients did not have normal angiograms during the acute phase (transient coronary thrombosis or spasm were usually suspected to be the cause). Information on the prevalence of truly normal coronary angiograms during the acute phase of a suspected ST-elevation myocardial infarction is lacking. PATIENTS AND METHODS: The PRimary Angioplasty in patients transferred from General community hospitals to specialized PTCA Units with or without Emergency thrombolysis-1 (PRAGUE-1) and PRAGUE-2 studies enrolled 1150 patients with ST-elevation acute myocardial infarction, in whom 625 coronary angiograms were performed within 2 h of the initial electrocardiogram. A simultaneous registry included an additional 379 coronary angiograms performed during the ST-elevation phase of a suspected myocardial infarction. Thus, a total of 1004 angiograms were retrospectively analyzed. A normal coronary angiogram was defined as one with the absence of any visible angiographic signs of atherosclerosis, thrombosis or spontaneous spasm. RESULTS: Normal coronary angiograms were obtained for 26 patients (2.6%). Among these, the diagnosis at discharge was a small myocardial infarction in seven patients (0.7%), acute (peri)myocarditis in five patients, dilated cardiomyopathy in four patients, hypertension with left ventricular hypertrophy in three patients, pulmonary embolism in two patients and misinterpretation of the electrocardiogram (ie, no cardiac disease) in five patients. Seven patients with small infarctions underwent angiography within 30 min to 90 min of complete relief of the signs of acute ischemia, and thus, angiograms during pain were not taken. None of the 898 patients catheterized during ongoing symptoms of ischemia had a normal coronary angiogram. Spontaneous coronary spasm as the only cause (without underlying coronary atherosclerosis) for the evolving infarction was not seen among these 898 patients. Thus, the causes of the seven small infarcts in patients with normal angiograms remain uncertain. CONCLUSIONS: The observed prevalence of normal coronary angiography in patients presenting with acute chest pain and ST elevations was 2.6%. Most of these cases were misdiagnoses, not infarctions. A normal angiogram during a biochemically confirmed infarction is extremely rare (0.7%) and was not seen during the ongoing symptoms of ischemia.