cardiology2016 91-100
cardiology2016 231-240
A1
Correct answer:E The anthracyclines (daunorubicin, doxorubicin, epirubicin and idarubicin) are chemotherapeutic agents associated with severe cardiotoxicity. The generation of free radicals is implicated in the unique ability of these agents to cause cardiotoxicity. Dilated cardiomyopathy is cumulative dose-dependent and may present many months after discontinuation of the drug. Swelling of the sarcoplasmic reticulum is the morphologic sign of an early stage of doxorubicin-associated cardiomyopathy. It is followed by loss of cardiomyocytes ("myofibrillar dropout"). Its symptoms are those of biventricular CHF including dyspnea on exertion, orthopnea, and peripheral edema. The most effective method of preventing doxorubicin cardiomyopathy is dexrazoxane. It is an iron-chelating agent that decreases formation of oxygen free radicals by doxorubicin and other anthracyclines. (Choice A) Right ventricular overload (cor pulmonale) presents with fatigue, dyspnea on exertion, and peripheral edema Physical examination reveals accentuation and splitting of the pulmonary component of S2, distended neck veins and hepatomegaly with hepatojugular reflux. Right ventricular failure is commonly a consequence of pulmonary hypertension or left heart failure. (Choice C) Restrictive cardiomyopathy is associated with hemochromatosis, amyloidosis, sarcoidosis and radiation therapy. (Choice D) Hypertrophic cardiomyopathy is an autosomal dominant disorder caused by mutation of the p-myosin heavy chain. (Choice B) Focal myocardial scarring commonly results following a myocardial infarction. (Choice F) Pericardial fibrosis usually follows cardiac surgery, radiation therapy or viral infections of the pericardium. Educational Objective:
100个常用英语词根
100个常用英语词根英语单词的构成方式有很多种,其中词根是最为基础的构词成分之一。
词根是指单词中最基础的词元素,具有不同的含义。
掌握常用英语词根十分重要,可以帮助我们快速准确的理解和记忆词汇,提高英语的阅读理解和写作能力。
下面就为大家介绍一些常用的英语词根。
1. act- 行动,做例如:actress (女演员), action (行动)2. ad- 向,朝例如:advance (前进), adhere (粘着)3. ambi- 两,双例如:ambidextrous (双手灵巧), ambiguous (模糊不清的)4. amphi- 两,双例如:amphibious (水陆两栖的), amphitheater (圆形露天剧场)5. ana- 再,重复例如:analysis (分析), anatomy (解剖)6. ante- 前,先例如:anterior (前面的), antecedent (先前的)7. anti- 反对,反抗例如:antibiotic (抗生素), anti-social (反社会的) 8. aqua- 水例如:aquarium (水族馆), aquamarine (海蓝宝石) 9. arch- 首例如:architect (建筑师), archbishop (大主教) 10. auto- 自己,自动例如:automatic (自动的), automobile (汽车) 11. bene- 仁慈,好例如:benefit (好处), benevolent (仁慈的)12. bio- 生命例如:biology (生物学), biography (传记)13. cardi- 心脏例如:cardiology (心脏病学), cardiogram (心电图) 14. cata- 下降,衰败例如:catastrophe (灾难), catalyst (催化剂)15. cede- 放弃,让步例如:concede (承认), secede (脱离)16. cent- 中心例如:centripetal (向心的), centimeter (厘米) 17. cerebr- 大脑例如:cerebral (大脑的), cerebrospinal (脑脊髓的) 18. chrom- 颜色例如:chromosome (染色体), chromatic (彩色的) 19. chron- 时间例如:chronology (年代学), chronic (慢性的) 20. cid- 杀,灭例如:homicide (杀人), insecticide (杀虫剂)21. circum- 环绕例如:circumference (周长), circumference (圆周) 22. co- 共同例如:cooperate (合作), coexist (共存)23. com- 一起例如:combine (结合), community (社区)24. contra- 相反例如:contradiction (矛盾), contraceptive (避孕的) 25. corp- 身体例如:corporation (公司), corpse (尸体)26. cosm- 宇宙例如:cosmic (宇宙的), cosmopolitan (世界性的) 27. crypto- 隐藏,秘密例如:cryptogram (密码), cryptic (神秘的) 28. cycl- 圆,周期例如:bicycle (自行车), cycle (周期)29. de- 向下,离开例如:decrease (减少), depart (离开)30. dec- 十例如:decade (十年), decimeter (十分米) 31. deca- 十例如:decathlon (十项全能), decagram (十克) 32. demo- 人民例如:democrat (民主党人), demotic (民间的) 33. dent- 牙齿例如:dentist (牙医), dental (牙科的)34. derm- 皮肤例如:dermatology (皮肤病学), dermatitis (皮炎) 35. dia- 通过,穿过例如:diameter (直径), diagonal (对角线)36. dic- 说例如:dictionary (词典), indicate (指示)37. di- 二例如:divisible (可分的), dioxide (二氧化物) 38. doc- 教育,教导例如:doctor (医生), document (文件)39. domin- 统治例如:dominate (支配), dominion (统治)40. don- 给予,赠送例如:donate (捐赠), pardon (宽恕)41. dub- 命名例如:dubious (可疑的), dub (配音)42. duc- 引导例如:produce (生产), introduce (介绍)43. dur- 持久例如:durable (持久的), endure (忍耐)44. dys- 不正常例如:dysfunctional (功能失调的), dyslexia (阅读障碍) 45. e- 电子例如:email (电子邮件), e-commerce (电子商务)46. eco- 环境例如:ecology (生态学), eco-friendly (环保的)47. ecto- 外部例如:ectoderm (外胚层), ectoplasm (外质)48. en- 使例如:enable (使能够), encourage (鼓励)49. end- 内部例如:endocrine (内分泌的), endoskeleton (内骨骼) 50. equi- 相等例如:equator (赤道), equidistant (等距离的)51. ex- 出,从例如:exit (出口), ex-boyfriend (前男友)52. extra- 在...之外例如:extraordinary (非凡的), extracurricular (课外的) 53. fac- 做,制造例如:factory (工厂), manufacture (制造)54. fid- 信任例如:confident (自信的), fidelity (忠诚)55. fin- 结束例如:finish (完成), final (最后的)56. fix- 固定例如:fixable (可固定的), fixture (装置)57. flam- 火焰例如:flamboyant (火焰般的), inflammation (炎症) 58. flex- 弯曲例如:flexible (灵活的), reflex (反射的)59. flu- 流动例如:fluid (流体), influence (影响)60. form- 形状例如:formation (形成), conform (遵循)61. fract- 打破例如:fracture (骨折), fracture-zone (断层带) 62. flect- 弯曲例如:reflect (反射), deflect (偏转)63. ger- 生产例如:germinate (发芽), generate (生产)64. geo- 地球,土地例如:geology (地质学), geography (地理学)65. gram- 记录,写例如:telegram (电报), grammar (语法)66. graph- 写,画例如:photography (摄影), autograph (亲笔签名) 67. hexa- 六例如:hexagonal (六边形的), hexapod (六足的) 68. hemo- 血液例如:hemoglobin (血红蛋白), hemophilia (血友病) 69. hetero- 不同的例如:heterogeneous (异质的), heterodox (异端的) 70. hex- 震动例如:hexagon (六边形), hexane (己烷)71. homo- 相同的例如:homogeneous (均质的), homosexual (同性恋的) 72. hydr- 水例如:hydraulic (水力的), hydrogen (氢)73. hyper- 超过,过度例如:hyperactive (活动过度的), hypertension (高血压) 74. hypo- 低于,不足例如:hypodermic (皮下的), hypotension (低血压) 75. icon- 图标例如:iconic (代表性的), iconoclast (打破旧习的人) 76. ign- 火例如:ignite (点火), ignition (点火)77. in- 不,非例如:incomplete (不完整的), invisible (不可见的) 78. inter- 在..之间,相互例如:interact (相互影响), intermission (间歇) 79. intra- 内部例如:intravenous (静脉内的), intrastate (州内的) 80. iso- 同等的例如:isometric (等距的), isosceles (等腰的)81. ject- 投掷例如:object (物体), reject (拒绝)82. jur- 法律,审判例如:jury (陪审团), jurisdiction (法律管辖权) 83. kilo- 千例如:kilometer (千米), kilogram (千克)84. lact- 乳汁例如:lactose (乳糖), lactate (乳酸盐)85. lat- 延长例如:latitude (纬度), lateral (侧边的)86. lex- 词语,字典例如:lexicographer (词典编撰者), lexical (词汇的) 87. leg- 法律例如:legal (合法的), legislature (立法机构)88. liber- 自由例如:liberation (解放), liberal (自由的)89. loc- 位置,地点例如:location (位置), local (本地的)90. log- 说话,理论例如:logic (逻辑), dialogue (对话)91. luc- 发光例如:lucid (清晰的), lucidite (光明)92. magn- 大的例如:magnify (放大), magnificent (壮丽的) 93. mal- 不好的例如:malfunction (功能失调), malign (恶意的) 94. mand- 命令例如:mandate (授权), command (命令)95. manu- 手工制作例如:manual (手工的), manufacture (制造) 96. mater- 母亲例如:maternal (母性的), maternity (产妇) 97. mega- 百万的例如:megabyte (兆字节), megawatt (兆瓦)98. meta- 超越,变化例如:metamorphosis (变形), metaphysics (形而上学)99. micro- 微小的例如:microscope (显微镜), microbe (微生物)100. migra- 迁移例如:migrate (迁移), emigrant (移民)以上就是100个常用的英语词根,涵盖了各个领域的词根。
cardiology2016 151-160
Correct answer:D The drug described is representative of a class 1 antiarrhythmic medication. These drugs preferentially bind to and block activated and inactivated voltage-gated sodium channels in cardiac pacemaker cells and myocytes. Dissociation of the drug from the channel occurs during the resting state, a conformational state distinct from the inactivated state that occurs following repolarization. Class 1 antiarrhythmics exhibit use dependence, a phenomenon in which tissues undergoing frequent depolarization become more susceptible to blockage. Use dependence occurs because the sodium channels in rapidly depolarizing tissue spend more time in the activated and inactivated states, thus allowing more binding time for the drug. For class 1 antiarrhythmics. sodium-channel-binding strength is 1C > 1A > 1B. Use dependence is more pronounced in class 1C antiarrhythmics because of their slow dissociation from the sodium channel, which allows their blocking effects to accumulate over multiple cardiac cycles. This effect is enhanced with tachycardia, and the resulting increase in sodium channel blockade helps to slow conduction speed and terminate tachyarrhythmias. The prominent use dependence effects of class 1C drugs can cause a delay in conduction speed that is out of proportion to prolongation of the refractory period. This can promote arrhythmias, especially in patients with ischemic or structural heart disease. Class 1B antiarrhythmics (eg, lidocaine, mexiletine, and tocainide) bind less avidly to sodium channels than the other class 1 antiarrhythmics (Choice D). Dissociation from the channels occurs so rapidly that there is minimal cumulative effect over multiple cardiac cycles, resulting in little use dependence. These drugs are more selective for ischemic myocardium because the reduced resting membrane potential delays sodium channel transition from the inactivated to the resting state, resulting in increased drug-channel binding. Class 1B antiarrhythmics are useful for treating ischemia-induced ventricular arrhythmias, one of the most common causes of death in the short term following acute myocardial infarction. (Choice A) Amiodarone is classified primarily as a class 3 antiarrhythmic medication although it has small class 1, 2? and 4 effects as well. The class 3 antiarrhythmics act by blocking potassium channels and prolonging phase 3 repolarization. (Choice B) Disopyramide, quinidine, and procainamide are class 1A antiarrhythmic dmgs. They are represented by line 2 on the graph because of their intermediate dissociation speed. (Choice C) Propafenone and flecainide are class 1C antiarrhythmic drugs. They are represented by line 3 on the graph because of their slow dissociation speed. (Choice E) Propranolol (a nonselective (3-adrenergic blocker) is categorized as a class 2 antiarrhythmic drug. It causes decreased chronotropy and inotropy via (31 blockade. (Choice F) Verapamil as a calcium channel blocker is classified as a class IV antiarrhythmic drug; diltiazem is another drug in this class. Although nifedipine is a calcium channel blocker as well, it is selective for vascular smooth muscle and does not have a notable effect on the heart. Educational objective: Use dependence describes the phenomenon in which higher rates of depolarization lead to increased sodium channel blockade due to the channels spending less time in the resting state. For class 1 antiarrhythmics, sodium-channel-binding strength is 1C>1A>1B. Class 1C antiarrhythmics demonstrate the most use dependence, and class 1B drugs have the least
cardiology-医学英语
Diagnostic, Symptomatic, and Terms
Term Meaning
hemostasis
arrest of bleeding or circulation
hyperlipidemia
excessive amounts of lipids(cholesterol, phospolipids, and triglycerides)in the blood Condition that is present when, on several separate occasions, blood pressure registers higher than normal
Combining Forms
Combining form atri/o cardi/o hemangi/o phleb/o ven/o thromb/o sphygm/o Meaning atrium heart blood vessel vein vein blood clot pulse Example atri/o/tome cardi/o/megaly hemangi/oma phleb/o/tomy ven/ous thromb/o/lysis sphygm/o/meter
Diagnostic, Symptomatic, and Terms
Term Meaning
embolus,emboli
mass of undissolved matter(foreign object,air, gas, tissue, thrombus)circulating in a blood or lymphatic channels until it becomes lodged in a vessel outside a vessel
cardiology2016 251-260
A2Q3Biblioteka A 43-year-old man is being evaluated for occasional retrosternal chest pressure that develops with moderate exertion and sometimes occurs when resting. He does not use alcohol, tobacco, or illicit drugs. The patient has an extensive family history of coronary artery disease. His temperature is 36.7 C (98 F), blood pressure is 124/72 mm Hg, pulse is 81/min, and respirations are 14/min. Physical examination shows no abnormalities. Coronary angiography shows mild luminal irregularities but no significant obstructive lesions. Acetylcholine infusion during the procedure results in dilation of epicardial coronary vessels. A reaction involving which of the following amino acids is most likely responsible for the observed dilation? A. Arginine B. Aspartate C. Glutamate D. Tryptophan E. Tyrosine
2016年04月急性冠脉综合征治疗新药临床研究指导原则.(英文版)
30 Churchill Place ● Canary Wharf ● London E14 5EU ● United Kingdom1 April 2016 1 EMA/CHMP/207892/20152 Committee for medicinal products for human use (CHMP)3 Guideline on clinical investigation of new medicinal 4products for the treatment of acute coronary syndrome 5(CPMP/EWP/570/98) 6Draft7 Draft agreed by Cardiovascular Working PartyFebruary 2016 Adopted by CHMP for release for consultation1 April 2016 Start of public consultation 27 April 2016 End of consultation (deadline for comments)31 October 2016 8 This guideline replaces 'Points to consider on the clinical investigation of new medicinal products for the 9 treatment of acute coronary syndrome (ACS) without persistent ST segment elevation' 10 (CPMP/EWP/570/98). 1112 Comments should be provided using this template . The completed comments form should be sent to CVSWPSecretariat@ema.europa.eu .13Keywords Acute coronary syndrome, STE-ACS, NSTE-ACS, guideline, CHMP1415Table of contents16Executive summary (4)171. Introduction (background) (4)182. Scope (5)193. Legal basis and relevant guidelines (5)204. Choice of efficacy criteria (endpoints) (6)214.1. All-cause mortality and CV mortality (6)224.2. New myocardial infarction (6)234.3. Revascularisation (6)244.4. Unstable angina pectoris necessitating hospitalisation (6)254.5. Stent thrombosis (6)264.6. Stroke (7)274.7. Left ventricular function and heart failure (7)284.8. Composite endpoints (7)294.9. Endpoints in fibrinolysis studies (7)305. Methods to assess efficacy (how to measure the endpoints) (8)315.1. Mortality (8)325.2. New myocardial infarction (8)335.3. Revascularisation (8)345.4. Unstable angina pectoris necessitating hospitalisation (8)355.5. Stent thrombosis (8)365.6. Ventricular function and heart failure (9)375.7. Angiographic endpoints (9)386. Selection of patients (9)396.1. Study population (9)406.1.1. STE-ACS (ST elevation acute coronary syndrome) (9)416.1.2. NSTE-ACS (Non-ST elevation acute coronary syndrome) (9)426.1.3. Unstable angina (9)436.2. Inclusion criteria for the therapeutic studies (10)446.3. Exclusion criteria for the therapeutic studies (10)456.4. Risk Stratification (10)466.5. Special populations (11)476.5.1. Older patients (11)487. Strategy and design of clinical trials (11)497.1. Clinical pharmacology (11)507.2. Therapeutic exploratory studies (12)517.2.1. Objectives (12)527.2.2. Design (12)537.3. Confirmatory Therapeutic Studies (12)547.3.1. Objectives (12)557.3.2. Background therapy (12)567.3.3. Choice of comparator (13)577.3.4. Duration of clinical studies (13)587.3.5. Analyses and subgroup analysis (13)598. Safety aspects (14)608.1. Bleedings (14)618.2. All-cause mortality (15)628.3. Thrombocytopenia (15)638.4. Rebound effect (15)648.5. Effects on laboratory variables (15)658.6. Effects on concomitant diseases (15)66References (16)6768Executive summary6970Two CHMP Guidelines have been previously developed to address clinical investigations of new71medicinal products for the treatment of acute coronary syndrome (ACS): (I) the CHMP points toconsider (PtC) on the clinical investigation of new medicinal products for the treatment of acute7273coronary syndrome without persistent ST-segment elevation (CPMP/EWP/570/98), published in 2000 74[1], and (II) the CHMP PtC on the clinical development of fibrinolytic products in the treatment of75patients with ST segment elevation myocardial infarction (CPMP/EWP/967/01), published in 2003 [2].76Since their finalisation, major developments have taken place in the definitions, diagnosis,77interventions and management of ACS, as reflected in the relevant European Society of Cardiology78(ESC) clinical practice guidelines (3, 4). Currently, an update of the above mentioned CHMP Guidelines 79is considered necessary to take these new developments into consideration based on literature review 80and experience gained with medicinal products intended for treatment during the acute phase and81beyond. The present update includes the following changes: 1) guidance addressing both ST-segment 82elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction83(NSTEMI), as well as unstable angina (UA), 2) update in their definitions, 3) risk stratification using84different scoring systems, 4) investigated endpoints, and 5) clinical developments of new medicinal85products beyond the acute stage, including agents other than antiplatelets and anticoagulants.1. Introduction (background)8687Cardiovascular diseases are currently the leading cause of death in industrialized countries and also 88expected to become so in emerging countries by 2020 [3, 4]. Among these, coronary artery disease 89(CAD) is the most prevalent manifestation and is associated with high mortality and morbidity. ACS 90has evolved as a useful operational term to refer to any constellation of clinical symptoms that are91compatible with acute myocardial ischemia. It encompasses (STEMI), NSTEMI, and UA.92ACS represents a life-threatening manifestation of atherosclerosis. It is usually precipitated by acute 93thrombosis induced by a ruptured or eroded atherosclerotic coronary plaque, with or without94concomitant vasoconstriction, causing a sudden and critical reduction in blood flow. In the complex95process of plaque disruption, inflammation was revealed as a key pathophysiological element. Non-96atherosclerotic aetiologies are rare e.g. such as arteritis and dissection.97The leading symptom of ACS is typically chest pain. Patients with acute chest pain and persistent (>20 min) ST-segment elevation have ST-elevation ACS (STE-ACS) that generally reflect an acute total9899coronary occlusion. Patients with acute chest pain but without persistent ST-segment elevation have 100rather persistent or transient ST-segment depression or T-wave inversion, flat T waves, pseudo-101normalization of T waves, or no ECG changes. At presentation, based on the measurement of102troponins, it is possible to further discriminate between the working diagnosis of non-ST-elevation ACS 103(NSTE-ACS) and unstable angina.104NSTE-ACS is more frequent than STE-ACS [5] with an annual incidence around 3 per 1000 inhabitants, 105but varying between countries [6]. Hospital mortality is higher in patients with STEMI than among 106those with NSTEMI (7% vs. 3–5%, respectively), but at 6 months the mortality rates are very similar 107in both conditions (12% and 13%, respectively) [5,7,8]. Long term follow-up shows that death rates 108were higher among patients with NSTE-ACS than with STE-ACS, with a two-fold difference at 4 years[8]. This difference in mid- and long-term evolution may be due to different patient profiles, since 109110NSTE-ACS patients tend to be older with more co-morbidities, especially diabetes and renal failure.2. Scope111112The aim of this guideline is to provide guidance when performing trials to develop medicinal products 113in the management of ACS. The primary goals of therapy for patients with ACS are to:1. Treat acute, life-threatening complications of ACS, such as serious arrhythmias, pulmonary 114115oedema, cardiogenic shock and mechanical complications of acute myocardial infarction (AMI). [9] 1162. Reduce the amount of myocardial necrosis that occurs in patients with AMI, thus preserving 117left ventricular (LV) function, preventing heart failure (HF), and limiting other cardiovascular118complications.1193. Prevent major adverse cardiac events like death, non-fatal myocardial infarction (MI), andneed for urgent revascularization.120121The focus in this Guideline concerns mainly the medical treatment of ACS (treatment goals 2 and 3). 122The choice of interventional procedures [percutaneous coronary intervention (PCI) or coronary artery 123bypass graft CABG)] falls outside the scope of this guideline.3. Legal basis and relevant guidelines124125This guideline has to be read in conjunction with the introduction and general principles and parts I 126and II of the Annex I to Directive 2001/83 as amended.127Pertinent elements outlined in current and future EU and ICH guidelines, should also be taken into 128account, especially those listed below:129•Dose-Response Information to Support Drug Registration (ICH E4; CPMP/ICH/378/95).130•Statistical Principles for Clinical Trials (ICH E9; CPMP/ICH/363/96).131•Choice of Control Group and Related Issues in Clinical Trials (ICH E10; CPMP/ICH/364/96).132•Points to consider on an Application with 1) Meta-analyses 2) One pivotal study133(CPMP/EWP/2330/99).134•Points to consider on multiplicity issues in clinical trials (CPMP/EWP/908/99).135•Investigation of subgroups in confirmatory clinical trials (EMA/CHMP/539146/2013).136•The Extent of Population Exposure to Assess Clinical Safety for Drugs (ICH E1A;137CPMP/ICH/375/95).138•Pharmacokinetic Studies in Man (3CC3A).139•Studies in Support of Special Populations: Geriatrics (ICH E7 CHMP/ICH/379/95) and related Q&A 140document (EMA/CHMP/ICH/604661/2009).141•Note for Guidance on the Investigation of Drug Interactions (CPMP/EWP/560/95).142•Reporting the Results of Population Pharmacokinetic Analyses (CHMP/EWP/185990/06).143•Reflection paper on the extrapolation of results from clinical studies conducted outside the EU to 144the EU-population (EMEA/CHMP/EWP/692702/2008).145•Draft Guideline on clinical investigation of medicinal products for the treatment of chronic heart 146failure (EMA/392958/2015 )•Guideline on clinical investigation of medicinal products for the treatment of acute heart failure147148(CPMP/EWP/2986/03 Rev. 1)4. Choice of efficacy criteria (endpoints)149150Definitions of clinical endpoints in confirmatory trials should be in line with the relevant clinical151guidelines to facilitate interpretation of the results, to allow comparisons across clinical studies and to 152extrapolate to clinical practice. Endpoints should be centrally adjudicated by a blinded committee. The 153following endpoints are relevant to the investigation of efficacy in patients with ACS.4.1. All-cause mortality and CV mortality154155As one of the goals of treatment of ACS is reduction of mortality, this is an important endpoint to156measure. There is an ongoing debate around the use of all-cause versus cardiovascular mortality in 157cardiovascular (CV) trials. All cause mortality is the most important endpoint in clinical trials for the 158estimation of the benefit-risk balance of a drug, in particular when investigating newer medicinal159products with possible safety issues. On the other hand, CV mortality is more specifically linked to the 160mode of action of CV medicinal products/intervention and is especially relevant when the earliest part 161of the follow up is assessed. The choice is also dependent on the objective of the study i.e. in non-162inferiority trials, CVmortality may be preferred while in superiority trials all cause mortality is usually 163used. In fibrinolysis studies, all cause mortality is preferred (see section 4.9).164As such, one of the two mortality endpoints should be included as a component of the primary165endpoint, with the other investigated as a key secondary endpoint.4.2. New myocardial infarction166167New onset MIis a relevant endpoint in studies of ACS and should always be investigated. The definition 168of MI has evolved through the years; at the time of drafting of this Guideline, the third universal169definition of MI is applicable [10]. Criteria of MI are the same as those used to define the index event 170(see below).4.3. Revascularisation171172Some clinical trials have included revascularization endpoints (PCI or CABG) as part of the primary 173composite with conflicting results [11, 12]. Such endpoints are considered more relevant tointerventional studies, and in the scope of this Guideline, their inclusion as a primary endpoint should 174175be clearly justified and their assessment pre-defined and systematically assessed.4.4. Unstable angina pectoris necessitating hospitalisation176177Unstable angina has been investigated in ACS clinical trials. Due to the varying definitions used, the 178associated subjectivity and the influence of local clinical practice, this endpoint is not encouraged to be 179included in the composite primary endpoint.4.5. Stent thrombosis180181Stent thrombosis (ST) is a rare event that can have fatal consequences. ST has been captured in some 182registration studies, but not consistently in the primary endpoint (PEP). The investigation of ST as part 183of the primary endpoint is not encouraged due to the uncertainty of the clinical relevance of all184captured events, except for the "definite" subcategory. Another category identified by the timing isintra-procedural stent thrombosis (IPST), which is a rare event indicating the development of occlusive 185186or non-occlusive new thrombus in or adjacent to a recently implanted stent before the PCI procedure is187completed. Some recent studies [13,14] show that these events may be of prognostic value. As such they should also be collected and presented as secondary endpoint but not included in the analysis of 188189ST.4.6. Stroke190191Stroke should be defined by a generally accepted definition [15]. Clinical studies in ACS have used192non-fatal stroke in the primary endpoint , including any types of strokes. However it is preferred to193include only ischemic strokes in the primary endpoint, as this is the true measure of efficacy;194haemorrhagic stroke should be included as a safety endpoint. An ischaemic stroke with haemorrhagic195conversion should be considered as “primary ischaemic”. The subgroup of “undefined strokes” should196be as small as possible in order to be able to properly assess the effect of the study treatment. In case 197all types of strokes are included in the primary endpoint, a sensitivity analysis including only ischemic198stroke should be submitted.4.7. Left ventricular function and heart failure199Some medicinal products such as modulators of reperfusion injury or inflammation, or gene/cell200201therapy are developed to improve myocardial function and reduce the occurrence of HF. In these202cases, measurement of myocardial function could be a relevant endpoint to investigate the mechanismof action. In phase III studies, these endpoints can be investigated as secondary endpoints to support 203204the clinical endpoints. Occurrence of HF should be considered as a clinical endpoint in phase III studies205aimed at showing benefit in long-term cardiovascular outcome. All-cause mortality and long term206follow-up are mandatory in studies with novel interventions.4.8. Composite endpoints207Due to the rather low incidence of cardiovascular events during the follow-up period after the acute 208209phase of the ACS, composite endpoints consisting of relevant components are acceptable, both as210primary and secondary endpoints. The composite of CV death, non-fatal MI and non-fatal stroke (Major211Adverse Cardiovascular Events, [MACE]) has commonly been used in registration studies, with non-212fatal strokes showing limited contribution to the results. As such, it is preferred to investigate the213composite of death and non-fatal MI in confirmatory studies; non-fatal ischaemic stroke could beincluded in the composite if justified. Sometimes different definitions of MACE are being used with214215novel therapies [16], that should be justified when used in place of MACE. The inclusion of less216objective and clinically derived outcomes in the same composite is generally not encouraged, as they217may either drive the efficacy or dilute the results. In case these endpoints are included they have to be218stringently defined, and adjudicated. Each component of the primary composite endpoint should be219analysed as secondary endpoint.220The net clinical benefit that includes both benefit and safety issues of the studied drug may be used as221a secondary endpoint to be evaluated if it contributes to the discussion on the benefit-risk balance of222the studied drug.4.9. Endpoints in fibrinolysis studies223224In fibrinolysis studies, angiographic studies using the TIMI (Thrombolysisi in Myocardial Infarction)perfusion grades as evaluation criteria are often used. However, complete recanalization cannot be 225226considered as a surrogate for survival when assessing fibrinolytic drugs, as some medicinal productsproviding higher complete recanalization rates than alteplase, failed to demonstrate additional survival 227228benefit. For this reason, all cause mortality is the most relevant endpoint or a combined endpoint as 229previously discussed (see 4.1). Secondary endpoints such as heart failure hospitalisations, left230ventricular function, ventricular arrhythmias, the need for rescue recanalization (emergent and/or231planned) should also be considered and justified.5. Methods to assess efficacy (how to measure the232endpoints)2335.1. Mortality234235Definition of CV death should be clearly defined, in line with acceptable standards [17]. It is mandatory 236to report and centrally adjudicate all mortality data where survival is an endpoint of the study.237Assessment of cardiovascular mortality will require censoring of other “types” of mortality, which may 238complicate its interpretation, in particular when non-CV deaths are in high proportion.5.2. New myocardial infarction239240The diagnostic of MI is based on the detection of a rise and/or fall of cardiac biomarker values241[preferably cardiac troponin (cTn)] with at least one value above the 99th percentile upper reference 242limit (URL). All MIs should be collected and also classified by their different sub types (i.e,243spontaneous, secondary to an ischemic imbalance, related to PCI, related to ST or CABG) [10]. This is 244particularly important considering the different prognostic values of each type of MI. For the same 245reason and to support the clinical relevance of post procedural MIs, these events should be presented 246with higher cut-off values (≥ 5 and ≥10x upper level of normal ULN, in case of CK-MB or ≥70x ULN of 247cTn) [18]. These higher cut-off values can also help in diagnosing MIs in the setting of elevated248baseline biomarkers, which is a problematic situation. In such cases, serial measurements of the249biomarkers are necessary, in addition to new ECG changes or signs of worsening of cardiac function, 250e.g. HFor hypotension [18].5.3. Revascularisation251252The underlying cause of revascularization should be identified: restenosis, ST or disease progression. 253In the latter case target vessel revascularization (TVR) could be included. Early target lesion eventsafter revascularization (before 30 days) are more likely to be caused by an angiographic complication 254255and should preferably be included as safety endpoint (see ST).5.4. Unstable angina pectoris necessitating hospitalisation256257When investigated, robust definitions should be employed. In order to support the seriousness of the 258event it should also be shown that it has led to a revascularisation procedure. Since a medicinalproduct that prevents death and/or new MI might result in more patients suffering from UA, the259260analysis of this endpoint should take into account censoring issues as well.5.5. Stent thrombosis261262ST should be collected and classified as definite, probable and possible in line with acceptable263definitions [19]. In addition, the timing of ST should be documented (acute, sub-acute, late and very 264late), as risk factors and clinical sequels differ with timing.5.6. Ventricular function and heart failure265266Investigation of cardiac function should follow state of the art methods. This can include among others 267measurement of ventricular function by isotopic method and/or by cardiac magnetic resonance imaging 268and/or echocardiography. Investigation of HFshould follow the relevant CHMP guidelines.5.7. Angiographic endpoints269270Angiograms should undergo central blinded reading. In principle, the rate of TIMI 3 flow (complete 271revascularization) of the infarct related artery at 90 minutes is considered the most relevant272angiographic endpoint, as it has been shown to correlate with an improved outcome in terms of273mortality and left ventricular function. An earlier evaluation of the patency pattern (i.e. 30 and 60274minutes) may provide important information on the speed of recanalization. Whatever is the time-point 275selected as primary outcome, it must be properly justified and pre-specified in the clinical trial.6. Selection of patients2766.1. Study population277The definition of the different ACS subtypes should be based on current guidelines/universal definition 278279of MI including STEMI and NSTEMI as well as UA [3, 4, 10].6.1.1. STE-ACS (ST elevation acute coronary syndrome)280281In patients with acute chest pain and persistent (>20 min) ST-segment elevation on ECG the282diagnostic of STE-ACS is made [3]. This condition generally reflects an acute total coronary occlusion.Most patients will ultimately develop an ST-elevation myocardial infarction (STEMI) with the criteria of 283284acute myocardial infarction described before [see 5.2].6.1.2. NSTE-ACS (Non-ST elevation acute coronary syndrome)285286In patients with acute chest pain but no persistent ST-segment elevation the diagnostic of NSTE-ACS is 287made [4]. ECG changes may include transient ST-segment elevation, persistent or transient ST-288segment depression, T-wave inversion, flat T waves or pseudo-normalization of T waves or the ECG 289may be normal. The clinical spectrum of non-ST-elevation ACS (NSTE-ACS) may range from patients 290free of symptoms at presentation to individuals with ongoing ischaemia, electrical or haemodynamic 291instability or cardiac arrest. The pathological correlate at the myocardial level is cardiomyocyte292necrosis (NSTEMI) or, less frequently, myocardial ischaemia without cell loss (UA). Currently, cardiac 293troponins play a central role in establishing a diagnosis and stratifying risk, and make it possible to 294distinguish between NSTEMI and UA[4].6.1.3. Unstable angina295296Unstable angina (UA) is defined as myocardial ischemia at rest or minimal exertion in the absence of 297cardiomyocytes necrosis, i.e. without troponin elevation. Among NSTE-ACS population, the higher298sensitivity of troponin has resulted in an increase in the detection of MI [4]; the diagnosis of UAis less 299frequently made.6.2. Inclusion criteria for the therapeutic studies300301Inclusion of both STEMI and NSTEMI and/or NSTE-ACS patients in the same clinical trial (or not)302should be justified based on the mechanism of action of the investigated product and the proposed 303time of intervention. If both subgroups are investigated in the same trial, both subgroups should be 304well represented. For interventions aimed at post-acute and longer term phases (secondary305prevention or plaque stabilisation) it may be justified to address both conditions in the same clinical 306trial. Time of inclusion of the patients in relation to the index event should be set and adequately307discussed a priori.308Patients with unstable angina represent a different risk category and prognosis that necessitates309different interventions than NSTEMI patients. However, during the acute presentation of NSTE-ACS it may be difficult to discriminate NSTEMI from UA so both groups have been included in some clinical 310311studies. In general, the investigation of interventions in these patients is encouraged, but preferably in 312separate clinical trials.If fibrinolysis is considered, inclusion criteria should be in line with the current treatment guidelines 313314concerning the inclusion for fibrinolysis [3].6.3. Exclusion criteria for the therapeutic studies315316If the patients do not fulfil the above criteria for ACS they should be excluded from the ACS studies. 317Other life-threatening conditions presenting with chest pain, such as dissecting aneurysm,318myopericarditis or pulmonary embolism may also result in elevated troponins and should always be 319considered as differential diagnoses [4].320If drugs interfering with the haemostatic system are tested, patients with a significant risk of bleeding 321(e.g. recent stroke, recent bleeding, major trauma or surgical intervention) and/or a propensity to 322bleed (e.g. thrombocytopenia, clotting disturbances, intracranial vascular diseases, peptic ulcers,323haemophilia) should be excluded from participation in the clinical studies.324Attention should be paid to the time elapsed between a previous application of antiplatelet or325anticoagulant acting agent beforehand and the administration of study drug (e.g. the pharmacokinetic 326[PK] and even more importantly, the pharmacodynamic [PD] half-life of these previously administered 327drugs).328For reasons of generalisability of the study results to the future target population it is strongly advised 329not to define the exclusion criteria too narrow, i.e. polymorbid patients (e.g. renal and/or hepatic330impairment, heart failure), should not automatically be excluded from the main therapeutic clinical 331trials.332When fibrinolysis is considered, exclusion criteria for fibrinolysis should be strictly respected [3].6.4. Risk Stratification333334In clinical trials, the ability of the therapy to demonstrate a treatment effect may depend on the335underlying risk and expected event rates. Enrichment strategies are sometimes used in trials to obtain 336the required number of events with a reasonable time in specific subgroups who are likely to exhibit a 337higher event rate than the overall target population and potentially larger treatment effect. In thatcase, it has to be shown that the results of this enriched study population can be extrapolated to the 338339general population.。
心血管杂志排名
No. 按期刊名称排列按期刊简称排列参考中文名称影响因子降序1 Circulation Circulation 循环↑2 Journal of the American College of Cardiology J Am Coll Cardiol 美国心脏病学会志↑3 Circulation Research Circ Res 循环研究↑4 European Heart Journal Eur Heart J 欧洲心脏杂志↑5 Hypertension Hypertension 高血压↑6 Arteriosclerosis, Thrombosis, and Vascular Biology Arterioscler Thromb Vasc Biol 动脉硬化、血栓形成与血管生物学↓7 Atherosclerosis Supplements Atheroscler Suppl 动脉粥样硬化↑8 Nature Clinical Practice Cardiovascular Medicine Nat Clin Pract Cardiovasc Med 自然临床诊疗:心血管医学↑9 Cardiovascular Research Cardiovasc Res 心血管研究↓10 Basic Research in Cardiology Basic Res Cardiol 心脏病学基础研究↑11 Journal of Hypertension J Hypertens 高血压杂志↑12 Journal of Molecular and Cellular Cardiology J Mol Cell Cardiol 分子与细胞心脏病学杂志↓13 Heart Heart 心脏↑14 Progress in Cardiovascular Diseases Prog Cardiovasc Dis 心血管病研究进展↑15 Atherosclerosis Atherosclerosis 动脉粥样硬化↑16 Heart Rhythm Heart Rhythm 心脏节律↑17 American Heart Journal Am Heart J 美国心脏杂志↑18 Trends in Cardiovascular Medicine Trends Cardiovasc Med 心血管医学趋势↓19 Cardiovascular Drug Reviews Cardiovasc Drug Rev 心血管药物评论↑20 Heart Failure Reviews Heart Fail Rev 心力衰竭评论↑21 American Journal of Cardiology Am J Cardiol 美国心脏病学杂志↑22 Thrombosis & Haemostasis Thromb Haemost 血栓形成和止血↑3 Seminars in Thrombosis and Hemostasis Semin Thromb Hemost 血栓形成与止血法论文集↑24 American Journal of Physiology - Heart and Circulatory Physiology Am J Physiol Heart Circ Physiol 美国生理学杂志-心脏与循环生理学↓25 Current Vascular Pharmacology Curr Vasc Pharmacol 最新血管药理学↓26 Nutrition, Metabolism, and Cardiovascular Diseases (NMCD) Nutr Metab Cardiovasc Dis 营养、代谢与心血管疾病↑27 European Journal of Heart Failure Eur J Heart Fail 欧洲心力衰竭杂志↑28 Shock Shock 休克↑29 Current Problems in Cardiology Curr Probl Cardiol 当前心脏病问题↑30 Hypertension Research Hypertens Res 高血压研究↑31 American Journal of Hypertension Am J Hypertens 美国高血压症杂志↑32 International Journal of Cardiology Int J Cardiol 国际心脏病学杂志↑33 Current Opinion in Cardiology Curr Opin Cardiol 心脏病学新见↑34 Revista Española de Cardiología Rev Esp Cardiol 西班牙心脏病学杂志↑35 Journal of Human Hypertension J Hum Hypertens 人类高血压杂志↑36 Journal of Atherosclerosis and Thrombosis J Atheroscler Thromb 动脉硬化与血栓症杂志↓37 Steroids Steroids 类固醇↑38 Resuscitation Resuscitation 复苏↓39 Cardiovascular Drugs and Therapy Cardiovasc Drugs Ther 心血管药物与治疗↑40 Thrombosis Research Thromb Res 血栓形成研究↑41 Clinical Research in Cardiology Clin Res Cardiol 临床心脏病学研究↑42 Circulation Journal Circ J 循环杂志↑43 European Journal of Cardiovascular Prevention & Rehabilitation Eur J Cardiovasc Prev Rehabil 欧洲心血管疾病预防与康复杂志↑44 Journal of Cardiovascular Pharmacology J Cardiovasc Pharmacol 心血管药理学杂志↑45 Journal of Thrombosis and Thrombolysis J Thromb Thrombolysis 血栓形成与血栓溶解杂志↑46 Cardiovascular Toxicology Cardiovasc Toxicol 心血管毒理学↑47 Journal of Cardiovascular Magnetic Resonance J Cardiovasc Magn Reson 心血管磁共振杂志↑48 Cardiovascular Pathology Cardiovasc Pathol 心血管病理学↑49 Current Hypertension Reports Curr Hypertens Rep 高血压症最新报告↑50 Cardiology Cardiology 心脏病学↑51 CardioVascular and Interventional Radiology Cardiovasc Intervent Radiol 心血管与介入放射学↑52 Europace Europace 欧洲心脏起搏、心律失常和心脏电生理会议↑53 Journal of Cardiovascular Pharmacology and Therapeutics J Cardiovasc Pharmacol Ther 心血管药物学与治疗学杂志↑54 Blood Pressure Blood Press 血压↑55 Blood Pressure Monitoring Blood Press Monit 血压监测↓56 Pacing and Clinical Electrophysiology Pacing Clin Electrophysiol 起搏与临床电生理学↑57 Journal of Cardiovascular Nursing J Cardiovasc Nurs 心血管病护理杂志↑58 Echocardiography: A Journal of Cardiovascular Ultrasound & Allied Techniques Echocardiography 超声心动图↑59 Clinical and Applied Thrombosis/Hemostasis Clin Appl Thromb Hemost 临床与应用血栓形成与止血研究↑60 Heart and Vessels Heart Vessels 心脏与脉管↑61 Coronary Artery Disease Coron Artery Dis 冠心病↓62 Clinical Cardiology Clin Cardiol 临床心脏病学↑63 Journal of Renal Nutrition J Ren Nutr 肾病营养学杂志↓64 Journal of Electrocardiology J Electrocardiol 心电学杂志↑65 Annals of Noninvasive Electrocardiology Ann Noninvasive Electrocardiol 无创心电学年鉴↓66 Heart & Lung: The Journal of Acute and Critical Care Heart Lung 心与肺;危急护理杂志↑67 Clinical and Experimental Hypertension Clin Exp Hypertens 临床与实验高血压↑68 Journal of Interventional Cardiac Electrophysiology J Interv Card Electrophysiol 心脏介入电生理学杂志↓69 Cardiology in the Young Cardiol Young 青少年心脏病↑70 International Heart Journal Int Heart J 国际心脏杂志↑71 Vascular Vascular 脉管↑72 Reviews in Cardiovascular Medicine Rev Cardiovasc Med 心血管医学评论↑73 Scandinavian Cardiovascular Journal Scand Cardiovasc J 斯堪的那维亚心血管杂志↓74 Texas Heart Institute Journal Tex Heart Inst J 德克萨斯心脏病学会志↑75 Cardiology Clinics Cardiol Clin 心脏病临床↓76 VASA Vasa 脉管病杂志↑77 Herz - Kardiovaskuläre Erkrankungen Herz 心脏↑78 Klinische Monatsblätter für Augenheilkunde Klin Monatsbl Augenheilkd 眼科学临床月刊↓79 Journal des Maladies Vasculaires J Mal Vasc 血管疾病杂志↑80 Archives des Maladies du Coeur et des Vaisseaux Arch Mal CoeurVaiss 法国心血管集刊↓81 Indian Heart Journal Indian Heart J 印度心脏病杂志 0 -82 Japanese Heart Journal Jpn Heart J 日本心脏杂志 0 -83 Minerva Cardioangiologica Minerva Cardioangiol 心脏脉管学 0 -84 Japanese Circulation Journal Jpn Circ J 日本循环杂志 0 -85 Kardiologia Polska / Polish Heart Journal Kardiol Pol 波兰心脏病杂志 0 -86 Revista Brasileira de Cirurgia Cardiovascular Rev Bras Cir Cardiovasc 巴西心血管外科杂志 0 -87 Advances in Cardiology Adv Cardiol 心脏学研究进展 0 -88 Arquivos Brasileiros de Cardiologia Arq Bras Cardiol 巴西心脏集刊 0 -89 Cardiovascular Diseases Cardiovasc Dis 心血管疾病 0 -90 Arteriosclerosis Arteriosclerosis 动脉硬化 0 -91 Zeitschrift für Kardiologie Z Kardiol 心脏病学杂志0 ↓92 Blood Pressure - Supplement Blood Press Suppl 血压-增刊 0 -93 Journal of Cardiopulmonary Rehabilitation (JCR) J Cardiopulm Rehabil 心肺疾病康复杂志 0 -94 Asian Cardiovascular & Thoracic Annals Asian Cardiovasc Thorac Ann 亚洲心血管与胸腔纪事 0 -95 General Pharmacology: The Vascular System Gen Pharmacol 普通药物学 0 -96 Cardiovascular Surgery Cardiovasc Surg 心血管外科 0 -97 Cardiovascular Journal of Southern Africa Cardiovasc J S Afr 南非心血管杂志 0 -98 Journal of Invasive Cardiology J Invasive Cardiol 侵袭性心脏病学杂志 0 -99 Seminars in Thoracic and Cardiovascular Surgery Semin Thorac Cardiovasc Surg 胸心血管外科论文集 0 -100 Journal of Hypertension - Supplement : J Hypertens Suppl 高血压杂志-增刊 0 -。
Sigma-1受体激活减轻心脏缺血再灌注损伤
Sigma-1受体激活减轻心脏缺血再灌注损伤廖小平;喻溥蛟;许嘉鸿【摘要】[目的]研究sigma-1受体的激活与抑制对心脏缺血再灌注损伤的作用.[方法]C57BL/6小鼠经过3 d尾静脉注射sigma-1受体抑制剂BD1047,sigma-1受体激动剂SA4503或生理盐水后施行心脏缺血再灌注手术.术后对小鼠心脏进行TTC/Evans蓝双染色并计算心脏梗死区(infarction area,INF)与危险区(area at risk,AAR)比值(INF/AAR),同时对心肌组织采用蛋白免疫印迹法检测凋亡相关蛋白Bcl-2,Bax,Caspase-3的表达水平.[结果]接受了sigma-1受体抑制剂BD1047预处理的小鼠,其INF/AAR值远大于对照组(P<0.05),心肌组织中促凋亡相关蛋白的表达水平升高,抗凋亡相关蛋白的表达水平降低.而接受sigma-1受体激动剂SA4503预处理的小鼠,其INF/AAR值远小于对照组(P<0.05),心肌组织中促凋亡相关蛋白的表达水平降低,抗凋亡相关蛋白的表达水平升高.[结论]Sigma-1受体的激活能够改善心脏缺血再灌注损伤,而抑制sigma-1受体则会加重心脏缺血再灌注损伤.【期刊名称】《上海大学学报(自然科学版)》【年(卷),期】2018(024)006【总页数】8页(P853-860)【关键词】Sigma-1受体;心肌梗死;缺血再灌注损伤【作者】廖小平;喻溥蛟;许嘉鸿【作者单位】上海市安亭医院心血管内科,上海 201805;同济大学附属同济医院心血管内科,上海 200065;同济大学附属同济医院心血管内科,上海 200065【正文语种】中文【中图分类】R541.4急性心肌梗死(acute myocardial infarction,AMI)已成为目前发病率及死亡率非常高的疾病之一[1].仅在美国,每年就有约150万人发生急性心肌梗死.而随着生活水平的提高以及生活方式的改变,目前我国的急性心肌梗死发病率也逐渐升高.而随着再灌注治疗技术的发展,急性的心肌梗死已能够在发生的短期内得到有效治疗.尽管极大地提高了急性心肌梗死患者的存活率,但也催生出了新的问题.心脏缺血再灌注损伤(myocardial ischemia reperfusion injury,MIRI)指的是心肌梗死罪犯血管打开后,快速血流重新流入心肌,在途经受损的心肌细胞时由血液中HbO2造成二次打击的氧化应激损伤[1-3].这种损伤往往会造成心肌细胞的进一步坏死和凋亡、存活心肌细胞的线粒体功能障碍、蛋白激酶的激活、大量的炎症反应等,继而导致患者的远期预后不良,甚至死亡[4-5].因此,如何改善心脏缺血再灌注损伤是目前心血管病领域一个亟待解决的重要问题.Sigma-1受体是一个长度为25 kD的分子伴侣,主要位于内质网以及线粒体相关的内质网膜上[6],可以通过调节钾离子通道、电压敏感性的钙离子通道来调节钙离子进入细胞膜的浓度,还可以调节胞浆内储存的钙离子流通,促进蛋白的折叠,提高细胞对于氧化应激反应的抗性[7-9].Sigma-1受体广发地分布在身体的各个组织中,包括心脏、大脑、肺脏、肾脏等[10].已有研究发现,sigma-1受体对于多种器官的缺血再灌注损伤(ischemia reperfusion injury,IRI)有着重要的调节作用[11-14].Sigma-1受体的配体之一——BHDP(N-benzyl-N'-(2-hydroxy-3,4-dimethoxybenzyl)-piperazine,N-苄基-N'-(2-羟基-3,4-二氧苄基)-哌嗪),能够有效改善肝脏受到的氧化应激反应[11].在大鼠肾脏缺血再灌注损伤模型中,使用sigma-1受体激动剂氟伏沙明,能够通过Akt介导的NO信号通路显著改善肾脏功能,提高大鼠的存活率[12].而在心脏相关的研究中,研究者也发现,sigma-1受体参与了心脏重构的病理生理过程[15-20],sigma-1受体激动剂SA4503以及氟伏沙明都可以改善压力负荷所致的心脏重构,保护心脏功能不受损.然而,sigma-1受体在心脏缺血再灌注损伤中的作用尚不清楚.因此,本工作的目的旨在探索sigma-1受体对于心脏缺血再灌注损伤的作用,以期为心脏缺血再灌注的诊疗提供一个全新的分子靶点.1 材料与方法1.1 实验材料与仪器1.1.1 实验动物雄性C57BL/6小鼠,8~10周龄,质量28±1 g,饲养于SPF级动物房,温度22±2°C,湿度50%~60%.所有操作均依照美国国立卫生院(National Institutes of Health,NIH)的相关规定.1.1.2 实验仪器多功能酶标仪、微量移液器、旋涡混匀器、恒温水浴锅、离心机、半干转膜槽、电泳仪、电泳凝胶成像系统、倒置显微镜、体视镜、显微手术器械、小动物呼吸机.1.1.3 实验试剂实验中所涉及的抗体包括一抗Bcl-2抗体、Bax抗体、Caspase-3、甘油醛-3-磷酸脱氢酶(glyceraldehyde-3-phosphate dehydrgenase,GAPDH)抗体,均购于Abclonal公司.Sigma-1受体激动剂SA4503以及抑制剂BD1047购于Sigma公司.1.2 实验方法1.2.1 动物实验方案采用冠脉结扎法构建小鼠的缺血再灌注模型.8周龄的C57BL/6小鼠经过3 d的尾静脉注射药物SA4503(1 mg·kg-1·d-1)以及BD1047(1 mg·kg-1·d-1)后进行手术. 手术步骤如下:①手术区域用75%的酒精擦拭消毒;②用1%戊巴比妥钠按0.01mL/g浓度腹腔注射麻醉小鼠;③在声门下两个气管软骨环之间切一个小孔,插入气管插管,固定;④打开胸腔,用7-0线将冠状动脉左前降支弓结扎;⑤逐层关胸,用6-0缝线固定肋骨,4-0缝线缝皮;⑥用5 mL注射器通过胸管边抽气边拔出胸管,避免术后发生气胸;⑦30 min后,再次打开胸腔,将结扎的线剪断,关闭胸腔,缝合肋骨和皮肤;⑧24 h后收取心脏样本.1.2.2 四氮唑红染色方法心脏损伤的评估方式采用TTC/Evans蓝双染色法,其中TTC为四氮唑红(2,3,5-triphenyl-2H-tetrazolium chloride).首先,将2%的Evans蓝通过冠脉结扎的方式,仅灌注于心脏未缺血部分,未着色的部分称为危险区(area at risk,AAR).接着从小鼠体内快速取出心脏,置于-20°C冰箱中冷冻,冰冻后用刀片将心脏横切为1~2 mm厚度的切片.将切片浸泡于37°C的1%TTC溶液中孵浴15 min后使用磷酸盐缓冲液(phosphate buffer saline,PBS)漂洗.TTC未着色部分心肌组织呈现白色,为坏死的心肌组织,视为梗死区(infarction area,INF),着色的红色区域为缺血但未坏死的组织.染色后使用倒置显微镜拍摄心肌切片照片,利用ImageJ软件对图形进行量化分析.1.2.3 蛋白的提取取适当大小的心肌组织样本,加入适量的细胞裂解液,用匀浆机将组织样本破碎.随后置于冰上裂解样本15 min.接下来,将蛋白样品置于离心机中以12 000 r/min离心30 min后,将蛋白上清液转移至新的离心管中,加入上样缓冲液后100°C使蛋白变性,迅速放入冰中冷却,短时离心.采用标准牛血清白蛋白(albumin from bovine serum,BCA)定量方法对样本进行蛋白含量均一化后待用.细胞裂解液配方(以1 mL 为例)如下:1 mL细胞裂解液,10µL磷酸酶抑制剂,10µL苯甲基磺酰氟(phenylmethanesulfonyl fluoride,PMSF).1.2.4 免疫印迹法根据目的蛋白的分子量配制不同浓度的分离胶,一般大多采用浓度为8%,10%与12%的分离胶.电泳条件如下:电压80 V(浓缩胶)~120 V(分离胶),电泳时间约2~3 h,溴酚蓝至胶底边即可停止电泳.选用聚偏二氟乙烯膜(polyvinylidene fluoride,PVDF)作为蛋白转膜载体,转膜条件为恒流200 mA转2 h.转在PVDF上的样品用PBS配制5%的BSA作为封闭液常温封闭处理1 h后,用PBST(PBS溶液加上Tween-20)清洗干净.一般按照1∶1 000的比例用5%BSA配置一抗,并将样品于4°C冰箱内孵育一抗过夜.第二天弃去一抗,用PBS清洗干净后,用5%BSA按照1∶10 000的比例配制二抗,并于常温孵育二抗2 h.使用化学发光显影试剂对蛋白表达情况进行检测.1.2.5 统计方法数据以均值±标准差(mean±SD)表示,使用SPSS 17.0统计软件进行方差分析,3组及3组以上单因素样本运用单因素方差分析(analysis of variance,ANOVA),方差齐性时再运用Bonferroni分析作两两比较.统计结果以P<0.05为具有统计学差异.2 结果2.1 Sigma-1受体抑制剂BD1047对小鼠心脏缺血再灌注损伤的影响为了明确sigma-1受体对于心脏缺血再灌注损伤的作用,首先检测了使用sigma-1受体抑制剂后小鼠心脏缺血再灌注损伤的面积.经过3 d的尾静脉注射sigma-1受体抑制剂BD1047后发现,接受了BD1047预处理后的小鼠心肌受损面积即梗死区与危险区比值(INF/AAR)要远大于对照组,如图1所示,图中LV为左心室(left ventricle),***代表P<0.01,n=6.图1 BD1047对心脏缺血再灌注损伤面积的影响Fig.1 Effects of BD1047 on myocardial infarction size induced by MIRI2.2 Sigma-1受体抑制剂BD1047对心肌细胞中凋亡相关蛋白表达的影响同时,在蛋白水平使用了蛋白免疫印迹法检测心肌组织中的凋亡相关蛋白,结果发现,相较于对照组,BD1047组的抗凋亡相关蛋白Bcl-2表达明显下调,而与促凋亡相关的蛋白Bax以及Capase-3的活化水平明显升高,如图2所示,图中*代表P<0.05,**代表P<0.01,***代表P<0.001,n=3.2.3 Sigma-1受体激动剂SA4503对小鼠心脏缺血再灌注损伤的影响在明确了抑制sigma-1受体对心脏缺血再灌注损伤有协同作用后,检测了sigma-1受体的激活对小鼠心脏缺血再灌注损伤的作用.经过3 d的尾静脉注射sigma-1受体激动剂SA4503后发现,接受了SA4503预处理后的小鼠心肌受损面积要远小于对照组(见图3,图中***代表P<0.001,n=6).2.4 Sigma-1受体激动剂SA4503对心肌细胞中凋亡相关蛋白表达的影响同样地,在蛋白水平使用蛋白免疫印迹法检测心肌组织中的凋亡相关蛋白,结果发现,相较于对照组,SA4503组的抗凋亡相关蛋白Bcl-2表达明显上调,而与促凋亡相关的蛋白Bax以及Capase-3的活化水平明显降低(见图4,图中*代表P<0.05,**代表P<0.01,n=3).图2 BD1047对Bax,Bcl-2以及Caspase-3蛋白表达的影响Fig.2 Effects of BD1047 on expression of Bax,Bcl-2 and Caspase-3 proteins图3 SA4503对心脏缺血再灌注损伤面积的影响Fig.3 Effects of SA4503 on myocardial infarction size induced by MIRI3 讨论随着药物溶栓、经皮冠状动脉介入治疗、冠脉旁路移植术等再灌注治疗技术日益完善且广泛普及,心脏再灌注损伤的干预治疗备受重视.目前,已有观点多集中于心肌梗死后缺血再灌注引起的氧化应激损伤及其产生的强烈炎症反应.这些损伤反应的最终结果是大片细胞的坏死和进一步的心肌细胞凋亡.图4 SA4503对Bax,Bcl-2以及Caspase-3蛋白表达的影响Fig.4 Effects of SA4503 on expression of Bax,Bcl-2 and Caspase-3 proteins通常来说,心肌细胞凋亡发生在心肌梗死缺血后的几分钟内[21-22]以及冠脉闭塞被打通后血液再灌注时[23].一些基础研究以及临床试验认为,凋亡是心脏缺血再灌注损伤最重要的病理生理机制[24].当再灌注发生时,血流快速恢复的同时带来了大量的氧分子以及细胞外pH值的变化,这些均导致氧自由基的释放以及钙离子的超载,继而发生线粒体膜渗透性的增加,线粒体通透性转换孔的开放,进而导致更多的促凋亡因子从线粒体中被释放出来[24-29].Sigma-1受体本身对于线粒体离子通道有着重要的调控作用.本工作的研究中发现了抑制sigma-1受体将会加重小鼠心脏缺血再灌注损伤时心肌细胞的凋亡水平,进而加重心脏的损伤程度.相反,激活sigma-1受体则可以改善心肌细胞的凋亡水平,减少心脏的损伤.从已有研究中可知,通过激动剂SA4503激活sigma-1受体后,线粒体钙离子通道的激活、三磷酸腺苷(adenosine triphosphate,ATP)的正常生产为心脏的收缩舒张功能提供了稳定的钙稳态环境以及充足的能量供给,从而改善了心脏的功能[15,30-31].除此之外,sigma-1受体对于Akt信号通路也有一定的激活作用,而这也是一条控制细胞凋亡、自噬、生长的经典信号通路[18].参考文献:【相关文献】[1]YELLOND M,HAUSENLOY D J.Myocardial reperfusion injury[J].NEngl JMed,2007,357:1121-1135.[2]HAUSENLOY D J,YELLOND M.Targeting myocardial reperfusion injury: the search continues[J].NEngl J Med,2015,373:1073-1075.[3]HAUSENLOY D J,YELLOND M.Myocardial ischemia-reperfusion injury:a neglectedtherapeutic target[J].J Clin Invest,2013,123:92-100.[4]IB´A˜NEz B,HEUSCH G,OVIzE M,et al.Evolving therapies for myocardialischemia/reperfusion injury[J].J Am Coll Cardiol,2015,65:1454-1471.[5]LEJAY A,FANG F,JOHNR,et al.Ischemia reperfusion injury,ischemic conditioning and diabetes mellitus[J].Journal of Molecular and Cellular Cardiology,2016,91:11-22.[6]HAYASHI T,SU T P.Sigma-1 receptor chaperones at the ER-mitochondrion interface regulate Ca2+signaling and cell survival[J].Cell,2007,131:596-610.[7]SU T P,HAYASHI T,MAURICE T,et al.The sigma-1 receptor chaperone as an inter-organelle signaling modulator[J].Trends Pharmacol Sci,2010,31:557-566.[8]FUJIMOTO M,HAYASHI T,URFER R,et al.Sigma-1 receptor chaperones regulate the secretion of brain-derived neurotrophic factor[J].Synapse,2012,66:630-639.[9]MEUNIER J,HAYASHI T.Sigma-1 receptors regulate Bcl-2 expression by reactive oxygen speciesdependent transcriptional regu lation of NFκB[J].J Pharmacol ExpTher,2010,332:388-397.[10]TSAI S Y,HAYASHI T,MORI T,et al.Sigma-1 receptor chaperones and diseases[J].Cent Nerv Syst Agents Med Chem,2009,9:184-189.[11]KLOUz A,SA¨ID D B,FERCHICHI H,et al.Protection of cellular and mitoc hondrial functions against liver ischemia by N-benzyl-N'-(2-hydroxy-3,4-dimethoxybenzyl)-piperazine(BHDP),a sigma1 ligand[J].Eur J Pharmacol,2008,578(2/3):292-299.[12]HOSSzU A,ANTAL Z,LENART L,et al.σ1-receptor agonism protects against renal ischemiareperfusion injury[J].J Am Soc Nephrol,2017,28(1):152-165.[13]BUCOLO C,DRAGO F.Neuroactive steroids protect retinal tissue through σ1 receptors[J].Basic Clin Pharmacol Toxicol,2007,100:214-216.[14]SHENY C,WANG Y H,CHOU Y C,et al.Dimemorfan protects rats against ischemic stroke through activation of sigma-1 receptor-mediated mechanisms by decreasing glutamate accumulation[J].J Neurochem,2008,104:558-572.[15]TAGASHIRA H,ZHANG C,LU Y M,et al.Stimulation of σ1-receptor restores abnormal mitochondrial Ca2+mobilization and ATP production following cardiachypertrophy[J].Biochim Biophys Acta,2013,1830:3082-3094.[16]TAGASHIRA H,BHUIYANM S,SHIODA N,et al.Fluvoxamine rescues mitochondrialCa2+transport and ATP production through σ1-receptor in hypertrophic cardiomyocytes[J].Life Sci,2014,95:89-100.[17]BHUIYANM S,FUKUNAGA K.Stimulation of sigma-1 receptor signaling by dehydroepiandrosterone ameliorates pressure overload-induced hypertrophy and dysfunctions in ovariectomized rats[J].Expert Opin Ther Targets,2009,13:1253-1265. [18]BHUIYANM S,TAGASHIRA H,FUKUNAGA K.Dehydroepiandrosterone mediated stimulation of sigma-1 receptor activates Akt-eNOS signaling in the thoracic aorta ofovariectomized rats with abdominal aortic banding[J].Cardiovasc Ther,2010,29:219-230. [19]BHUIYANM S,TAGASHIRA H,FUKUNAGA K.Sigma-1 receptor stimulation with fluvoxamine activates Akt-eNOS signaling in the thoracic aorta of ovariectomized rats with abdominal aortic banding[J].Eur J Pharmacol,2011,650:621-628.[20]ITO K,HIROOKA Y,MATSUKAWA R,et al.Decreased brain sigma-1 receptor contributes to the relationship between heart failure and depression[J].Cardiovas Res,2012,93:33-40.[21]DUMONT E A,HOFSTRA L,VANHEERDE W L,et al.Cardiomyocyte death induced by myocardial ischemia and reperfusion:measurement with recombinant human annexin-Ⅴina mouse model[J].Circulation,2000,102:1564-1568.[22]DUMONT E A,REUTELINGSPERGER C P,SMITS J F,et al.Real-time imaging of apoptotic cell-membrane changes at the single-cell level in the beating murine heart[J].Nature Medicine,2001,7(12):1352-1355.[23]WHELANR S,KAPLINSKIY V,KITSIS R N.Cell death in the pathogenesis of heart disease:mechanisms and significance[J].Annu Rev Physiol,2010,72:19-44.[24]HAUSENLOY D J,YELLOND M.The mitochondrial permeability transition pore:its fundamental role in mediating cell death during ischaemia and reperfusion[J].J Mol Cell Cardiol,2003,35:339-341.[25]ONG S B,SAMANGOUEI P,KALKHORANS B,et al.The mitochondrial permeability transition pore and its role in myocardial ischemia reperfusion injury[J].J Mol Cell Cardiol,2015,78:23-34.[26]FLISS H,GATTINGER D.Apoptosis in ischemic and reperfused rat myocardium[J].Circ Res,1996,79:949-956.[27]DI LISA F,CANTONM,MENABO R,et al.Mitochondria and reperfusion injury:the role of permeability transition[J].Basic Res Cardiol,2003,98:235-241.[28]HALESTRAP A P,RICHARDSONA P.The mitochondrial permeability transition:a current perspective on its identity and role in ischaemia/reperfusion injury[J].J Mol Cell Cardiol,2015,78:129-141.[29]ELTzSCHIG H K,ECKLE T.Ischemia and reperfusion:from mechanism totranslation[J].Nat Med,2011,17:1391-1401.[30]SHIMAzAWA M,SUGITANI S,INOUE Y,et al.Effect of a sigma-1 receptoragonist,cutamesine dihydrochloride(SA4503),on photoreceptor cell death against light-induced damage[J].Exp Eye Res,2015,132:64-72.[31]URFER R,MOEBIUS H J,SKOLOUDIK D,et al.Cutamesine stroke recovery study group.PhaseⅡtrial of the sigma-1 receptor agonist cutamesine(SA4503)for recovery enhancement after acute ischemic stroke[J].Stroke,2014,45:3304-3310.。
cardiology2016 71-80
Q2
A 35-year-old previously healthy man is brought to the emergency department after being involved in a motor vehicle accident He has significant blunt chest and head trauma. Shortly after he arrives, his blood pressure drops suddenly and he begins experiencing respiratory distress. On physical examination, the patient is tachycardic and tachypneic. His lungs are clear to auscultation with vesicular breath sounds heard bilaterally. He has jugular venous distention, and his systolic blood pressure falls 15 mm Hg with inspiration. Which of the following is the most likely cause of this patient's deterioration? A. Tension pneumothorax B. Epidural hematoma C. Hemothorax D. Aortic rupture E. Cardiac tamponade
Q1
Correct answer:G The cause of death was most likely an acute myocardial infarction. In myocardial infarction, changes on light microscopy are usually not apparent until 4 hours after the onset of severe ischemia. Although a variable waviness of myofibrils at the border of the infarct (due to myofibril relaxation) might be observed before this, more definite signs of early coagulative necrosis, such as cytoplasmic eosinophilia and nuclear pyknosis, take at least 4 hours to develop. Other potentially lethal causes of chest pain, diaphoresis, and palpitations/tachycardia include aortic dissection and/or rupture, massive pulmonary embolism, and tension pneumothorax. The chest pain of aortic dissection is typically tearing in nature and often radiates to the back. Dyspnea is typically the most prominent symptom in the event of a pulmonary embolus or tension pneumothorax. (Choices A & B) Cytoplasmic hypereosinophilia on light microscopy is one of the earliest signs of coagulative necrosis of cardiac myocytes. It begins approximately 4 hours after the onset of lethal ischemia. Light microscopy may also reveal edema and punctate hemorrhages in infarcted myocardium starting also at about 4 hours after the ischemic event. (Choice C) An interstitial infiltrate of neutrophils around a zone of myocardial infarction is not seen until 1 to 3 days after the onset of severe ischemia. (Choice D) Extensive macrophage phagocytosis of the dead cells generally does not develop until at least 5 days after myocardial infarction, and is most prominent during post-infarction days 7 to 10. (Choice E) Fibrovascular granulation tissue with neovascularization generally begins to develop 7 days after myocardial infarction, and is most prominent on post-infarction days 10 to 14. (Choice F) Increased collagen deposition and decreased cellularity in a zone of infarcted myocardium is not generally evident until 2 weeks post-infarction. Fibrosis continues during weeks 2 to 8, producing a dense collagenous scar by two months post-infarction.
cardiology2016 61-70
A 62-year-old Caucasian female hospitalized with acute myocardial infarction dies suddenly on day four of her hospitalization. Findings at autopsy are pictured below (RV = right ventricle, LAD = left anterior descending coronary artery): Which of the following statements best describes the condition that caused this patient's death? A. It is the most common cause of death in patients hospitalized with 一 myocardial infarction B. It typically occurs 3 to 7 days after the onset of myocardial infarction C. It is a frequent complication of fibrinolytic therapy D. It is more common in patients with repetitive myocardial infarction E. Patients with left ventricular hypertrophy are especially susceptible
A2
Correct answer:E Headaches and epistaxis may be caused by hypertension in the arteries supplying the head and neck. Lower extremity muscle weakness or fatigue with exercise may be caused by inadequate lower body perfusion. In adult-type aortic coarctation, the stenosis is post-ductal (in contrast to the infantile form, where the coarctation is generally preductal and fatal soon after birth without surgical repair). Adult-type aortic coarctation can produce hypertension in the upper aortic circulation and simultaneously low perfusion in the distal aorta supplying the legs. The likelihood of an adult-type, postductal coarctation in this patient is greatly increased by the finding of enlarged, palpable intercostal vessels, which indicate the development of a collateral arterial circulation to the region of the aorta distal to the coarctation. On radiographic exam, patients with adult-type aortic coarctation often have notching of the ribs as a result of the enlarged, tortuous intercostal arteries. (Choice D) The initial left-to-right t of an isolated patent ductus arteriosus generally does not result in poor exercise tolerance until the persistent pulmonary hypertension causes pulmonary vascular sclerosis and shunt flow reversal (Eisenmenger syndrome). One would not expect to find epistaxis or enlarged intercostal arteries in these patients. (Choice F) Tetralogy of Fallot could decrease exercise tolerance via increased right-to-left shunting and hypoxemia in response to vasodilation in active skeletal muscles. However, one would not expect epistaxis or enlarged intercostal arteries in these patients. Educational Objective: The adult (postductal) type of congenital aortic coarctation can present with symptoms/signs of hypertension in the arterial tree proximal to the coarctation, and of hypoperfusion of the lower extremities, especially during ambulation. Collateral circulation to the distal aorta results in dilated intercostal arteries. The triad of upper body hypertension, diminished lower extremity pulses, and enlarged intercostal artery collaterals is typical of adult-type coarctation and is not seen in other congenital cardiovascular malformations.
急性胸痛的评估发现与诊断ppt
心肌标志物指标CARDIAC MARKER
1000 100
Myoglobin
CK-MB
MB Isoforms Troponin T
Troponin I
10
Upper Reference Interval
1
0
0
12
24
36
48
60
72
Hours After Chest Pain Onset
Antman EM、 In: Braunwald E, ed、 Heart Disease: A Textbook in Cardiovascular Medicine, 5th ed、 Philadelphia, Pa: WB Saunders; 1997、
• 既往冠心病史Prior Medical Conditions
• 危险因素 Risk factors • ECG • 酶学指标 enzymes
11
需询问并记录得胸痛特点?
• 性质:挤压、烧灼、刀割样? Character of ACP • 程度:1-10级? Degree:1—10? • 特征:突发、渐起? • 持续时间:数分或数小时? Duration; • 放射:背、臂、颈?Radiation: arm(s), neck, jaw? • 影响因素:加重或缓解因素Eliciting factors:
40% 14% 7% 5% 4、5%
J AM Geriatr Soc 1986
22
胸痛病史得价值与局限性
• Medline 与OVID搜索1970 – 2005 • 复习了88篇文献 • 超过11000病例 • 客观评价医师纳入与排除得能力
JAMA 2005 294:2623-2629
cardiology2016 221-230
A1
Correct answer:B Beta blockers are useful for treating hypertensive patients with comorbid conditions such as migraine, essential tremor, angina pectoris/prior myocardial infarction, and atrial fibrillation. Beta blockers lower blood pressure via 2 mechanisms: 1.Reducing myocardial contractility and heart rate 2.Decreasing renin release by the kidney Renin release is mediated in part through sympathetic stimulation of beta-1 receptors located on juxtaglomerular cells. Therefore, beta-adrenergic blocking drugs (eg, metoprolol) act to inhibit renin release, which in turn reduces the conversion of angiotensinogen to angiotensin I and reduces the levels of angiotensin II (a potent vasoconstrictor) and aldosterone (decreasing renal sodium and water retention) (Choice D). (Choice A) Beta blockers block the action of endogenous catecholamines on adrenergic beta receptors but have no significant effect on circulating levels of catecholamine. (Choice C) Beta-adrenergic receptor antagonists depress conduction through the atrioventricular (AV) node and can cause varying degrees of AV block. (Choice E) Long-term use of beta blockers will cause either no change or modest decreases in the peripheral vascular resistance due to their effects on the rGnin-angiot©nsin-3ldost6ron0 systGm. Educational objective: Beta blockers inhibit release of renin from renal juxtaglomerular cells through antagonism of beta-1 receptors on these cells. Inhibition of renin release prevents activation of the reninangiotensin-aldosterone pathway, which results in decreased vasoconstriction and decreased renal sodium and war-old man is evaluated for recurrent syncope. He has had 3 episodes of dizziness and palpitations followed by brief loss of consciousness over the last 6 months. He has no chest pain or dyspnea. The patient has a history of hypertension and hyperlipidemia There is no family history of sudden death. Initial evaluation shows normal ECG and echocardiogram. A cardiac electrophysiologic study is performed. During the study, intravenous infusion of a medication is administered and produces the responses shown below. Which of the following medications was most likely administered to this patient? A. Acetylcholine B. Adenosine C. Clonidine D. Esmolol E. Isoproterenol F. Norepinephrine G. Phenylephrine
老年心功能衰竭患者血清NT-proBNP和hs-TnT水平检测与NYHA分级的相关性分析
老年心功能衰竭患者血清NT-proBNP和hs-TnT水平检测与NYHA分级的相关性分析杨宏斌;黄巧平【摘要】目的探讨血清N末端B型钠尿肽原(NT-proBNP)和心肌肌钙蛋白(hs-TnT)联合定量检测在老年心功能衰竭患者心功能分级(NYHA分级)中的应用价值.方法选取2016年10月~2018年10月心内科住院的慢性心功能衰竭患者1 019例,对照组选取健康体检者96例,心功能衰竭诊断以临床医生依据病史、症状、客观检查等作出的综合判断为金标准.依据美国纽约心脏病协会(NYHA)分级方案将心功能衰竭患者分类为A组(Ⅰ级)和B组(Ⅱ级~Ⅳ级),采用电化学发光法测定其血清中NT-proBNP和hs-TnT的水平,应用方差分析和受试者工作特征曲线(ROC曲线)判断NT-proBNP,hs-TnT的诊断价值及其与NYHA分级的相关性.结果①心功能衰竭组与对照组的血清NT-proBNP,hs-TnT中位数水平分别为275.2pg/m1,35.3ng/L和79.3 pg/m1,19.2 ng/L,与对照组比较,心功能衰竭组显著高于对照组,差异具有统计学意义(t=3.20,2.543,均P<0.01),而组间年龄和性别无显著差异(P>0.05).②A组,B组患者人数分别为293例和726例.NT-proBNP和hs-TnT在A组的cutoff值分别为98.3 pg/ml和20.1 ng/L,曲线下面积分别为0.818(95%CI:0.804~0.823)和0.816(95%CI:0.792~0.833),灵敏度分别为64.7%和58.3%,特异度为90.1%和100%,阳性预测值为86%和85%,阴性预测值为67%和59%.B组的cutoff值分别为131.9 pg/ml和28.9 ng/L,曲线下面积分别为0.816(95%CI:0.792~0.833),灵敏度分别为90.4%和91.2%,特异度为90.4%和100%,阳性预测值均为100%,阴性预测值为85%和91%.NT-proBNP联合hs-TnT诊断心功能衰竭的cutoff值分别为133.4 pg/m1,35.3 ng/L,曲线下面积为0.943 (95%CI:0.901~0.951),灵敏度分别为74%和87%,特异度均为100%,阳性预测值均为100%,阴性预测值为86%和72%.B组诊断临界值明显高于在A组,差异有统计学意义(P<0.05).结论 NT-proBNP及hs-TnT的水平变化与老年心衰患者NYHA分级呈显著正相关(r=0.894,P<0.01),随着分级增加而呈递增趋势,联合检测结果优于单项检测,二者联合检测可为HF患者的诊断及分级严重程度的评估提供依据.【期刊名称】《现代检验医学杂志》【年(卷),期】2019(034)002【总页数】5页(P64-67,71)【关键词】N末端B型钠尿肽原;高敏心肌肌钙蛋白T;心功能分级;心功能衰竭【作者】杨宏斌;黄巧平【作者单位】甘肃天水市中医医院,甘肃天水741000;天水407医院,甘肃天水741000【正文语种】中文【中图分类】R541.6;R446.112心功能衰竭(heart failure,HF)是指在静脉回流正常的情况下,由于原发的心脏损害引起心排血量减少,不能满足组织代谢需要的一种综合征,是心血管疾病的终末期表现及最主要的死亡原因,随着年龄的增加患病率也迅速上升,准确而及时的诊断是挽救患者生命的迫切需求。
Cardiology
Cardiology1.An 8-year-old Caucasian male experiencing severe chest pain is diagnosed with an acutemyocardial infarction. Laboratory work-up reveals an increased serum methionine level. Which of the following amino acids is most likely essential in this patient?A.CysteineB.GlycineC.ProlineD.TyrosineE.SerineF.Asparagine2. A 62-year-old Caucasian male who recently underwent a mitral valve replacement is having low-grade fevers. He also complains of dyspnea and malaise. Repeated blood cultures grow Gram-positive cocci in clusters that are catalase-positive and coagulase-negative. Which of thefollowing is the best initial treatment for this patient?A.Penicillin GB.NafcillinC.VancomycinD.CiprofloxacinE.ErythromycinF.Ceftriaxone3. A 34-year-old immigrant from South Asia presents to your office complaining of heartpalpitations that are particularly prominent at night. He also notes that with moderate exertion, he experiences head “pounding” accompanied by involuntary head bobbing. He remembersbeing diagnosed with a heart murmur years before, but he cannot recall the type and has never received any treatment. Based on this patient’ s history, you suspect:A.Restricted left ventricular fillingB.Impaired left ventricular contractilityC.Left ventricular outflow obstructionD.Systolic-diastolic hypertensionE.Widening of the pulse pressure4. A 45-year-old Caucasian male dies two hours after the onset of severe chest pain, diaphoresis,and palpitations. At autopsy, the left anterior descending artery shows 100% occlusion. Lightmicroscopy of th e affected area of this patient’s myocardium would most likely demonstrate:A.Edema and punctate hemorrhagesB.Myocyte hypereosinophilaC.Dense interstitial neutrophil infiltrateD.Extensive macrophage phagocytosis of the dead cellsE.Fibrovascular granulation tissue with neovascularizationF.Dense collage scarG.Normal myocardium5.Cardiac catheterization is performed in a 7-year-old Caucasian male, demonstrating thefollowing pattern of oxygen saturation in cardiac chambers and outflow tracts.The patient most likely has which of the following findings on physical examination?A.Decreased femoral-to-brachial blood pressure ratioB.Fixed splitting of S2 on cardiac auscultationC.Holosystolic murmur over the left sternal borderD.Mucosal cyanosis and fingernail clubbingE.Machinery-like murmur over the upper precordiumF.Spike-and-dome carotid pulse upstroke6.Mr. J is an 83-year-old male who you have followed in your clinic for years. He is a retiredjeweler, and you have been following him regularly for management of his diabetes andhypertension. Most recently you cared for him as an inpatient after he suffered a minormyocardial infarction. He presents to your clinic today for a post-hospitalization follow-up.While speaking with him he mentions that he is very grateful for the work you have done for him over the years, and he presents with an antique watch as a gift. What is the mostappropriate reply?A.“It is inappropriate for you to offer me a gift in an attempt to secure preferential service.”B.“Thank you for this very nice gift, but we should keep this between you and me.”C.“That is a very kind gesture; what can I do for you in return?”D.“Thank you very much, but I am simply giving you the same care I would provide for any ofmy patients.”E.“I cannot accept this extravagant gift beca use it is unethical to accept gifts from patients,but thank you for the thought.”7. A medical intern is working on the inpatient wards at a busy community hospital. During rounds,the team evaluates a new patient who was admitted for an exacerbation of congestive heart failure. The patient’s past medical history includes atherosclerotic coronary artery disease,diabetes mellitus and osteoarthritis. The attending physician asks the intern to start a beta-adrenergic antagonist on this patient. After rounds, the intern recalls that during medical school she learned that beta-adrenergic antagonists can blunt the symptoms of hypoglycemia in a diabetic patient. What is the most appropriate course of action?A.Do not administer the beta-adrenergic antagonist because the most important principle inmedicine is to “do no harm.”B.Discuss concerns about the administration of this drug with the patient, and let the patientdecide whether to take the drug or not.C.Discuss concerns about this drug with the nurses, ask for their input, and ask them to keep aclose eye on the patient to avoid hypoglycemia on this drug.D.Administer the drug because the attending physician is in charge of the team and toundermine his authority is unethicalE.Do not administer the drug until you have discussed your concerns with the attendingphysician and asked him how to proceed8. A 50-year-old Caucasian male is brought to the ER with severe dizziness and confusion. He statesthat he had an episode of chest pain and took several tablets of nitroglycerin. His currentmedications include a daily aspirin for heart attack prevention, an occasional acetaminophen for headaches and occasionally tadalafil for erectile dysfunction. His blood pressure is 50/20 mmHg and his heart rate is 120 beats/min. Which of the following cellular changes is most likelyresponsible for this patient’s symptoms?A.Receptor downregulationB.Gs protein phosphorylationC.Cyclic GMP accumulationD.Tyrosine kinase overactivityE.Enhanced phospholipid metabolismF.Tolerance development9.An 8-year-old Caucasian boy is brought to your office with throat pain, fever and malaise.Physical examination reveals white exudates on his tonsils and swollen anterior cervical lymph nodes. If the boy returns in a month with fatigue, joint pain and chest pain and later in life he develops a heart murmur, which of the following would be most likely explanation for hiscondition?A.Protein A-mediated opsonization blockB.Bacterial and human epitope homologyC.Immune complex depositionD.Exotoxin-induced T-cell receptor activationE.Coronary artery aneurysm formation10.A 68-year-old male is admitted to the hospital for heart palpitations. EKG shows an irregularlyirregular rhythm and absent P waves. The patient is started on warfarin for long-termanticoagulation to prevent atrial thrombus formation. Which of the following should bemonitored in this patient?A.Bleeding timeB.Prothrombin time (PT)C.Activated partial thrmoboplastin time (aPTT)D.Fibrinogen levelsE.Fibrin split products11.Investigators are designing a randomized control trial to test the hypothesis that drug B willdecrease the mortality associated with acute ST elevation compared to standard of care. In order to ensure that they will not miss a difference between drug B and standard of care if one truly exists, they want to maximize:a.Type I errorb.Type II errorc.Alphad.Betae.1-beta12.In certain adults, the myocytes of the cardiac ventricles express mRNA for natriuretic peptidestypically synthesized by the atria. This finding is associated with which of the followingconditions?A.HyperplasiaB.HypertrophyC.Malnutrition atrophyD.Sublethal ischemic injuryE.Reperfusion injuryF.Normal aging13.A study to assess spironolactone’s efficacy is patients with heart failure is performed. 450patients receive either spironolactone or placebo for two years. Neither the patients norphysicians are aware of who takes the drug or placebo. The study setup described above is most effective in preventing:A.Beta errorB.Recall biasC.Observer biasD.Effect modificationE.Selection bias14.While playing soccer, an 18-year-old Caucasian male collapses suddenly and dies. He had nosignificant past medical history, nor had he taken any medications recently. This patient’sautopsy is likely to demonstrate:A.Fresh area of myocardial necrosisB.Multiple foci of mycocardial fibrosisC.Cardiac chamber dilatation and flabby ventricular wallsD.Massive cardiac hypertrophyE.Endocardial thickening and non-compliant ventricular walls15.Membrane potential changes of some atrial myocytes are recorded on the graph below.Which of the following stimuli was most likely applied to the cardiac muscle at the pointindicated by the arrow?A.NorepinephrineB.AdenosienC.GlycineD.Angiotensin IIE.AldosteroneF.Glucagon16.A 15-year-old male suffers severe cardiomyopathy following an infective myocarditis fromCoxsackie virus and is placed on the cardiac transplant list. Two weeks following his cardiac transplantation from a matched donor, he is suffering dyspnea on exertion. Extensive evaluation is undertaken in this patient including cardiac catheterization and endomyocardial biopsy.Which of the following findings is most consistent with acute graft rejection?A.Concentric coronary atherosclerosisB.Dense interstitial lymphocytic infiltrateC.Perivascular infiltrate with abundant eosinophilsD.Patchy necrosis with granulation tissueE.Scant inflammatory cells and interstitial fibrosis17.A 52-year-old Caucasian male presents to your office with two weeks history of progressivefatigue and exertional dypnea. He brings with him the report from a recent cardiaccatheterization (shown below). Cardiac auscultaton reveals a murmur that is best heard when the patient sits up and leans forward. Which of the time points pictured below corresponds to the peak murmur intensity?18.A 72-year-old Caucasian male is hospitalized after complaining of chronic fatigue and exertionaldyspnea. His left ventricular pressure-volume curve is pictured below (curve 2).Assuming heart failure is responsible for this patient’s symptoms, which of the following is the most likely cause of this patient’s condi tion?A.Viral myocarditisB.Alcoholic cardiomyopathyC.AmyloidosisD.Diphtheritic myocarditisE.High-dose doxorubicin19.The results of study investigating a new diagnostic test in diagnosing acute myocardial infarctionare given in the table below.Myocardial infarction No myocardial infarctionTest positive 75 20Test negative 25 80What is the sensitivity of the new diagnostic test?A.25%B.37%C.55%D.70%E.75%F.80%20.A 45-year-old Caucasian female is hospitalized with exertional dyspnea and fatigue. She recentlyemigrated from Eastern Europe and has no significant past medical history. Her blood pressure is 110/80 and her heart rate is 90 beats/min and regular. You suspect mitral stenosis. Which of the following is the best indicator of the severity of stenosis?A.Diastolic murmur intensityB.Presystolic accentuation of the murmurC.S2-to-opening snap time intervalD.Audible S3E.Audible S421.Two atrial (LA) compliance curves in patients with mitral regurgitation are given in the diagrambelow.Compared to the patient having LA compliance shown by curve 1 the patient with the curve 2reading is most likely to suffer:A.Severe fatigue and exhaustionB.Atrial fibrillationC.Acute pulmonary edemaD.Lower extremity swellingE.Arterial embolism22.A Caucasian neonate born to a 22-year-old primigravida has severe tachypnea and cyanosis.Echocardiography shows an aorta that lies anterior to and to the right of the pulmonary artery.Failure of which of the following embryonic processes is most likely responsible for this patient’s condition?A.FusionB.DifferentiationC.SeptationD.ProliferationE.ApoptosisF.Obliteration23.A 43-year-old man is rushed to the emergency room following repeated episode of coffee-ground-appearing emesis. He has a blood pressure of 70/40 mmHg, a heart rate of 130/min, and his extremities are cool to the touch. Immediate infusion of 2L of normal saline is expected to increase:A.Total peripheral resistanceB.Ventricular muscle contraction velocityC.End-diastolic sarcomere lengthD.Heart rateE.Diastolic ventricular compliance24.A group of investigators studies patterns of blood flow in various tissues. One of the patternsthey obtain is shown on the slide below.The flow curve most likely reflects the flow pattern in which of the following tissues?A.Subcortical nucleiB.Brain cortexC.Subendocardial myocardiumD.Renal medullaE.Renal cortexF.Adrenal medulla25.The volume and pressure tracings for the left ventricle of a 34-year-old male are shown below.Which of the following points corresponds to aortic valve opening?26.A 21-year-old Caucasian male presents to your office complaining of repeated episodes ofpalpitations that start and stop abruptly. After completing a careful work-up, you belive that there is an abnormal muscle tract in this patient’s heart that bypasses the AV node. If yourdiagnosis is c orrect, which of the following parts of the patient’s ECG is most likely to be affected at baseline?27.A 65-year-old male loses consciousness while buttoning a tight shirt collar. He reports that thishas happened several times in the past. His blood pressure was 70/40 mmHg and his heart rate was 45/min during one of the episodes. Stimulation of which of the following nerves is most likely responsible?A.HypoglossalB.AccessoryC.TrigeminalD.GlossopharyngealE.Vagal28.The cardiac and venous return curves of a healthy person are shown below in solid lines.Which of the following is the most likely cause of the change depicted by the dashed lines?A.Chronic arteriovenous fistulaB.Acute gastrointestinal bleedC.Phenylephrine infusionD.Myocardial infarctionE.Anaphylaxis29.A new class of drugs called vasopeptidase inhibitors is developed. The drugs in this class inhibitthe angiotensin-converting enzyme and inhibit degradation of natriuretic peptide. Which of the following adverse effects should be expected due to these pharmacologic properties?A.Cold extremitiesB.Throbbing headachesC.Sodium and fluid retentionD.AngioedemaE.Cardiac arrhythmias30.A 23-year-old male is rushed to the emergency room after being involved in a street fight.Physical examination reveals a stab wound at the left sternal border in the fourth intercostal space. Which of the following structures is most likely to have been damaged?A.Pulmonary trunkB.Right ventricleC.Left atriumD.Left ventricleE.Inferior vena cava31.A 64-year-old patient begins aspirin therapy for exertional chest pain. After the first dose,however, he experiences shortness of breath and wheezing. Which of the following medications would serve as a suitable aspirin alternative in this patient?A.HeparinB.WarfarinC.ClopidogrelD.StreptokinaseE.Vitamin KF.AllopurinolG.Paclitaxel32.A 60-year-old male is hospitalized with an arrhythmia. The agent used to treat this patient’scondition is known to significantly prolong the QT interval on EKG, but despite this the drug is associated with a low incidence of torsade de pointes. Which of the following agents was most likely used in this patient?A.AmiodaroneB.EsmololC.LidocaineD.ProcainamideE.VerapamilF.AdenosineG.Digoxin33.A 49-year-old female is brought to the emergency room with squeezing chest pain and profusesweating. ECG reveals ST segment elevation in leads I, aVL and V4-V6. Cardiac troponin levels are high. Soon after hospitalization ventricular tachycardia is noted and thereforeantiarrhythmic therapy is considered. Which of the following antiarrhythmic drugs has thehighest selectivity for ischemic myocardium compared to normal cardiac tissue?A.LidocaineB.ProcainamideC.VerapamilD.AdenosineE.DigoxinbetololG.Amlodipine34.Infective endocarditis is known to be caused by different bacterial species. Which of thefollowing scenarios is most consistent with infective endocarditis caused by Staphylococcus aureus?A. A 34-year-old Asian female with known mitral stenosis develops low-grade fevers andnegative blood culturesB. A 45-year-old Caucasian male complains of fatigue and exertional dyspnea three weeks aftertooth extractionC. A 62-year-old African American female has persistent fever after being diagnosed with coloncancerD. A 64-year-old Caucasian male with fever and malaise has repeatedly negative blood culturesand a small mitral vegetation on transesophageal echocardiogramE. A 29-year-old Caucasian male with persistently high fevers with tricuspid vegetations andtricuspid regurgitation on transthoracic echocardiogram35.A 20-year-old woman undergoes a bilateral oophorectomy. The overies are small andunderdeveloped. On light microscopic examination, the ovaries are found to consist ofconnective tissue with no follicles present. This patient is at increased risk for which of thefollowing:A.Mitral valve prolapseB.Aortic coarctationC.Lens displacementD.Vaginal adenosisE.Pancreatic insuffiency36.A 50-year-old male begins treatment with an antiarrhythmic medication for recurrent atrialfibrillation. The arrhythmia resolves, and there is now mild bradycardia and significant QTinterval prolongation on his EKG recording. Which of the following drugs was most likely used in this patient?A.MetoprololB.PropranololC.SotalolD.CarvedilolE.VerapamilF.Diltiazem37.In a patient with severely impaired left ventricular function, IV digoxin administration increasescardiac output and decreases right atrial pressure and pulmonary capillary wedge pressure.Which of the following is the initial cellular event triggering this response to digoxin?A.Decreased sodium effluxB.Increased calcium influxC.Increased potassium influxD.Increased cAMP concentrationE.Troponin sensitization to calcium38.A 36-year-old Caucasian female with a three week history of progressive fatigue and low-gradefevers is brought to the emergency department with sudden-onset right-sided weakness and speech difficulty. She is admitted, but dies two hours later. Gross autopsy specimen of her heart is shown below (LA=left atrium, LV=left ventricle):Which of the following conditions is most likely to have predisposed to this patient’s disease?A.Rheumatic heart diseaseB.Atrial septal defectC.Mitral annulus calcificationD.Coronary heart diseaseE.Hypertrophic cardiomyopathyF.Mitral valve prolapsed39.A 34-year-old male is admitted to the hospital with acute chest pain. An ECG obtained in the ERshows ST segment elevation in leads II, III and avF. A sample of blood is taken from the patient and the plasma homocysteine level is measured three times using a new test. The results are12.2 umol/L, 13.5 umol/L, and 15.0 umol/L. These results suggest that concerns should be raisedabout which of the following with the new test?A.ReliabilityB.ValidityC.AccuracyD.SensitivityE.Specificity40.A 65-year-old male presents to your office complaining of worsening exertional dyspnea andlower extremity edema. His past medical history is significant for hypertension, diabetes mellitus and a myocardial infarction two years ago. His medications include aspirin andhydrochlorothiazide. Addition of which of the following agents is most likely to decrease long-term mortality in this patient?A.FurosemideB.NitratesC.AmiodaroneD.CarvediolrnoneF.Digoxin41.A 7-year-old Caucasian male is brought to your office because of recurrent episodes of dyspneaand “turning blue,” to which the boy responds by assuming a squatting posture. This patient most likely suffers from:A.Primum-type atrial septal defectB.Secundum-type atrial septal defectC.Ventricular septal defectD.Patent ductus arteriosusE.Coarctation of the aortaF.Tetralogy of Fallot42.A new born is being evaluated for cyanosis. Echocardiography demonstrates apical displacementof the tricuspid valve leaflets, increased right ventricular volume, and atrialization of the right ventricle. If this neonate’s condition is due to a drug side effect, the mother most likely has which of the following conditions?A.Gestational diabetesB.SchizophreniaC.Narcotic abuseD.Alcohol abuseE.Cocaine abuseF.Seizure disorderG.Bipolar disorderH.HypothyroidismI.Down syndrome43.A 19-year-old Caucasian male presents to your office for a routine check-up. His body habitus ispictured below.This patient is most likely to die from:A.Myocardial infarctionB.Renal failureC.Aortic diseaseD.Overwhelming infectionE.Liver disease44.A group of physicians in a developing country is advocating the early empiric use of penicillin inthe treatment of clinically diagnosed bacterial pharyngitis, a condition that is quite common in children of that nation. What would you expect to decrease as a result of their policy in the long term?A.Expensive antibiotic requirementB.Nephritic diseaseC.Deaths caused by diarrheaD.Bronchial asthma hospitalizationsE.Cardiac surgeriesF.Vaccination needs45.A 10-year-old immigrant from Eastern Europe is brought to your office complaining of exertionaldyspnea and easy fatigability. According to his parents, he was diagnosed with a congenital heart disease (type unknown) in infancy, for which they refused surgical correction. Physical examination reveals toe cyanosis and clubbing but no finger abnormalities. This patient most likely suffers from:A.Primum-type atrial septal defectB.Secundum-type atrial septal defectC.Ventricular septal defectD.Patent ductus arteriosusE.Coarctation of the aortaF.Tetralogy of Fallot46.A 32-year-old Caucasian male is brought to the emergency department with a several dayhistory of high-grade fever, dyspnea and fatigue. Physical examination reveals a newholosystolic murmur with a blowing quality, heard best over the cardiac apex. On physical examination, the lesions pictured below are observed on the sole of the foot:These lesions most likely represent:A.Primary infection fociB.Immune complex-mediated vascular lesionsC.Microthrombi to skin vesselsD.Areas of local vascular growthE.Foci of granulomatous inflammation47.In order to maintain constant fluid flow through a tube with varying diameters, which of thefollowing would be true (where A1 and A2 represent cross-sectional areas, and V1 and V2 represent the corresponding flow velocities)?A.V1=V2B.V1=A1*V2C.A2=A1*V1/V2D.V1=A1*A2/V2E.V1*A2=A2*A148.A 34-year-old female who recently emigrated from Russia complains of weakness, exertionaldyspnea and orthopnea. On cardiac auscultation, a snap followed by a rumbling diastolicmurmur is heard over the cardiac apex. Which of the following points best corresponds to the occurrence of the snap?49.A 5-year-old child develops cyanosis with minimal exertion. On medical evaluation, he is foundto have an enlarged right ventricle. Which of the following early developmental events most likely underlies his condition?A.Abnormal neural crest cell migrationB.Endocardial cushion defectC.Aortic arch constrictionD.Pulmonary hypertensionE.Abnormal primitive heart tube looping50.A 5-year-old child who recently moved from Eastern Europe is brought to the emergency roomwith difficulty breathing and a low-grade fever. Physical examination reveals a grayishpharyngeal exudates, enlarged cervical lymph nodes and partial soft palate paralysis. Bacteria isolated from the pharyngeal exudates demonstrate exotoxin production in the laboratory. This exotoxin acts via the following mechanism:A.Intracellular protein ribosylationB.Degradation of lecithinC.Increased sensitivity to histamineD.Inactivation of the 60s ribosomal subunitE.Autoimmune activation by antigenic mimicry51.A 60-year-old Caucasian male is diagnosed with exertional angina and isosorbide dinitrate isprescribed for chronic therapy. The patient is concerned about the possible side effects of this therapy. Which of the following is most likely to occur in this patient?A.AV conduction delayB.Nocturnal wheezingC.ConstipationD.Urinary retentionE.Throbbing headachesF.Joint painG.Cold extremities52.A 32-year-old Caucasian female who has suffered from progressive exertional dyspnea overseveral years dies suddenly. At autopsy, her heart has the following appearance (RV=right ventricle, LV=left ventricle):This patient most likely suffered from:A.Essential hypertensionB.Dialted cardiomyopathyC.Primary pulmonary hypertensionD.Myocardial infarctionE.Acquired aortic stenosisF.Wolf-Parkinson-white syndrome53.You are caring for a 56-year-old male who was admitted for chest pain. His cardiac troponins areelevated and a cardiac catheterization is planned for that evening. When you are exiting the patient’s room after discussing the catheterization with him you encounter his wife who has just arrived at the hospital. She quickly asks what has happened to her husband and what is planned.What is the most appropriate course of action?rm the patient’s wife of his condition because she is his legal next of kin.B.Discuss end of life care and “Do Not Resuscitate” orders with the patient’s wife because ofhis serious condition.C.Do not discuss the patient’s status with the patient’s wife because the patient has notgranted permission for his medical care to be discussed with her.D.Do not discuss the patient’s status with the patient’s wife because she may not have thepatient’s best wishes in mindrm the patient’s wife that the patient has had a heart attack, but also tell her that shemust discuss details with her husband.54.A 56-year-old homeless man presents to the ER with increased fatigability and exertionaldyspnea. Physical examination shows significant lower extremity edema and decreasedsensation over the ankles and feet. Further evaluation reveals cardiac dilation and increased cardiac output. Which of the following nutrient deficiency is most likely responsible for this p atient’s symptoms?A.Vitamin AB.Vitamin B1C.Vitamin B2D.PyridoxineE.NiacinF.Ascorbic acidG.Vitamin B1255.A 46-year-old Caucasian female presents to your office because of easy fatigability andexertional dyspnea. Auscultation of the heart reveals a diminished first heart sound and an apical holosystolic murmur radiating to the axilla. Lungs have bibasilar crackles. There is no elevation of jugular venous pressure or peripheral edema. Which of the following would most likely increase forward-to-regurgitant volume ratio in this patient?A.Decreasing left ventricular preloadB.Increasing left ventricular contractilityC.Decreasing left ventricular afterloadD.Decreasing heart rateE.Increasing left ventricular volume56.Transient bacteremia is demonstrated in a healthy 22-year-old male after a dental procedure.The Gram-positive bacteria isolated from the blood synthesize dextrans from sucrose. Which of the following would be the most likely adherence site for these bacteria?A.Endothelial surface glycoproteinsB.Subendothelial collagenC.Subendothelial glycosaminoglycansD.Circulating heparinsE.Fibrin-platelet aggregates57.A 52-year-old Caucasian male presents to your office for a routine check-up. He says that ‘somecardiac problems’ were detected during his previous visit to the doctor. Ph ysical examination reveals a holosystolic murmur at the apex that radiates to the axilla. Which of the following is the best indicator of the severity of this patient’s problem?A.Holosystolic murmur intensityB.Presystolic component of the murmurC.S2 to opening snap (OS) time intervalD.Presence of audible S3E.Presence of audible S458.Plasma homocysteine levels are measured in patients with acute coronary syndrome who aretreated in a large community hospital. The mean plasma homocysteine level in this group is determined to be 11.1 umol/L with a standard deviation of 1.2 umol/L. In a separate group of patients hospitalized on the general ward in the same hospital, the mean plasma level is 9.5 umol/L and standard deviation is 1.3 umol/L. Which of the following tests should be used to compare the mean homocysteine level s of these two groups of patients?A.Two-sample t testB.Two-sample z testC.Analysis of variance (ANOVA)D.Chi-square testE.Meta-analysis59.A 60-year-old male non-smoker with a history of type II diabetes mellitus, hypertension,hypercholesterolemia and mild renal insufficiency presents to your office complaining of a dry cough during the past month. His blood pressure is 130/80 mmHg. His medications include aspirin, glipizide, lovastatin, hydrochlorothiazide, a nd captopril. In order to relieve the patient’s cough, which of the following drugs would it be best to substitute for one of the patient’scurrent medications?A.MetforminB.PropranololC.PrazosinD.LosartanE.Tolbutamide。
血浆脑钠肽检测在心力衰竭诊断中的应用评价
血浆脑钠肽检测在心力衰竭诊断中的应用评价王元芬【摘要】目的:探讨血浆脑钠肽(brain natriuretic peptide,BNP)检测在心力衰竭(心衰)诊断中的应用价值.方法:选取心衰患者71例为观察组,同时选取71例健康体检者为对照组,比较两组血浆BNP、左心室射血分数(left ventricular ejectionfraction,LVEF)、不同心功能分级BNP水平及阳性检出情况.结果:观察组LVEF比对照组低,血浆BNP水平比对照组高,差异均有统计学意义(P<0.05);观察组心功能Ⅰ级患者血浆BNP阳性检出率53.33%,Ⅱ级阳性检出率76.47%,Ⅲ级阳性检出率95.00%,Ⅳ级阳性检出率100.00%;心功能Ⅳ级患者血浆BNP水平高于Ⅲ级、Ⅱ级及Ⅰ级患者,差异均有统计学意义(t=36.535、24.466、19.305,均P<0.05);心功能Ⅲ级患者血浆BNP水平高于Ⅰ级患者,差异有统计学意义(t=2.732,P <0.05);但心功能Ⅱ级患者血浆BNP水平与Ⅰ级和Ⅲ级比较,差异均无统计学意义(t=1.904、1.104,均p>0.05).结论:血浆BNP检测在心衰诊断中效果较好,有助于早期诊断,且心衰越严重其阳性检出率与检测值越高.%Objective:To investigate the clinical value of brain natriuretic peptide (BNP) in the diagnosis of heart failure.Methods:A total of 71 cases of patients with heart failure were selected as observation group.In the same period,71 healthy subjects were selected as the control group.The levels of BNP,left ventricular ejection fraction (LVEF),BNP grade with different cardiac function and positive rate were compared between the two groups.Results:The LVEF in the observation group was significantly lower than that in the control group,and the levels of BNP was higher than that in the control group,the difference was statistically significant (P <0.05).The positive rate of gradeⅠ was 53.33%,the positive rate of grade Ⅱ was 76.47%,the positive rate of grade Ⅲ was 95.00%,the positive rate of grade Ⅳ was 100.00%.The level of BNP in patients with grade Ⅳ cardiac function was significantly higher than that in grade Ⅰ,Ⅱ and Ⅲ patients,the difference was statistically significant (t =36.535,24.466,19.305,P <0.05).The level of BNP in patients with heart function grade Ⅲ was higher than that of patients with grade Ⅰ,and the difference was statistically significant (t =2.732,P <0.05).However,there was no significant difference between the level of BNP in the patients with cardiac function grade Ⅱ with these in the grade Ⅰ and Ⅲ.Conclusion:BNP detection has a good effect in the diagnosis of heart failure,which is helpful for early diagnosis,and the more serious the heart failure is,the higher the positive detection rate and detection value are.【期刊名称】《川北医学院学报》【年(卷),期】2017(032)006【总页数】3页(P821-823)【关键词】血浆脑钠肽;心力衰竭;检测率;诊断;应用价值【作者】王元芬【作者单位】安顺市人民医院心内科,贵州安顺561000【正文语种】中文【中图分类】R446.61心肌收缩力降低引发的一种临床综合征为心力衰竭(心衰),是造成心源性死亡的主要原因[1]。
cardiology2016 191-200
儿童暴发性心肌炎病例分析及文献复习
儿童暴发性心肌炎病例分析及文献复习刘冉'李艳2,黄琰琰3,邹庆梅4,徐南平2,余婧2I.深圳市龙华区人民医院,广东深圳5丨8109;2.南吕大学附属儿童医院,江西南昌330006;3.深圳市第二人民医院,广东深圳518035, 3惠州市第三人民医院,广东惠州516002摘要:通过分析1例不典型儿重晷发性心肌炎(fulminant myocarditis, F M C)临床资料结合近年相关文献,探讨儿重F M C的临床特 点及早期识别与治疗的方法,有助临床尽早识别和诊断F M C,采取积极抢救措施,降低死亡率关键词:儿童,心肌酶谱,暴发性心肌炎,临床特点中图分类号:R542. 2+1 文献标识码:丨5文章编号:1673-6966(2021)03-0338-03病例报告\中国急救复苏与灾‘H、2()2丨年3月第16卷第3期(:丨丨i" J丨:丨削名Krs丨丨S••丨)iwsu‘r Med,March2021 丨丨.Ift\〇.3儿童暴发性心肌炎是最严重的心肌炎,特点为病 情发展迅速,可引起心力衰竭,血液动力学障碍和心 源性休克等严重结果'2019年南昌大学附属儿童 医院收治了 1例以发热、腹痛、呕吐及口唇发绀为主 要症状的F M C,现报道如下。
1病例简介患者,男,6岁10月,因“发热3 d,腹痛伴呕吐 1 (!, 口唇发绀半天”于2019年9月19丨_】20:29人 院。
病史采集:患儿3 (丨前出现发热,无咳嗽,无流 涕,无头痛,1c l前呕吐1次,伴腹痛,跻周痛为主,无腹泻,人院当天呕吐3次,腹痛加剧,口唇发绀 半天人院。
既往无心脏病及家族遗传病史。
查 体:T:36.9X:,R:30 次/m i n,P: 198 次 /m i n,B P:78/51 m m H s神志清楚,精神差,呼吸急促,面色苍白,口唇发绀,心音低钝,心律不齐,未闻及杂音。
脐周有 压痛,无反跳痛3肝肋下3 m m,睥肋下未触及。
总缺血时间与门球时间对急性心肌梗死病人主要心脏不良事件发生率的影响
总缺血时间与门球时间对急性心肌梗死病人主要心脏不良事件发生率的影响王 潇,潘一龙,常 程,谢瑶峰,李晓东摘要 目的:探究总缺血时间与门球时间对急性心肌梗死病人主要心脏不良事件发生率的影响㊂方法:选取2019年12月 2021年6月因急性心肌梗死于我院行经皮冠状动脉介入治疗的病人255例㊂计算病人的总缺血时间㊁门球时间,并根据冠状动脉造影结果计算SYNTAX 评分,利用SYNTAX 评分评估冠状动脉病变的严重程度,并根据SYNTAX 评分分为低危组㊁中危组㊁高危组㊂对病人进行为期1个月的随访,记录病人主要心脏不良事件(MACE )的发生情况㊂结果:低危组㊁中危组㊁高危组门球时间㊁总缺血时间比较,差异均无统计学意义(P >0.05),MACE 发生率差异有统计学意义(P <0.05)㊂尚未发现低危组㊁中危组㊁高危组MACE 的发生与门球时间㊁总缺血时间有相关性㊂结论:冠状动脉病变中㊁高危病人MACE 发生率较高,缩短病人的门球时间㊁总缺血时间对改善短期预后无影响㊂关键词 急性心肌梗死;冠状动脉病变;总缺血时间;门球时间;SYNTAX 评分d o i :10.12102/j.i s s n .1672-1349.2023.10.029 近年来,我国急性心肌梗死的死亡率仍然呈上升趋势,根据流行病学调查显示,我国心血管病负担日益加重,其中,急性心肌梗死占据了相当大的一部分,且农村死亡率持续高于城市,由于术后并发症的发生,急性心肌梗死的住院总费用也在增加[1-2]㊂因此,加强急性心肌梗死的诊治已成为刻不容缓的公共卫生问题㊂ 时间就是心肌 ,使缺血的心肌立即得到再灌注是治疗的关键㊂研究表明,经皮冠状动脉介入治疗(percutaneous coronary intervention ,PCI )每延迟1h ,死亡率就会增加约10%[3]㊂虽然PCI 可以实现心肌的再灌注,但每年仍有很多病人尚未到达医院就已死亡㊂因此,缩短救治时间是控制死亡率的重中之重㊂门球时间(door to balloon ,D to B )最早由美国心脏病学会(ACC )/美国心脏协会(AHA )提出,是指从病人进入医院大门到首次球囊扩张开通罪犯血管的时间,推荐时间为90min 以内[4-6]㊂目前已有多项研究表明,积极缩短门球时间具有降低急性心肌梗死病人死亡率㊁减少术后并发症等改善预后的效果[7-10]㊂总缺血时间(total ischemic time ,TIT )是指病人出现急性胸痛等心肌缺血症状至首次球囊扩张的时间,理论上等同于门球时间加上病人从出现症状至进入医院大门的时间,它也是评价救治时间的一项客观指标[11-12]㊂研究表明,总缺血时间控制在120min 以内的病人获益最为基金项目 十二五 国家科技支撑计划(No.2014BAL11B04)作者单位 中国医科大学附属盛京医院(沈阳110004)通讯作者 李晓东,E -mail :****************引用信息 王潇,潘一龙,常程,等.总缺血时间与门球时间对急性心肌梗死病人主要心脏不良事件发生率的影响[J ].中西医结合心脑血管病杂志,2023,21(10):1877-1880.显著[13]㊂然而,救治时间并非是影响死亡率的唯一变量,病人冠状动脉病变的严重程度也会对死亡率产生影响㊂SYNTAX 评分是一种能够通过造影来判断冠状动脉病变严重程度的评判积分,往往更直观㊁更准确㊂本研究采用SYNTAX 评分评估病人冠状动脉病变的严重程度,旨在研究在控制SYNTAX 评分情况下,总缺血时间与门球时间对急性心肌梗死病人短期预后的影响㊂1 资料与方法1.1 研究对象 选取2019年12月 2021年6月因急性心肌梗死就诊于我院行PCI 的病人255例,计算病人的总缺血时间㊁门球时间,并根据冠状动脉造影结果计算SYNTAX 评分,利用SYNTAX 评分评估冠状动脉病变的严重程度㊂对病人进行为期1个月的随访,记录病人主要心脏不良事件(MACE )的发生情况,并统计其发生率㊂纳入标准:①临床诊断为急性ST 段抬高型心肌梗死,胸痛并伴有心电图相邻两个或以上导联ST 段抬高ȡ0.10mV (<40岁男性V 2~V 3导联ST 段抬高ȡ0.25mV ;ȡ40岁男性V 2~V 3导联ST 段抬高ȡ0.20mV 或女性V 2~V 3导联ST 段抬高ȡ0.15mV )或新发左束支传导阻滞;②发病时间12h 以内;③高危的急性非ST 段抬高型心肌梗死病人,即GRACE 评分大于140分者;④病人及家属同意行PCI 者㊂排除标准:①非急性胸痛而择期行冠状动脉造影的病人;②溶栓后行补救PCI 治疗者;③选择非血运重建治疗的病人;④行PCI 前病人死亡或不同意行PCI 者㊂1.2 方法1.2.1 分组 根据SYNTAX 评分,将病人分为高危组㊁中危组㊁低危组(根据SYNTAX 评分危险分层,SYNTAX评分ɤ22分为低危组;SYNTAX评分23~ 32分为中危组,SYNTAX评分ȡ33分为高危组),计算各组病人的总缺血时间㊁门球时间,通过随访记录各组病人MACE的发生情况㊂每组分别按照总缺血时间㊁门球时间再分为各亚组,比较各亚组MACE发生情况㊂1.2.2研究方法收集病人一般资料,计算门球时间㊁总缺血时间㊂利用SYNTAX评分评估冠状动脉病变的严重程度㊂SYNTAX评分:经动脉穿刺Judkins法行冠状动脉造影,由至少2名高年资心内科冠状动脉介入主任医师对冠状动脉病变做出评估,至少2名心内科冠状动脉介入医师按照SYNTAX评分要求计算评分结果㊂随访并记录病人1个月内MACE的发生情况,包括再发急性心肌梗死㊁心力衰竭㊁心源性休克㊁心因性死亡㊁再住院㊁再灌注心律失常等㊂1.3统计学处理采用SPSS22.0统计软件进行数据分析㊂不符合正态分布的定量资料用中位数㊁四分位数[M(P25,P75)]表示,采用Mann-Whitney U检验㊂定性资料以例数㊁百分率(%)表示,采用χ2检验㊂以P<0.05为差异有统计学意义㊂2结果2.13组门球时间㊁总缺血时间比较低危组㊁中危组㊁高危组门球时间㊁总缺血时间比较,差异均无统计学意义(P>0.05)㊂详见表1㊂表13组门球时间㊁总缺血时间比较[M(P25,P75)]单位:min 组别例数门球时间总缺血时间低危组130108.50(77.00,173.00)371.00(263.75,631.75)中危组90105.50(79.95,186.75)405.50(250.75,713.50)高危组3596.00(77.00,141.00)358.00(257.00,657.00) P>0.05>0.052.2各组MACE发生情况比较各组MACE发生率比较,差异有统计学意义(P<0.05)㊂详见表2㊂表2各组MACE发生情况比较单位:例(%)组别例数MACE低危组1307(5.38)中危组9032(35.55)高危组3522(62.86)P<0.052.3各组门球时间㊁总缺血时间与MACE的关系低危组㊁中危组㊁高危组MACE的发生均与门球时间㊁总缺血时间相关性无统计学意义(P均>0.05)㊂详见表3~表5㊂表3低危组不同门球时间㊁总缺血时间的MACE发生情况单位:例总缺血时间门球时间>90minɤ90min合计>120min516ɤ120min101合计617注:P=1.000㊂表4中危组不同门球时间㊁总缺血时间的MACE发生情况单位:例总缺血时间门球时间>90minɤ90min合计>120min21930ɤ120min022合计211132注:P=0.111㊂表5高危组不同门球时间㊁总缺血时间的MACE发生情况单位:例总缺血时间门球时间>90minɤ90min合计>120min12719ɤ120min033合计121022注:P=0.078㊂3讨论自心肌再灌注治疗的理念提出以来,尽可能地缩短心肌缺血时间,挽救更多的濒死心肌成为治疗的关键,门球时间㊁总缺血时间也作为一种量化指标被提出,用以评价救治的及时性㊂本研究根据SYNTAX评分对病人进行分组,发现急性心肌梗死病人MACE的发生和门球时间㊁总缺血时间的相关性无统计学意义㊂这可能是由于低危组病人的血管病变较轻,其他血管可为其提供短暂的侧支循环以保证心肌的血供㊂中危组㊁高危组MACE的发生与门球时间㊁总缺血时间无关可能与纳入样本量少有关㊂门球时间是国内推荐的经典指标,目前,国内各医疗机构胸痛中心急救绿色通道也都倡导缩短门球时间㊂研究表明,门球时间每增加30min,急性心肌梗死病人的死亡率增加约17%[14-16]㊂有研究证实了门球时间延迟的急性心肌梗死病人死亡率较高,且短期死亡率与中长期死亡率之间无明显相关性[17-25]㊂Brodie 等[25-26]对急性心肌梗死病人进行了7个月的随访,发现门球时间延迟病人的射血分数较门球时间90min以内的病人明显降低㊂因此,近年来各医疗机构不断优化流程,尽管门球时间提高了,但病人住院期间死亡率与出院后短期死亡率并没有如预期一样随门球时间缩短而下降[27]㊂Flynn等[27]研究得出门球时间与死亡率无明显相关性的结论㊂因此,如果病人入院前已经延误了很长时间,即使将门球时间尽可能地缩短,也达不到预期的治疗效果㊂由此可见,仅仅以门球时间评价预后是片面的,病人从发病到进入医院这段时间的长短也至关重要㊂2013年ACC‘急性ST段抬高型心肌梗死病人管理指南“提出了总缺血时间㊂有研究表明,虽然门球时间的延误与MACE有相关性,但门球时间与MACE并非线性关系,在发病早期或晚期,门球时间与短期死亡率的相关性是不同的㊂院前延误时间较短者的门球时间与短期死亡率的相关性更强,在评价预后方面总缺血时间也许是一个比门球时间更全面的指标[28-31]㊂Denktas等[11]研究发现,将总缺血时间控制在120 min以内会使病人获益最显著㊂有研究利用总缺血时间与门球时间预测病人30d MACE发生率及心肌梗死面积,最终证实了其预测急性心肌梗死病人预后的可靠性[32]㊂然而,总缺血时间的影响因素也较多,病人的就医意识㊁医患关系及医疗系统的延误等均会影响总缺血时间㊂此外,诊断明确㊁相对禁忌证较少㊁愿意配合病人的总缺血时间较短㊂病情的严重程度会影响预后,对于冠状动脉病变较为复杂的病人,尽管尽可能缩短门球时间㊁总缺血时间,但仍无法避免出现不良预后,因此,在利用总缺血时间㊁门球时间评价预后时应当控制各组病情的严重程度㊂参考文献:[1]陈伟伟,高润霖,刘力生,等.‘中国心血管病报告2017“概要[J].中国循环杂志,2018,33(1):1-8.[2]胡盛寿,高润霖,刘力生,等.‘中国心血管病报告2018“概要[J].中国循环杂志,2019,34(3):209-220.[3]IBANEZ B,JAMES S,AGEWALL S,et al.2017ESC guidelines forthe management of acute myocardial infarction in patientspresenting with ST-segment elevation:the Task Force for themanagement of acute myocardial infarction in patientspresenting with ST-segment elevation of the European Society ofCardiology(ESC)[J].European Heart Journal,2018,39(2):119-177.[4]MENEES D S,PETERSON E D,WANG Y F,et al.Door-to-balloontime and mortality among patients undergoing primary PCI[J].The New England Journal of Medicine,2013,369(10):901-909. [5]MÜLLER U M,EITEL I,ECKRICH K,et al.Impact of minimisingdoor-to-balloon times in ST-elevation myocardial infarction toless than30min on outcome:an analysis over an8-year period ina tertiary care centre[J].Clinical Research in Cardiology,2011,100(4):297-309.[6]WEN E R,SIM J,TAN M C,et al.TCTAP A-133treatment delay indoor-to-balloon time in south-east Asian patients undergoingprimary percutaneous coronary intervention for ST-segmentelevation myocardial infarction:a key process analysis of patientfactors[J].Journal of the American College of Cardiology,2015,65(17):S66.[7]RA THORE S S,CURTIS J P,NALLAMOTHU B K,et al.Association ofdoor-to-balloon time and mortality in patients65years with ST-elevation myocardial infarction undergoing primary percutaneouscoronary intervention[J].The American Journal of Cardiology,2009,104(9):1198-1203.[8]RATHORE S S,CURTIS J P,CHEN J,et al.Association of door-to-balloon time and mortality in patients admitted to hospital with STelevation myocardial infarction:national cohort study[J].BMJ,2009,338:b1807.[9]BRENNAN A L,ANDRIANOPOULOS N,DUFFY S J,et al.Trendsin door-to-balloon time and outcomes following primarypercutaneous coronary intervention for ST-elevation myocardialinfarction:an Australian perspective[J].Internal Medicine Journal,2014,44(5):471-477.[10]ZAHN R,VOGT A,ZEYMER U,et al.In-hospital time to treatmentof patients with acute ST elevation myocardial infarction treatedwith primary angioplasty:determinants and outcome.Results fromthe registry of percutaneous coronary interventions in acutemyocardial infarction of the Arbeitsgemeinschaft LeitenderKardiologischer Krankenhausarzte[J].Heart,2005,91(8):1041-1046.[11]DENKTAS A E,ANDERSON H V,MCCARTHY J,et al.Totalischemic time:the correct focus of attention for optimal ST-segmentelevation myocardial infarction care[J].JACC CardiovascularInterventions,2011,4(6):599-604.[12]SOLHPOUR A,CHANG K W,ARAIN S A,et al.Ischemic time is abetter predictor than door-to-balloon time for mortality and infarctsize in ST-elevation myocardial infarction[J].Catheterization andCardiovascular Interventions,2016,87(7):1194-1200. [13]DE ANDRADE P B,TEBET M A,NOGUEIRA E F,et al.Impact ofinter-hospital transfer on the outcomes of primary percutaneouscoronary intervention[J].Revista Brasileira De Cardiologia Invasiva,2012,20(4):361-366.[14]IANTORNO M,SHLOFMITZ E,ROGERS T,et al.Should non-ST-elevation myocardial infarction be treated like ST-elevationmyocardial infarction with shorter door-to-balloon time?[J].TheAmerican Journal of Cardiology,2020,125(2):165-168. [15]NALLAMOTHU B K,NORMAND S L,WANG Y F,et al.Relationbetween door-to-balloon times and mortality after primarypercutaneous coronary intervention over time:a retrospectivestudy[J].Lancet,2015,385(9973):1114-1122.[16]MCNAMARA R L,WANG Y F,HERRIN J,et al.Effect of door-to-balloon time on mortality in patients with ST-segment elevationmyocardial infarction[J].Journal of the American College ofCardiology,2006,47(11):2180-2186.[17]RA THORE S S,CURTIS J P,NALLAMOTHU B K,et al.Association ofdoor-to-balloon time and mortality in patients65years with ST-elevation myocardial infarction undergoing primary percutaneouscoronary intervention[J].The American Journal of Cardiology,2009,104(9):1198-1203.[18]LAMBERT L,BROWN K,SEGAL E,et al.Association betweentimeliness of reperfusion therapy and clinical outcomes in ST-elevation myocardial infarction[J].JAMA,2010,303(21):2148-2155.[19]KODAIRA M,KAWAMURA A,MIYATA H,et al.Door to balloontime:how short is enough under highly accessible nationwideinsurance coverage?Analysis from the Japanese MulticenterRegistry[J].International Journal of Cardiology,2013,168(1):534-536.[20]NAKAMURA M,YAMAGISHI M,UENO T,et al.Current treatmentof ST elevation acute myocardial infarction in Japan:door-to-balloon time and total ischemic time from the J-AMI registry[J].Cardiovascular Intervention and Therapeutics,2013,28(1):30-36.[21]SONG Y B,HAHN J Y,GWON H C,et al.The impact of initialtreatment delay using primary angioplasty on mortality amongpatients with acute myocardial infarction:from the Korea AcuteMyocardial Infarction Registry[J].Journal of Korean MedicalScience,2008,23(3):357-364.[22]WONGPRAPARUT N,CHOTINAIW A TT ARAKUL C,PANCHA VINNIN P,et al.First medical contact to device time in the ThailandPercutaneous Coronary Intervention(PCI)Registry[J].Chotmaihet Thangphaet,2014,97(12):1247-1253.[23]BRODIE B R,STONE G W,MORICE M C,et al.Importance of timeto reperfusion on outcomes with primary coronary angioplasty foracute myocardial infarction(results from the stent primaryangioplasty in myocardial infarction trial)[J].The AmericanJournal of Cardiology,2001,88(10):1085-1090.[24]SOON C Y,CHAN W X,WU Y J,et al.The impact of time-to-balloon on outcomes in patients undergoing modern primaryangioplasty for acute myocardial infarction[J].Annals of theAcademy of Medicine,Singapore,2004,33(5Suppl):S68-S70. [25]BRODIE B R,STONE G W,COX D A,et al.Impact of treatmentdelays on outcomes of primary percutaneous coronaryintervention for acute myocardial infarction:analysis from theCADILLAC trial[J].American Heart Journal,2006,151(6):1231-1238.[26]BRODIE B R,HANSEN C,STUCKEY T D,et al.Door-to-balloontime with primary percutaneous coronary intervention for acutemyocardial infarction impacts late cardiac mortality in high-riskpatients and patients presenting early after the onset ofsymptoms[J].Journal of the American College of Cardiology,2006,47(2):289-295.[27]FLYNN A,MOSCUCCI M,SHARE D,et al.Trends in door-to-balloon time and mortality in patients with ST-elevationmyocardial infarction undergoing primary percutaneous coronaryintervention[J].Archives of Internal Medicine,2010,170(20):1842-1849.[28]REIMER K A,LOWE J E,RASMUSSEN M M,et al.The wavefrontphenomenon of ischemic cell death.1.Myocardial infarct size vsduration of coronary occlusion in dogs[J].Circulation,1977,56(5):786-794.[29]GARCIA-DORADO D,THÉROUX P,ELIZAGA J,et al.Myocardialreperfusion in the pig heart model:infarct size and duration ofcoronary occlusion[J].Cardiovascular Research,1987,21(7):537-544.[30]BRODIE B R,STUCKEY T D,WALL T C,et al.Importance of timeto reperfusion for30-day and late survival and recovery of leftventricular function after primary angioplasty for acutemyocardial infarction[J].Journal of the American College ofCardiology,1998,32(5):1312-1319.[31]LUCA G D,SURYAPRANATA H,ZIJLSTRA F.Symptom-onset-to-balloon time and mortality in patients with acute myocardialinfarction treated by primary angioplasty[J].ACC CurrentJournal Review,2004,13(1):45.[32]ALSAMARA M,DEGHEIM G,GHOLKAR G,et al.Is symptom toballoon time a better predictor of outcomes in acute ST-segmentelevation myocardial infarction than door to balloon time?[J].American Journal of Cardiovascular Disease,2018,8(4):43-47.(收稿日期:2021-07-24)(本文编辑王丽)。
心血管类英文杂志
缩写名/全名影响因子投稿难易一审周期international journal of cardiology 6.175命中率约35.62%平均4.5月American journal of cardiology 3.425命中率约37.5% 平均1月journal of the American college ofcardiology 15.343命中率约5%平均1月pediatric cardiology 1.55命中率约50% 平均12月Canadian journal of cardiology 3.94命中率约50% 平均1月journal of molecular and cellularcardiology 5.218命中率约41.66%平均1月Journal of Invasive Cardiology 0.824 容易一般,3-8周Experimental & Clinical Cardiology 0.758命中率约81.66% 平均1月Journal of geriatric cardiology1.056新增容易较慢,6-12周Nature reviews cardiology 10.154 很难较慢,6-12周cardiology clinics 1.064 容易>12周,或约稿Cardiology review 3.238>12周,或约稿current problems in cardiology 2.167 较易>12周,或约稿Hellenic journal of cardiology 0.785 容易>12周circulation journal 3.685命中率约25%平均1.6月microcirculation 2.263 较易较慢6-12周Netherlands Heart Journal 2.263 较易较慢6-12周international heart journal 1.127 较易较慢6-12周heart and vessels 2.109 命中率约62.5%平均1.2月atherosclerosis 3.971 命中率约37.5%平均2.6月Scurrent atherosclerosis reports 3.059较慢,6-12周journal of atherosclerosis and thrombosis 2.77 命中率约75%平均1月atherosclerosis supplements9.667 命中率约50%1月catheterization and cardiovascularinterventions2.396 80% 2月cardiovascular diabetology3.706 1月journal of cardiovascular pharmacology 2.111 命中率约71.87%1月circulation-cardiovascular quality andoutcome5.04 6-12周journal of cardiovascular pharmacologyand therapeutics3.072 50% 1月progress in cardiovascular diseases 2.443 较易6-12周cardiovascular drugs and therapy 2.952 62.5% 1.7月。
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Q2
A 62-year-old man with a long history of hypertension comes to the physician for a routine physical examination. His blood pressure is 150/90 mm Hg and heart rate is 74/min and regular. Cardiac auscultation shows a presystolic sound that immediately precedes the first heart sound and is best heard during expiration when the patient is lying on his left side. Chest x-ray reveals extensive calcification around the mitral and aortic valves. Which of the following is the most likely explanation for the additional heart sound? A. Increased flow velocity through the aortic valve B. Increased stiffness of the left ventricular wall C. Rapid passive filling of the ventricles D. Restricted motion of the aortic valve cusps E. Systolic anterior motion of the mitral valve
cardiology2016 91-100
A 65-year-old man comes to the office due to exertional dyspnea and easy fatigability. He has no other medical problems. The patient has not seen a physician in the last 10 years. He takes no medications but smokes a pack of cigarettes per day and drinks approximately 7-10 alcoholic beverages a week His blood pressure is 170/90 mm Hg and pulse is 80/min. Physical examination reveals bilateral lung crackles. Which of the following sets of diagnostic findings would be most consistent with isolated diastolic heart failure?
Q1
Correct answer:E Diastolic heart failure (DHF) is a common cause of acute decompensated HF. It is characterized by normal or nearnormal left ventricular ejection fraction (LVEF, >50%) and end-diastolic volume in the setting of increased LV filling pressures Diastolic dysfunction can be due to conditions that decrease LV compliance, such as impaired myocardial relaxation (eg. from ischemia) or increased intrinsic ventricular wall stiffness (eg, from amyloid deposition). This patient most likely has long-standing hypertension leading to LV wall hypertrophy, which can impair myocardial relaxation and increase intrinsic wall stiffness LV diastolic pressure is determined by the blood volume in the LV cavity and compliance of the left ventricle. Conditions that reduce ventricular compliance lead to increased LV end-diastolic pressures (LVEDP) at the same LVED volumes. This causes a shift in the pressure-volume curve that goes upward and to the left (point a - b). As diastolic dysfunction worsens, LVEDP continues to rise as the heart attempts to maintain a near-normal stroke volume and cardiac output. Decompensation occurs when the increased LVEDP (transmitted to the left atrium and pulmonary veins) causes pulmonary edema and dyspnea. Cardiac reserve also diminishes as the stiffened ventricle becomes less effective at accommodating increased blood volumes (limiting the ability to use the Frank-Stariing mechanism). (Choice A) In contrast to diastolic HF. systolic HF is caused by a primary decrease in myocardial contractility rather than ventricular compliance. As a result, systolic HF is characterized by a reduced LVEF (<50%), along with progressive chamber dilation with increased LV volume and elevated LVEDP. (Choices B, C, and F) LVEDP is elevated (not normal) in patients with diastolic HF. This increase in LVEDP is transmitted to the left atrium, pulmonary veins, and capillaries; the result is pulmonary congestion, dyspnea, and exercise intolerance. Educational objective: