2019年整理2009欧洲感染性心内膜炎防治指南的解读
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随着置入式心脏电装置( ICED )置入率逐渐增加, ICED 感染风险也随之增加。
目前针对 ICED 感染的诊治和预防策略证据支持有限,近期,英国多个学科协会发布相关指南,进一步标准化 ICED 感染管理,来自英国利兹大学的 Sandoe 博士等对多部指南进行要旨总结,全文发表于 Heart 杂志上。
ICED 包括永久起搏器( PPM )、置入式心脏复律除颤仪( ICD )和心脏再同步化治疗( CRT)装置,英国 ICED 置入率正在增加,随着指征的放宽,置入率将进一步增加,但 ICED 感染及其伴有的致残和致死率也随着增加。
ICED 感染诊断和管理非常具有挑战性,感染可累及囊袋、导线和心内膜结构,心内膜感染明显增加死亡率,装置移除同样显著增加严重并发症和死亡风险,拯救感染装置也往往以失败告终。
预防和管理 ICED 感染的策稍不少,但支持证据有限。
目前为止,惟一针对该领域发布的指南为 2022 年美国心脏协会 ICED 感染指南。
近期,英国心脏节律协会、英国心血管协会和英国心脏瓣膜协会等发布的指南进一步推动了 ICED 感染的标准化诊断和管理方案。
本文主要总结其中要旨。
全球范围内, ICED 感染率约为 0.5%-2.2% ,置入 ICD/CRT 感染率高于 PPM ,再次置入感染率高于初次置入。
肾功能受损、心衰和糖尿病患者 ICED 置入率处于增长趋势。
三、诊断:指南将 ICED 分为 5 类,分别为早期置入后炎症、非复杂性囊袋感染、复杂性囊袋感染、 ICED 感染性心内膜炎( ICED-IE )和 ICED 导线感染(ICED-LI)(表1)。
囊袋感染以局部蜂窝组织炎、肿胀、放电、开裂或者疼痛为特征。
伤口炎症很快发生于装置置入后,其可以是囊袋感染的早期症状,也可能由非感染性疾病导致。
当皮肤因侵蚀浮现裂口时,应考虑装置感染,囊状感染往往同时合并 ICED-IE/ICED-LI ,浮现发热、寒颤、盗汗、精神委靡和厌食等症状。
2015年欧洲心脏病学会关于感染性心内膜炎治疗指南解读梁峰;胡大一;沈珠军;方全【期刊名称】《中国心血管病研究》【年(卷),期】2017(015)004【总页数】8页(P302-309)【关键词】心内膜炎;感染;指南;抗菌疗法;心脏手术【作者】梁峰;胡大一;沈珠军;方全【作者单位】102600北京市,首都医科大学大兴教学医院心内科;北京大学人民医院心脏中心;中国协和医科大学北京协和医院心内科;中国协和医科大学北京协和医院心内科【正文语种】中文【中图分类】R542.4+1感染性心内膜炎(IE)是一种致死性疾病,虽然其治疗获得进展,但仍然导致很高的死亡率和各种严重并发症。
之前由于该病发病率低,缺乏随机试验而仅有有限数量的荟萃分析,IE的指南基本上基于专家意见。
2009年欧洲心脏病学会(ESC)关于IE预防、诊断和治疗指南,推出各种创新理念,包括极高危患者预防性抗生素的限制使用、关注医疗相关IE以及手术最佳时机的确定。
但是多种进展要求ESC更新原来的指南,大系列的IE文章发表,包括手术治疗的第一项随机研究;影像诊断的重要进展,尤其核素显像领域;与以前不同指南的巨大差异。
另外最近多种新指南确立并强调“心内膜炎团队”,即需要一种多科协作治疗方法。
该指南工作组的主要目的是提供明确和简洁的建议,帮助医务人员进行临床决策制订。
这些推荐通过对现有文献全面回顾,达成专家共识。
但是强调,无论如何指南不可能无视医务工作者对每一例个体患者合适准确的判断决策,以及合适和(或)必要时与患者和监护者的沟通协商,同时医务工作人员有责任验证药物和器械使用的原则和规定。
本文解读2015年ESC关于IE治疗的指南。
1.1 总体原则 IE的成功治疗取决于抗生素对微生物的根除,手术清除感染物和引流脓肿有助于根除微生物,自身防御抵抗力几乎无用。
这可解释为何杀菌方案较抑菌治疗更有效,动物实验和人体结果均相同。
氨基糖苷类与细菌胞壁抑制剂(如β内酰胺类和糖肽类抗生素)具有协同杀菌作用,有助于缩短治疗时间(如口腔链球菌),以及根除致病微生物(如肠球菌)。
欧洲心血管病预防指南解读(全文)指南的要点解读如下:1. 何时进行评估总心血管危险以下三种情况评估总心血管危险:(1)病人要求(2)在咨询期间:面对中年吸烟者;有一种或多种危险因素如高血压。
(3)有早发心血管病家族史或重要心血管危险因素如高血脂或已提示有心血管病症状。
2. 评估危险:医生应该做什么?用SCORE(除非病人已知有心血管病,糖尿病或很高的危险因素)进行危险评估。
(1)过去史:心血管病(CVD)早发家族史,疾病史,吸烟,运动及饮食习惯。
(2)体检:血压(BP)、心率(HR)、足背动脉、心肺听诊、身高、体重、腰围。
(3)实验室检验:尿糖、尿蛋白,空腹血糖、血脂(Tc、HDL-c、TG)、肌酐。
(4)心电图,心绞痛时做运动心电图。
(5)年轻或严重高血压者检查心电图,超声心动图。
(6)早发CVD或早发家族史者检查hs-CRP、脂蛋白、纤维蛋白元、血红蛋白。
3. 评估后处理a:如确定CVD、糖尿病(DM)伴微蛋白尿、显著单个危险因素、SCORE危险≥5%,则采取以下措施:(1)生活方式改善不吸烟减轻体重(BMI≥25kg/m2)(或腰围升高者)。
每周大多数天中进行中度运动30分钟。
健康膳食:摄入多种食物,能量摄入避免超重,鼓励摄入水果,蔬菜,鱼类,全麦。
减少盐摄入量,减少饱和脂肪酸摄入。
(2)药物治疗SCORE大于10%的用药治疗,5%~10%的伴特殊情况的用药治疗BP≥140/90mmHg,用降压药TC≥5.0mmol/L或LDL-C≥3.Ommol/L用他汀治疗。
CVD者,大多数用阿司匹林,他汀。
糖尿病者用降糖药。
b:如SCORE危险<5%,则采取以下措施,改善生活方式,以避免增加危险因素。
有规律地再评估总危险。
[注:SCORE——指欧洲以10年心血管病死亡率为指标的危险评估] 4. 为什么要在临床实践中搞预防策略(1)心血管病是欧洲过早死亡的丰要原因,是致残的主要原因,是健康医疗的重要负担。
·标准与指南·2015年欧洲心脏病学会关于感染性心内膜炎指南的解读梁峰1沈珠军2方全2胡大一3感染性心内膜炎(infective endocarditis,IE)是一种致死性疾病,虽然其治疗获得重要进展,但死亡率仍然居高不下并导致各种严重并发症。
目前IE指南基本上基于专家意见[1]。
2009年欧洲心脏病学会(European Society of Cardiology,ESC)关于IE预防、诊断和治疗指南,推出各种创新理念,包括极高危患者预防性抗生素的限制性使用,关注医疗相关IE以及手术最佳时机的确定[2]。
但是多种进展要求ESC更新原来的指南,如大系列IE文章的发表,包括手术治疗的第一项随机研究;影像诊断的重要进展,尤其核素显像领域;以及以前不同指南的巨大差异。
另外最近多种新指南确立并强调“IE团队”,即需要一种多科协作的治疗方法。
而该指南主要目的是提供明确和简单的建议,帮助医务人员进行临床决策的制订。
但是必须强调,无论何种指南,需正视医务工作者对每例个体患者准确的判断决策和(或)必要时与患者和监护人的沟通协商,同时医务人员有责任验证药物和器械使用原则和规定。
一、IE最高危患者行高危手术使用预防性抗生素,但强调非特异性感染预防措施的重要性IE最高危患者进行高危手术时应该考虑预防性使用抗生素:(1)瓣膜置换的所有患者,包括经导管置入瓣膜或瓣膜修复使用人工材料的患者;(2)既往IE患者;(3)先天性心脏病(congenital heart disease,CHD)患者:①任何类型紫绀型CHD;②用人工材料修补的任何类型CHD,无论外科手术修补或经皮介入技术置入,直到术后6个月;但如果残留分流或瓣膜反流则需终身(ⅡaC)。
其他类型的瓣膜性心脏病或CHD不推荐预防性使用抗生素(ⅢC)。
牙科操作:只有对牙龈和牙齿根尖区操作或口DOI:10.3877/cma.j.issn.1674-0785.2017.06.019基金项目:北京市卫生系统高层次卫生技术人才培养项目(2009-3-68)作者单位:102600 北京,首都医科大学大兴医院心内科1;100730 中国医学科学院北京协和医学院北京协和医院心内科2;100044 北京大学人民医院心脏中心3通信作者:胡大一,Email: dayi.hu@ 腔黏膜穿孔的操作,才应考虑抗生素预防(ⅡaC)。
《2019年欧洲心脏病学会急性肺栓塞诊断和管理指南》要点更新及解读急性肺栓塞(pulmonary embolism,PE)是全球第三大常见的心血管病死因,仅次于冠心病和卒中,其年发病率为(39~115)人/10万人。
随着近年来PE领域积累的大量新的循证医学证据,2019年8月31日欧洲心脏病学会(ESC)携手欧洲呼吸学会(ERS)共同制定的《2019年欧洲心脏病学会急性PE诊断和管理指南》(以下简称《2019年PE指南》)应运而生。
1 诊断和管理规范急性PE由于发病隐匿经常被忽略,严重性也经常被低估。
因此,其早期的识别与诊断、及时的抢救与治疗、规范的随访与管理至关重要。
ESC工作组强调从以下十个方面来规范医师对PE的诊断和管理:(1)对于出现血流动力学不稳定的患者,快速、即时地检测床旁经胸超声心动图(transthoracic echocardiography,TTE),以区分疑似高危PE与其他急性危及生命的情况。
(2)如果怀疑急性PE,在排除患者出血或绝对禁忌证的情况下,尽快进行抗凝治疗,同时进行诊断检查。
(3)使用推荐的、经过验证的PE诊断流程,包括(测试前)临床概率和D-二聚体测试的标准化评估方法,价格低廉,同时也避免了不必要的成像检测和电离辐射的伤害。
(4)如果CT肺血管造影(CT pulmonary angiography,CTPA)提示单个亚段PE,应与放射科医师共同会诊以排除假阳性,避免不必要、可能有害的抗凝治疗。
(5)应对血流动力学稳定的PE患者进行进一步的风险评估,包括临床表现、右心室(right ventricular,RV)大小和(或)功能以及相关实验室生物标志物,对高风险患者行再灌注治疗和生命体征监测,考虑低风险患者应选择早期出院和持续抗凝治疗。
(6)一旦诊断(或高度怀疑)高风险PE,应结合患者的风险状况和现有医疗条件选择最佳的再灌注方案,包括全身溶栓、手术取栓或导管导向治疗。
感染性心内膜炎的病因治疗与预防感染性心内膜炎(infectiveendocarditis)指由细菌、真菌等微生物(如病毒、立克次体、衣原体、螺旋体等)直接感染引起的心瓣膜或心室壁内膜炎,不同于风湿热、类风湿、系统性红斑狼疮引起的非传染性心内膜炎。
这种疾病过去被称为细菌性心内膜炎(bacterialendocarditis),由于不够全面,不再使用。
传染性心内膜炎的典型临床表现包括发热、噪音、贫血、栓塞、皮肤病变、脾肿大和血液培养阳性。
感染性心内膜炎常多发于原已有病的心脏,近年来发生于原无心脏病变者日益增多,尤其见于接受长时间经静脉治疗、静脉注射麻醉药成瘾、由药物或疾病引起免疫功能抑制的患者。
人工瓣膜置换术后的感染性心内膜炎也有增多。
左心心内膜炎主要涉及主动脉瓣和二尖瓣,尤其是轻至中度关闭不完全的患者。
右心心内膜炎罕见,主要涉及三尖瓣。
在各种先天性心脏病中,动脉导管未闭、室间隔缺损和法乐四联症最为常见。
在单个瓣膜病变中,二叶主动脉瓣狭窄最容易发生,瓣膜脱垂(主动脉瓣和二尖瓣)也容易发生。
上海中山医院1980~1995年,82例传染性心内膜炎行人工瓣膜置换术切除的标本病理检查结果显示,先天性二叶主动脉瓣畸形占55例原心脏器质性病变的20例(36例)%),主动脉瓣脱垂为10例(18%)。
肥厚型梗阻型心肌病、退行性瓣膜病变、冠心病患者也有报道。
急性感染性心内膜炎常由化脓性细菌侵入心内膜引起,多由毒性病原体感染引起。
金黄色葡萄球菌占50%%以上。
抗生素临床应用前应用亚急性感染性心内膜炎%它是由非溶血性链球菌引起的,主要是由草绿色链球菌感染引起的。
近年来,由于广谱抗生素的广泛使用,致病菌种发生了显著变化。
几乎所有已知的致病微生物都可以引起这种疾病。
同一病原体可产生急性病程或亚急性病程。
过去罕见的耐药微生物病例增加。
草绿色链球菌的发病率正在下降,但仍有优势。
金黄色葡萄球菌、肠球菌、表皮葡萄球菌、革兰阴性菌或真菌的比例显著增加。
欧洲心血管疾病预防临床实践指南要点解读完整版《欧洲心脏杂志》发布了欧洲心血管疾病预防临床实践指南[1]。
指南分为四个部分论述心血管疾病(cardiovascular disease,CVD)预防的关键问题,可概括为"4W"(What、Who、How、Where),即什么是CVD预防?谁将从中受益,什么时候、如何进行风险分析和优先考虑?如何实施CVD预防?在什么机构进行干预?在此我们解读如下主要内容。
1 什么是CVD预防?为什么需要预防CVD?CVD预防被定义为在人群或个体水平,通过一系列相互协同的综合措施,消除或减少CVD的影响及其带来的身心障碍。
公众教育和高风险的预防策略应该是相辅相成的,一项措施仅限于高危人群不会太有效;公众教育项目仍然是需要的。
CVD与生活方式密切相关,特别与吸烟、不良饮食习惯、缺乏体力活动以及心理压力关系密切。
世界卫生组织指出,充分的改变生活习惯可减少80%的CVD发生,甚至降低40%癌症发生。
当代欧洲CVD死亡率比80年代降低50%,主要归功于人群胆固醇水平、血压降低和戒烟措施,这些效果被其他危险因素的影响,如肥胖、糖尿病的增长以及人口老龄化部分抵消。
理想的CVD的预防从怀孕开始直至生命终结。
在日常实践中,CVD 预防工作通常针对患有CVD的人群(即二级预防)或主要心血管事件的高危人群,如吸烟、血压升高、糖尿病或血脂紊乱(即一级预防);而在年轻的或仅有中等或轻微CVD风险的老年人群中有限,而对这些人群加强CVD预防会有更多获益。
指南推荐针对人群的促进健康生活方式的措施干预(Ⅱa/B)。
2 何人可受益?何时、如何进行风险分析和优先考虑?2.1 首先评估总体心血管风险基于动脉粥样硬化是危险因素的产物,所以CVD预防指南推荐评估总体心血管风险。
CVD的预防有赖于其风险级别,级别越高,干预措施越强。
指南推荐用SCORE量表评估总体心血管风险。
该量表来源于欧洲人群的流行病学调查研究,主要用于高加索人种的心血管风险评估;对蒙古人种、尼罗格人种是否适用尚缺乏循证医学证据[2]SCORE量表是由年龄、性别、吸烟、收缩压和总胆固醇各心血管相关危险因素作为"经纬度",形成的危险分数"地图",临床医生可根据个体存在的危险因素情况,快捷地对心血管风险"定位"和判断;针对高风险和低风险发病地区有不同的预测模型。
ESC GUIDELINESGuidelines on the prevention, diagnosis, and treatment of infective endocarditis (newversion 2009The Task Force on the Prevention, Diagnosis, and Treatment of Infective Endocarditis of the European Society of Cardiology (ESCEndorsed by the European Society of Clinical Microbiology and Infectious Diseases (ESCMIDand by the International Society of Chemotherapy (ISCfor Infection and CancerAuthors/TaskForce Members:Gilbert Habib (Chairperson(France*, Bruno Hoen (France,Pilar Tornos (Spain,Franck Thuny (France,Bernard Prendergast (UK,Isidre Vilacosta (Spain,Philippe Moreillon (Switzerland,Manuel de Jesus Antunes (Portugal,Ulf Thilen (Sweden,John Lekakis (Greece,Maria Lengyel (Hungary,Ludwig Mu¨ller (Austria,Christoph K. Naber (Germany,Petros Nihoyannopoulos (UK,Anton Moritz (Germany,Jose Luis Zamorano (SpainESC Committee for Practice Guidelines (CPG:Alec Vahanian(Chairperson(France,Angelo Auricchio(Switzerland,Jeroen Bax (TheNetherlands, Claudio Ceconi (Italy,Veronica Dean (France,Gerasimos Filippatos (Greece,Christian Funck-Brentano (France,Richard Hobbs (UK,Peter Kearney (Ireland,Theresa McDonagh (UK,Keith McGregor (France,Bogdan A. Popescu (Romania,Zeljko Reiner (Croatia,Udo Sechtem (Germany,Per Anton Sirnes (Norway,Michal Tendera (Poland,Panos Vardas (Greece,Petr Widimsky (CzechRepublic Document Reviewers:Alec Vahanian (CPGReview Coordinator (France,Rio Aguilar (Spain,Maria Grazia Bongiorni (Italy,Michael Borger (Germany,Eric Butchart (UK,Nicolas Danchin (France,Francois Delahaye (France,Raimund Erbel (Germany,Damian Franzen (Germany,Kate Gould (UK,Roger Hall(UK,Christian Hassager (Denmark,Keld Kjeldsen (Denmark,Richard McManus (UK,Jose´M. Miro ´(Spain,Ales Mokracek (CzechRepublic, Raphael Rosenhek (Austria,Jose´A. San Roma ´n Calvar (Spain,Petar Seferovic (Serbia,Christine Selton-Suty (France,Miguel Sousa Uva (Portugal,Rita Trinchero (Italy,Guy van Camp (BelgiumThe disclosure forms of the authors and reviewers are available on the ESC website/guidelines*Corresponding author. Gilbert Habib, Service de Cardiologie, CHU La Timone, Bd Jean Moulin, 13005Marseille, France. Tel:þ33491386379, Email:gilbert.habib@free.frThe content of these European Society of Cardiology (ESCGuidelines has been published for personal and educational use only. No commercial use is authorized. No part of the ESC Guidelines may be translated or reproduced in any form without written permission from the ESC. Permission can be obtained upon submission of a writtenrequest to Oxford University Press, the publisher of the European Heart Journal and the party authorized to handle such permissions on behalf of the ESC.Disclaimer. The ESC Guidelines represent the views of the ESC and were arrived at after careful consideration of the available evidence at the time they were written. Health professionals are encouraged to take them fully into account when exercising their clinical judgement. The guidelines do not, however, override the individual responsibility of health professionals to make appropriate decisions in the circumstances of the individual patients, in consultation with that patient, and where appropriate and necessary the patient’s guardian or carer. It is also the health professional’s responsibility to verify the rules and regulations applicable to drugs and devices at the time of prescription.&The European Society of Cardiology 2009. All rights reserved. For permissions please email:journals.permissions@.European Heart Journaldoi:10.1093/eurheartj/ehp285Table of ContentsA. Preamble . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3B. Justification/scopeof the problem . . . . . . . . . . . . . . . . . . . 4C. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 A changing epidemiology . . . . . . . . . . . . . . . . . . . . . . . 4 Incidence of infectiveendocarditis . . . . . . . . . . . . . . . . . 5 Types of infectiveendocarditis . . . . . . . . . . . . . . . . . . . 5Microbiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5D. Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6E. Preventive measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 Evidence justifying the use of antibiotic prophylaxis forinfective endocarditis in previous ESC recommendations . . 7 Reasons justifying revision of previous ESC Guidelines . . . 7 Principles of the new ESCGuidelines. . . . . . . . . . . . . . . 8 Limitations and consequences of the new ESC Guidelines . 10 F. Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10 Clinical features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10Echocardiography . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11 Microbiologicaldiagnosis . . . . . . . . . . . . . . . . . . . . . . . 12 Diagnostic criteria and theirlimitations. . . . . . . . . . . . . . 14G. Prognostic assessment at admission . . . . . . . . . . . . . . . . . 15H. Antimicrobial therapy:principles and methods . . . . . . . . . . 15 General principles . . . . . . . . . . . . . . . . . . . . . . . . . . . 15 Penicillin-susceptible oral streptococci and group Dstreptococci . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 Penicillin-resistant oral streptococci and group Dstreptococci . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 Streptococcus pneumoniae , b -haemolytic streptococci (groups A, B, C, and G . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 Nutritionally variant streptococci . . . . . . . . . . . . . . . . . 16 Staphylococcus aureus and coagulase-negative staphylococci . 18 Methicillin-resistant and vancomycin-resistant staphylococci 19 Enterococcus spp. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19 Gram-negative bacteria . . . . . . . . . . . . . . . . . . . . . . . . 19 Blood culture-negative infective endocarditis . . . . . . . . . . 19 Fungi . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20 Empirical therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20 Outpatient parenteral antibiotic therapy for infectiveendocarditis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21 I. Complications and indications for surgery in left-sided native valve infectiveendocarditis. . . . . . . . . . . . . . . . . . . . . . . . . . 23 Part 1. Indications and optimal timing of surgery . . . . . . . . . . . 23 Heart failure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23 Uncontrolled infection . . . . . . . . . . . . . . . . . . . . . . . . 24 Prevention of systemic embolism. . . . . . . . . . . . . . . . . . 25 Part 2. Principles, methods, and immediate results of surgery. . . 26 Pre-and peri-operative management . . . . . . . . . . . . . . . 26 Surgical approach and techniques . . . . . . . . . . . . . . . . . 26 Operative mortality, morbidity, and post-operativecomplications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26 J. Other complications of infective endocarditis . . . . . . . . . . . . 27 Part 2. Other complications (infectiousaneurysms, acute renal failure, rheumatic complications, splenic abscess, myocarditis,pericarditis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28 K. Outcome after discharge and long-term prognosis . . . . . . . . 29 Recurrences:relapses andreinfections . . . . . . . . . . . . . . 29 Heart failure and need for valvular surgery . . . . . . . . . . .30 Long-term mortality . . . . . . . . . . . . . . . . . . . . . . . . . . 30 Follow-up . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 L. Specificsituations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 Part 1. Prosthetic valveendocarditis . . . . . . . . . . . . . . . . . . . 30 Part 2. Infective endocarditis on pacemakers and implantabledefibrillators . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32 Part 3. Right-sided infective endocarditis . . . . . . . . . . . . . . . . 33 Part 4. Infective endocarditis in congenital heart disease . . . . . . 35 Part 5. Infective endocarditis in the elderly . . . . . . . . . . . . . . . 36 Part 6. Infective endocarditis during pregnancy . . . . . . . . . . . . 36 M.References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36Abbreviations and acronyms BCNIE blood culture-negative infective endocarditisCD cardiac deviceCDRIE cardiac device-related infective endocarditis CHD congenital heart diseaseCNS coagulase-negative staphylococciCT computed tomographyELISA enzyme-linked immunosorbent assayHF heart failureIA infectious aneurysmICD implantable cardioverter defibrillatorICE International Collaboration on EndocarditisIE infective endocarditisIVDA intravenous drug abuserLDI local device infectionMBC minimal bactericidal concentrationMIC minimal inhibitory concentrationMRI magnetic resonance imagingMRSA methicillin-resistant Staphylococcus aureus MSSA methicillin-susceptible Staphylococcus aureus NBTE non-bacterial thrombotic endocarditisNVE native valve endocarditisOPAT outpatient parenteral antibiotic therapyPBP plasma-binding proteinPCR polymerase chain reactionPET positron emission tomographyPMP platelet microbicidal proteinPPM permanent pacemakerPVE prosthetic valve endocarditisTEE transoesophagal echocardiographyTTE transthoracic echocardiographyESC GuidelinesPage 2of 45Guidelines and Expert Consensus Documents summarize and evaluate all currently available evidence on a particular issue with the aim of assisting physicians in selecting the best management strategy for an individual patient suffering from a given condition, taking into account the impact on outcome, as well as the risk/ benefit ratio of particulardiagnostic or therapeutic means. Guide-lines are no substitutes for textbooks. The legal implications of medical guidelines have been discussed previously.A great number of Guidelines and Expert Consensus Docu-ments have been issued in recent years by the European Society of Cardiology (ESCas well as by other societies and organizations. Because of the impact on clinical practice, quality criteria for devel-opment of guidelines have been established in order to make all decisions transparent to the user. The recommendations for for-mulating and issuing ESC Guidelines and Expert Consensus Docu-ments can be found on the ESC website (/ knowledge/guidelines/rules.In brief, experts in the field are selected and undertake a com-prehensive review of the published evidence for management and/ or prevention of a given condition. A critical evaluation of diagnos-tic and therapeutic procedures is performed including assessment of the risk/benefit ratio. Estimates of expected health outcomes for larger societies are included, where data exist. The level of evi-dence and the strength of recommendation of particular treatment options are weighed and graded according to predefined scales, as outlined in Tables 1and 2.The experts of the writing panels have provided disclosure statements of all relationships they may have which might be per-ceived as real or potential sources ofconflicts of interest. These disclosure forms are kept on file at the European Heart House, headquarters of the ESC. Any changes in conflict of interest that Task Force report received its entire financial suppor t from the ESC and was developed without any involvement of the pharma-ceutical, device, or surgical industry.The ESC Committee for Practice Guidelines (CPGsupervises and coordinates the preparation of new Guidelines and Expert Consensus Documents produced by Task Forces, expert groups, or consensus panels. The Committee is also responsible for the endorsement process of these Guidelines and Expert Consensus Documents or statements.Once the document has been finalized and approved by all the experts involv ed in the Task Force, it is sub-mitted to outside specialists for review. The document is revised, and finally approved by the CPG and subsequently published.After publication, dissemination of the message is of paramount importance. Pocket-sized versions and personal digital assistant (PDA-downloadableversions are useful at the point of care. Some surveys have shown that the intended users are sometimes unaware of the existence of guidelines, or simply do not translate them into practice. Thus, implementation programmes for new guidelines form an important component of knowledge dissemina-tion. Meetings are organized by the ESC, and directed towards its member National Societies and key opinion leaders in Europe. Implementation meetings can also be undertaken at national levels, once the guidelines have been endorsed by the ESC member societies, and translated into the national language. Implementation programmes are needed because it has been shown that the outcome of disease may be favourably influenced by the thorough application of clinical recommendations.Thus, the task of writing Guidelines or Expert Consensus docu-ments covers not only the integration of the most recent research, but also the creation of educational tools and implementation programmes for the recommendations. The loop between clinical research, writing of guidelines, and implementing them into clinicalTable 1Classes of recommendationspractice can then only be completed if surveys and registries are performed to verify that real-life daily practice is in keeping with what is recommended in the guidelines. Such surveys and registries also make it possible to evaluate the impact of implementation of the guidelines on patient outcomes. Guidelines and recommen-dations should help the physicians to make decisions in their daily practice, However, the ultimate judgement regarding the care of an individual patient must be made by the physician in charge of his/hercare.B. Justification/scopeof the problemInfective endocarditis (IEis a peculiar disease for at least three reasons:First, neither the incidence nor the mortality of the disease have decreased in the past 30years. 1Despite major advances in both diagnostic and therapeutic procedures, this disease still carries a poor prognosis and a high mortality.Secondly, IE is not a uniform disease, but presents in a variety of different forms, varying according to the initial clinical manifestation, the underlying cardiac disease (ifany, the microorganism involved, the presence or absence of complications, and underlying patient characteristics. For this reason, IE requires a collaborative approach, involving primary care physicians, cardiologists, surgeons, microbiol-ogists, infectious disease specialists, and frequently others, including neurologists, neurosurgeons, radiologists, and pathologists. 2Thirdly, guidelines are often based on expert opinion because of the low incidence of the disease, the absence of randomized trials, and the limited number of meta-analyses. 3,4Several reasons justify the decision of the ESC to update the pre-vious guidelines published in 2004. 3IE is clearly an evolving disease, with changes in its microbiological profile, a higher incidence of health care-associated cases, elderly patients, and patients with intra-cardiac devices or prostheses. Conversely, cases related to rheu-matic disease have become less frequent in industrialized nations. In addition, several new national and international guidelines or state-of-the-art papers have been published in recent years. 3–13Unfortunately, their conclusions are not uniform, particularly in the field of prophylaxis, where conflicting recommendations have been formulated. 3,4,6,8–13Clearly, an objective for the next few years will be an attempt to harmonize these recommendations. The main objective of the current Task Force was to provide clear and simple recommendations, assisting health care providersin clinical decision making. These recommendations were obtained by expert consensus after thorough review of the available litera-ture. An evidence-based scoring system was used, based on a classification of the strength of recommendation and the levels of evidence.C. EpidemiologyA changing epidemiologyThe epidemiological profile of IE has changed substantially over the la st few years, especially in industrialized nations. 1Once a disease affecting young adults with previously well-identified (mostlyrheu-matic valve disease, IE is now affecting older patients who more often develop IE as the result of health care-associated procedures, either in patients with no previously known valve disease 14or in patients with prosthetic valves. 15A recent systematic review of 15population-based investi-gations accounting for 2371IE cases from seven developed countries (Denmark,France, Italy, The Netherlands, Sweden, the UK, and the USA showed an increasing incidence of IE associated with a prosthetic valve, an increase in cases with underlying mitral valve prolapse, and a decrease in those with underlying rheumatic heart disease. 16Newer predisposing factors have emerged—valve prostheses, degenerative valve sclerosis, intravenous drug abuse—associated with increased use of invasive procedures at risk for bacteraemia, resulting in health care-associated IE. 17In a pooled analysis of 3784episodes of IE, it was shown that oral streptococci had fallen into second place to staphylococci as the leading cause of IE. 1However, this apparent temporal shift from predominantly streptococcal to predominantly staphylococcal IE may be partly due to recruit-ment/referralbias in specialized centres, since this trend is not evident in population-based epidemiological surveys of IE. 18In developing countries, classical patterns persist. In Tunisia, for instance, most cases of IE develop in patients with rheumatic valve disease, streptococci predominate, and up to 50%may be associated with negative blood cultures. 19In other African countries, the persistence of a high burden of rheumatic fever, rheumatic valvular heart diseases, and IE has also been highlighted. 20In addition, significant geographical variations have been shown. The highest increase in the rate of staphylococcal IE has been reported in the USA, 21where chronic haemodialysis, diabetes mellitus, and intravascular devices are the three main factorsTable 2Levels of evidenceESC GuidelinesPage 4of 45associated with the development of Staphylococcus aureus endocar-ditis. 21,22In other countries, the main predisposing factor for S. aureus IE may be intravenous drug abuse. 23Incidence of infective endocarditisThe incidence of IE ranges from one country to another within 3–10episodes/100000person-years. 14,24–26This may reflect methodological differences between surveys rather than true vari-ation. Of note, in these surveys, the incidence of IE was very low in young patients but increased dramatically with age—the peak inci-dence was 14.5episodes/100000person-years in patients between 70and 80years of age. In all epidemiological studies of IE, the male:femaleratio is ! 2:1,although this higher proportion of men is poorly understood. Furthermore, female patients may have a worse prognosis and undergo valve surgery less frequently than their male counterparts. 27Types of infective endocarditisIE should be regarded as a set of clinical situations which are some-times very different from each other. In an attempt to avoid overlap, the following four categories of IE must be separated, according to the site of infection and the presence or absence of intracardiac foreign material:left-sided native valve IE, left-sided prosthetic valve IE, right-sided IE, and device-related IE (the latter including IE developing on pacemaker or defibrillator wires with or without associated valve involvement (Table 3. With regard to acquisition, the following situations can be identified: community-acquired IE, health care-associated IE (nosocomial and non-nosocomial, and IE in intravenous drug abusers (IVDAs. MicrobiologyAccording to microbiological findings, the following categories are proposed:1. Infective endocarditis with positive blood cultures This is the most important category, representing 85%of all IE. Causative microorganisms are most often staphylococci, strepto-cocci, and enterococci. 28a. Infective endocarditis due to streptococci and enterococciOral (formerlyviridans streptococci form a mixed group of microorganisms, which includes species such as S. sanguis , S. mitis , S. salivarius , S. mutans , and Gemella morbillorum. Microorganisms of this group are almost always susceptible to penicillin G. Members of the ‘ S. milleri ’ or ‘ S. anginosus ’ group (S. anginosus , S. intermedius , and S. constellatus must be distinguished since theyTable 3Classification and definitions of infective endocarditisESC Guidelines Page 5of 45tend to form abscesses and cause haematogenously disseminated infection,often requiring a longer duration of antibiotic treat-ment.Likewise,nutritionallyvariant‘defective’streptococci, recently reclassified into other species(Abiotrophia and Granulica-tella,should also be distinguished since they are often tolerant topenicillin[minimal bactericidal concentration(MBCmuch higher than the mimimal inhibitory concentration(MIC]. Group D streptococci form the‘Streptococcusbovis/Streptococcus equinus’complex,including commensal species of t he human intestinal tract,and were until recently gathered under the name of Streptococcus bovis.They are usually sensitive to penicillin G,like oral streptococci.Among enterococci, E.faecalis, E.faecium,and to a lesser extent E.durans,are the three species that cause IE.b.Staphylococcal infective endocarditisTraditionally,native valve staphylococcal IE is due to S.aureus, which is most often susceptible to oxacillin,at least in community-acquired IE.In contrast,staphylococcal prosthetic valve IE is more frequently due to coagulase-negative staphylococci (CNSwithoxacillin resistance.However,in a recent study of 1779cases of IE collected prospectively in16countries,S.aureus was the most frequent cause not only of IE but also of prosthetic valve IE.22Conversely,CNS can also cause native valve IE,29–31 especiallyS.lugdunensis,which frequently has an aggressive clinical course.2.Infective endocarditis with negative blood cultures because of prior antibiotic treatmentThis situation arises in patients who received antibiotics for unexplained fever before any blood cultures were performed and in whom the diagnosis of IE was not considered;usually the diagnosis is eventually considered in the face of relapsing febrile episodes following antibiotic discontinuation.Blood cul-tures may remain negative for many days after antibiotic discon-tinuation,and causative organisms are most often oral streptococci or CNS.3.Infective endocarditis frequently associated with negative blood culturesThey are usually due to fastidious organisms such as nutritionally variant streptococci,fastidious Gram-negative bacilli of the HACEK group(Haemophilus parainfluenzae,H.aphrophilus, H.paraphrophilus,H.influenzae,Actinobacillus actinomycetemcomi-tans,Cardiobacterium hominis,Eikenella corrodens,Kingella kingae, and K.denitrificans,Brucella,and fungi.4.Infective endocarditis associated with constantly negative blood culturesThey are caused by intracellular bacteria such as Coxiella burnetii,Bartonella,Chlamydia,and,as recently demonstrated,Tropheryma whipplei,the agent of Whipple’s disease.32Overall,these account for up to5%of all IE.Diagnosis in such cases relies on serological testing,cell culture or gene amplification.D.PathophysiologyThe valve endotheliumThe normal valve endothelium is resistant to colonization and infection by circulating bacteria.However,mechanical disruption of the endothelium results in exposure of underlying extracellular matrix proteins,the production of tissue factor,and the deposition offibrin and platelets as a normal healing process.Such non-bacterial thrombotic endocarditis(NBTEfacilitates bacterial adherence and infection.Endothelial damage may result from mechanical lesions provoked by turbulent bloodflow,electrodes or catheters,inflammation,as in rheumatic ca rditis,or degenerative changes in elderly individuals,which are associated with inflam-mation,microulcers,andmicrothrombi.Degenerative valve lesions are detected by echocardiography in upto50%of asymp-tomatic patients over60years,33and in a similar proportion of elderly patients with IE.This might account for the increased risk of IE in the elderly.Endothelial inflammation without valve lesions may also promote IE.Localinflammation triggers endothelial cells to express integrins of the b1family(very late antigen.Integrins are transmembrane proteins that can connect extracellular deter-minants to the cellular cytoskeleton.Integrins of the b1family bind circulatingfibronectin to the endothelial surface while S.aureus and some other IE pathogens carryfibronectin-binding proteins on their surface.Hence,when activated endothelial cells bindfibro-nectin they provide an adhesive surface to circulating staphylo-cocci.Once adherent,S.aureus trigger their active internalization into valve endothelial cells,where they can either persist and escape host defences and antibiotics,or multiply and spread to distantorgans.34Thus,there are at least two scenarios for primary valve infection:one involving a physically damaged endo-thelium,favouring infection by most types of organism,and one occurring on physically undamaged endothelium,promoting IE due to S.aureus and other potential intracellular pathogens. Transient bacteraemiaThe role of bacteraemia has been studied in animals with catheter-induced NBTE.Both the magnitude of bacteraemia and the ability of the pathogen to attach to damaged valves are important.35Of note,bacteraemia does not occur only after invasiveprocedures, but also as a consequence of chewing and tooth brushing.Such spontaneous bacteraemia is of low grade and short duration[1–100colony-forming units(cfu/ml of blood for,10min],but its high incidence may explain why most cases of IE are unrelated to invasive procedures.26,36Microbial pathogens and host defences Classical IEpathogens(S.aureus,Streptococcus spp.,and Enterococ-cus spp.share the ability to adhere to damaged valves,trigger local procoagulant activity,and nurture infected vegetations in which they can survive.37They are equipped with numerous surface determinants that mediate adherence to host matrix mol-ecules present on damagedvalves(e.g.fibrinogen,fibronectin, platelet proteinsand trigger plateletactivation.Following coloni-zation,adherent bacteria must escape host defences.Gram-positive bacteria are resistant to complement.However,they may be the target of platelet microbicidal proteins(PMPs,which are produced by activated platelets and kill microbes by disturbing their plasma membrane.Bacteria recovered from patients with IE are consistently resistant to PMP-induced killing,whereas similar bacteria recovered from patients with other types of infection are susceptible.38Thus,escaping PMP-induced killing is a typical characteristic of IE-causing pathogens.E.Preventive measuresEvidence justifying the use of antibiotic prophylaxis for infective endocarditis in previous ESC recommendationsThe principle of prophylaxis for IE was developed on the basis of observational studies in the early20th century.39The basic hypoth-esis is based on the assumption that bacteraemia subsequent to medical procedures can cause IE,particularly in patients with pre-disposing factors,and that prophylactic antibiotics can prevent IE in these patients by minimizing or preventing bacteraemia,or by altering bacterial properties leading to reduced bacterial adherence on the endothelial surface.The recommendations for。
2019版:欧洲心脏病学会/欧洲动脉粥样硬化学会血脂管理指南要点解读(全文)2019年欧洲心脏病学会/欧洲动脉粥样硬化学会(European Society of Cardiology / European Atherosclerosis Society,ESC/EAS)血脂管理指南(以下简称2019欧洲血脂指南)的问世被列为2019年心血管领域重要事件之一绝不过分,其首要的理由是动脉粥样硬化性心血管疾病(atherosclerotic cardiovascular disease,ASCVD)的全球发病态势明显增加,而血脂领域研究的突出进展与成就也功含其中。
事实上,胆固醇尤其是低密度脂蛋白胆固醇(low density lipoprotein cholesterol,LDL-C),作为ASCVD发生的病因性危险因素可以说是人人皆知[1,2,3,4,5],但其与ASCVD的关系仍旧令人困惑。
LDL-C到底多低为好?为什么积极降LDL-C治疗存在残余心血管风险(residual cardiovascular risk,RCVR )?新型调脂药物如前蛋白转化酶枯草杆菌蛋白酶/kexin9型(proprotein convertase subtilisin/kexin type 9,PCSK9)抑制剂如何应用?这些问题常常影响着临床血脂防治工作的质量。
2019欧洲血脂指南的及时问世,为现今我国的血脂管理提供了新的方向,笔者就2019欧洲血脂指南的要点作一概述。
首先,2019欧洲血脂指南进一步扩大了极高危人群的范围并提出更细致的高、中、低心血管风险分层。
在极高危人群的定义中,对ASCVD人群确诊方面强调了影像学检查的重要性,且定义中涵盖了多发性血管病变患者(伴两个主要心外膜动脉狭窄>50%的多支冠状动脉疾病),颈动脉超声检测发现有显著的斑块以及伴其他主要危险因素的家族性高胆固醇血症(familial hypercholesterolemia,FH)的一级预防人群。
ESC GUIDELINESGuidelines on the prevention,diagnosis,and treatment of infective endocarditis (new version 2009)The Task Force on the Prevention,Diagnosis,and Treatment of Infective Endocarditis of the European Society of Cardiology (ESC)Endorsed by the European Society of Clinical Microbiology and Infectious Diseases (ESCMID)and by the International Society of Chemotherapy (ISC)for Infection and CancerAuthors/Task Force Members:Gilbert Habib (Chairperson)(France)*,Bruno Hoen (France),Pilar Tornos (Spain),Franck Thuny (France),Bernard Prendergast (UK),Isidre Vilacosta (Spain),Philippe Moreillon (Switzerland),Manuel de Jesus Antunes (Portugal),Ulf Thilen (Sweden),John Lekakis (Greece),Maria Lengyel (Hungary),Ludwig Mu¨ller (Austria),Christoph K.Naber (Germany),Petros Nihoyannopoulos (UK),Anton Moritz (Germany),Jose Luis Zamorano (Spain)ESC Committee for Practice Guidelines (CPG):Alec Vahanian (Chairperson)(France),Angelo Auricchio(Switzerland),Jeroen Bax (The Netherlands),Claudio Ceconi (Italy),Veronica Dean (France),Gerasimos Filippatos (Greece),Christian Funck-Brentano (France),Richard Hobbs (UK),Peter Kearney (Ireland),Theresa McDonagh (UK),Keith McGregor (France),Bogdan A.Popescu (Romania),Zeljko Reiner (Croatia),Udo Sechtem (Germany),Per Anton Sirnes (Norway),Michal Tendera (Poland),Panos Vardas (Greece),Petr Widimsky (Czech Republic)Document Reviewers:Alec Vahanian (CPG Review Coordinator)(France),Rio Aguilar (Spain),Maria Grazia Bongiorni (Italy),Michael Borger (Germany),Eric Butchart (UK),Nicolas Danchin (France),Francois Delahaye (France),Raimund Erbel (Germany),Damian Franzen (Germany),Kate Gould (UK),Roger Hall(UK),Christian Hassager (Denmark),Keld Kjeldsen (Denmark),Richard McManus (UK),Jose´M.Miro ´(Spain),Ales Mokracek (Czech Republic),Raphael Rosenhek (Austria),Jose´A.San Roma ´n Calvar (Spain),Petar Seferovic (Serbia),Christine Selton-Suty (France),Miguel Sousa Uva (Portugal),Rita Trinchero (Italy),Guy van Camp (Belgium)The disclosure forms of the authors and reviewers are available on the ESC website/guidelines*Corresponding author.Gilbert Habib,Service de Cardiologie,CHU La Timone,Bd Jean Moulin,13005Marseille,France.Tel:þ33491386379,Email:gilbert.habib@free.frThe content of these European Society of Cardiology (ESC)Guidelines has been published for personal and educational use only.No commercial use is authorized.No part of the ESC Guidelines may be translated or reproduced in any form without written permission from the ESC.Permission can be obtained upon submission of a written request to Oxford University Press,the publisher of the European Heart Journal and the party authorized to handle such permissions on behalf of the ESC.Disclaimer.The ESC Guidelines represent the views of the ESC and were arrived at after careful consideration of the available evidence at the time they were written.Health professionals are encouraged to take them fully into account when exercising their clinical judgement.The guidelines do not,however,override the individual responsibility of health professionals to make appropriate decisions in the circumstances of the individual patients,in consultation with that patient,and where appropriate and necessary the patient’s guardian or carer.It is also the health professional’s responsibility to verify the rules and regulations applicable to drugs and devices at the time of prescription.&The European Society of Cardiology 2009.All rights reserved.For permissions please email:journals.permissions@.European Heart Journaldoi:10.1093/eurheartj/ehp285Table of ContentsA.Preamble (3)B.Justification/scope of the problem (4)C.Epidemiology (4)A changing epidemiology (4)Incidence of infective endocarditis (5)Types of infective endocarditis (5)Microbiology (5)D.Pathophysiology (6)E.Preventive measures (7)Evidence justifying the use of antibiotic prophylaxis forinfective endocarditis in previous ESC recommendations..7 Reasons justifying revision of previous ESC Guidelines (7)Principles of the new ESC Guidelines (8)Limitations and consequences of the new ESC Guidelines.10 F.Diagnosis (10)Clinical features (10)Echocardiography (11)Microbiological diagnosis (12)Diagnostic criteria and their limitations (14)G.Prognostic assessment at admission (15)H.Antimicrobial therapy:principles and methods (15)General principles (15)Penicillin-susceptible oral streptococci and group Dstreptococci (16)Penicillin-resistant oral streptococci and group Dstreptococci (16)Streptococcus pneumoniae,b-haemolytic streptococci(groupsA,B,C,and G) (16)Nutritionally variant streptococci (16)Staphylococcus aureus and coagulase-negative staphylococci.18 Methicillin-resistant and vancomycin-resistant staphylococci19 Enterococcus spp (19)Gram-negative bacteria (19)Blood culture-negative infective endocarditis (19)Fungi (20)Empirical therapy (20)Outpatient parenteral antibiotic therapy for infectiveendocarditis (21)plications and indications for surgery in left-sided native valve infective endocarditis (23)Part1.Indications and optimal timing of surgery (23)Heart failure (23)Uncontrolled infection (24)Prevention of systemic embolism (25)Part2.Principles,methods,and immediate results of surgery (26)Pre-and peri-operative management (26)Surgical approach and techniques (26)Operative mortality,morbidity,and post-operativecomplications (26)J.Other complications of infective endocarditis............27Part2.Other complications(infectious aneurysms,acute renal failure,rheumatic complications,splenic abscess,myocarditis, pericarditis).. (28)K.Outcome after discharge and long-term prognosis (29)Recurrences:relapses and reinfections (29)Heart failure and need for valvular surgery (30)Long-term mortality (30)Follow-up (30)L.Specific situations (30)Part1.Prosthetic valve endocarditis (30)Part2.Infective endocarditis on pacemakers and implantabledefibrillators (32)Part3.Right-sided infective endocarditis (33)Part4.Infective endocarditis in congenital heart disease (35)Part5.Infective endocarditis in the elderly (36)Part6.Infective endocarditis during pregnancy (36)M.References (36)Abbreviations and acronymsBCNIE blood culture-negative infective endocarditisCD cardiac deviceCDRIE cardiac device-related infective endocarditisCHD congenital heart diseaseCNS coagulase-negative staphylococciCT computed tomographyELISA enzyme-linked immunosorbent assayHF heart failureIA infectious aneurysmICD implantable cardioverter defibrillatorICE International Collaboration on EndocarditisIE infective endocarditisIVDA intravenous drug abuserLDI local device infectionMBC minimal bactericidal concentrationMIC minimal inhibitory concentrationMRI magnetic resonance imagingMRSA methicillin-resistant Staphylococcus aureusMSSA methicillin-susceptible Staphylococcus aureusNBTE non-bacterial thrombotic endocarditisNVE native valve endocarditisOPAT outpatient parenteral antibiotic therapyPBP plasma-binding proteinPCR polymerase chain reactionPET positron emission tomographyPMP platelet microbicidal proteinPPM permanent pacemakerPVE prosthetic valve endocarditisTEE transoesophagal echocardiographyTTE transthoracic echocardiographyESC GuidelinesPage2of45Guidelines and Expert Consensus Documents summarize and evaluate all currently available evidence on a particular issue with the aim of assisting physicians in selecting the best management strategy for an individual patient suffering from a given condition, taking into account the impact on outcome,as well as the risk/ benefit ratio of particular diagnostic or therapeutic means.Guide-lines are no substitutes for textbooks.The legal implications of medical guidelines have been discussed previously.A great number of Guidelines and Expert Consensus Docu-ments have been issued in recent years by the European Society of Cardiology(ESC)as well as by other societies and organizations. Because of the impact on clinical practice,quality criteria for devel-opment of guidelines have been established in order to make all decisions transparent to the user.The recommendations for for-mulating and issuing ESC Guidelines and Expert Consensus Docu-ments can be found on the ESC website(/ knowledge/guidelines/rules).In brief,experts in thefield are selected and undertake a com-prehensive review of the published evidence for management and/ or prevention of a given condition.A critical evaluation of diagnos-tic and therapeutic procedures is performed including assessment of the risk/benefit ratio.Estimates of expected health outcomes for larger societies are included,where data exist.The level of evi-dence and the strength of recommendation of particular treatment options are weighed and graded according to predefined scales,as outlined in Tables1and2.The experts of the writing panels have provided disclosure statements of all relationships they may have which might be per-ceived as real or potential sources of conflicts of interest.These disclosure forms are kept onfile at the European Heart House, headquarters of the ESC.Any changes in conflict of interest that Task Force report received its entirefinancial support from the ESC and was developed without any involvement of the pharma-ceutical,device,or surgical industry.The ESC Committee for Practice Guidelines(CPG)supervises and coordinates the preparation of new Guidelines and Expert Consensus Documents produced by Task Forces,expert groups, or consensus panels.The Committee is also responsible for the endorsement process of these Guidelines and Expert Consensus Documents or statements.Once the document has beenfinalized and approved by all the experts involved in the Task Force,it is sub-mitted to outside specialists for review.The document is revised,and finally approved by the CPG and subsequently published.After publication,dissemination of the message is of paramount importance.Pocket-sized versions and personal digital assistant (PDA)-downloadable versions are useful at the point of care. Some surveys have shown that the intended users are sometimes unaware of the existence of guidelines,or simply do not translate them into practice.Thus,implementation programmes for new guidelines form an important component of knowledge dissemina-tion.Meetings are organized by the ESC,and directed towards its member National Societies and key opinion leaders in Europe. Implementation meetings can also be undertaken at national levels,once the guidelines have been endorsed by the ESC member societies,and translated into the national language. Implementation programmes are needed because it has been shown that the outcome of disease may be favourably influenced by the thorough application of clinical recommendations. Thus,the task of writing Guidelines or Expert Consensus docu-ments covers not only the integration of the most recent research, but also the creation of educational tools and implementation programmes for the recommendations.The loop between clinical research,writing of guidelines,and implementing them into clinicalTable1Classes of recommendationspractice can then only be completed if surveys and registries are performed to verify that real-life daily practice is in keeping with what is recommended in the guidelines.Such surveys and registries also make it possible to evaluate the impact of implementation of the guidelines on patient outcomes.Guidelines and recommen-dations should help the physicians to make decisions in their daily practice,However,the ultimate judgement regarding the care of an individual patient must be made by the physician in charge of his/her care.B.Justification/scope of the problemInfective endocarditis (IE)is a peculiar disease for at least three reasons:First,neither the incidence nor the mortality of the disease have decreased in the past 30years.1Despite major advances in both diagnostic and therapeutic procedures,this disease still carries a poor prognosis and a high mortality.Secondly,IE is not a uniform disease,but presents in a variety of different forms,varying according to the initial clinical manifestation,the underlying cardiac disease (if any),the microorganism involved,the presence or absence of complications,and underlying patient characteristics.For this reason,IE requires a collaborative approach,involving primary care physicians,cardiologists,surgeons,microbiol-ogists,infectious disease specialists,and frequently others,including neurologists,neurosurgeons,radiologists,and pathologists.2Thirdly,guidelines are often based on expert opinion because of the low incidence of the disease,the absence of randomized trials,and the limited number of meta-analyses.3,4Several reasons justify the decision of the ESC to update the pre-vious guidelines published in 2004.3IE is clearly an evolving disease,with changes in its microbiological profile,a higher incidence of health care-associated cases,elderly patients,and patients with intra-cardiac devices or prostheses.Conversely,cases related to rheu-matic disease have become less frequent in industrialized nations.In addition,several new national and international guidelines or state-of-the-art papers have been published in recent years.3–13Unfortunately,their conclusions are not uniform,particularly in the field of prophylaxis,where conflicting recommendations have been formulated.3,4,6,8–13Clearly,an objective for the next few years will be an attempt to harmonize these recommendations.The main objective of the current Task Force was to provide clear and simple recommendations,assisting health care providersin clinical decision making.These recommendations were obtained by expert consensus after thorough review of the available litera-ture.An evidence-based scoring system was used,based on a classification of the strength of recommendation and the levels of evidence.C.EpidemiologyA changing epidemiologyThe epidemiological profile of IE has changed substantially over the last few years,especially in industrialized nations.1Once a disease affecting young adults with previously well-identified (mostly rheu-matic)valve disease,IE is now affecting older patients who more often develop IE as the result of health care-associated procedures,either in patients with no previously known valve disease 14or in patients with prosthetic valves.15A recent systematic review of 15population-based investi-gations accounting for 2371IE cases from seven developed countries (Denmark,France,Italy,The Netherlands,Sweden,the UK,and the USA)showed an increasing incidence of IE associated with a prosthetic valve,an increase in cases with underlying mitral valve prolapse,and a decrease in those with underlying rheumatic heart disease.16Newer predisposing factors have emerged—valve prostheses,degenerative valve sclerosis,intravenous drug abuse—associated with increased use of invasive procedures at risk for bacteraemia,resulting in health care-associated IE.17In a pooled analysis of 3784episodes of IE,it was shown that oral streptococci had fallen into second place to staphylococci as the leading cause of IE.1However,this apparent temporal shift from predominantly streptococcal to predominantly staphylococcal IE may be partly due to recruit-ment/referral bias in specialized centres,since this trend is not evident in population-based epidemiological surveys of IE.18In developing countries,classical patterns persist.In Tunisia,for instance,most cases of IE develop in patients with rheumatic valve disease,streptococci predominate,and up to 50%may be associated with negative blood cultures.19In other African countries,the persistence of a high burden of rheumatic fever,rheumatic valvular heart diseases,and IE has also been highlighted.20In addition,significant geographical variations have been shown.The highest increase in the rate of staphylococcal IE has been reported in the USA,21where chronic haemodialysis,diabetes mellitus,and intravascular devices are the three main factorsTable 2Levels of evidenceESC GuidelinesPage 4of 45associated with the development of Staphylococcus aureus endocar-ditis.21,22In other countries,the main predisposing factor for S.aureus IE may be intravenous drug abuse.23Incidence of infective endocarditisThe incidence of IE ranges from one country to another within 3–10episodes/100000person-years.14,24–26This may reflect methodological differences between surveys rather than true vari-ation.Of note,in these surveys,the incidence of IE was very low in young patients but increased dramatically with age—the peak inci-dence was14.5episodes/100000person-years in patients between70and80years of age.In all epidemiological studies of IE,the male:female ratio is!2:1,although this higher proportion of men is poorly understood.Furthermore,female patients may have a worse prognosis and undergo valve surgery less frequently than their male counterparts.27Types of infective endocarditisIE should be regarded as a set of clinical situations which are some-times very different from each other.In an attempt to avoid overlap,the following four categories of IE must be separated, according to the site of infection and the presence or absence of intracardiac foreign material:left-sided native valve IE,left-sided prosthetic valve IE,right-sided IE,and device-related IE(the latter including IE developing on pacemaker or defibrillator wires with or without associated valve involvement)(Table3).With regard to acquisition,the following situations can be identified: community-acquired IE,health care-associated IE(nosocomial and non-nosocomial),and IE in intravenous drug abusers(IVDAs). MicrobiologyAccording to microbiologicalfindings,the following categories are proposed:1.Infective endocarditis with positive blood cultures This is the most important category,representing 85%of all IE. Causative microorganisms are most often staphylococci,strepto-cocci,and enterococci.28a.Infective endocarditis due to streptococci and enterococciOral(formerly viridans)streptococci form a mixed group of microorganisms,which includes species such as S.sanguis,S.mitis, S.salivarius,S.mutans,and Gemella morbillorum.Microorganisms of this group are almost always susceptible to penicillin G.Members of the‘leri’or‘S.anginosus’group(S.anginosus, S.intermedius,and S.constellatus)must be distinguished since theyTable3Classification and definitions of infective endocarditisESC Guidelines Page5of45to penicillin[minimal bactericidal concentration(MBC)much higher than the mimimal inhibitory concentration(MIC)]. Group D streptococci form the‘Streptococcus bovis/Streptococcus equinus’complex,including commensal species of the human intestinal tract,and were until recently gathered under the name of Streptococcus bovis.They are usually sensitive to penicillin G,like oral streptococci.Among enterococci, E.faecalis, E.faecium,and to a lesser extent E.durans,are the three species that cause IE.b.Staphylococcal infective endocarditisTraditionally,native valve staphylococcal IE is due to S.aureus, which is most often susceptible to oxacillin,at least in community-acquired IE.In contrast,staphylococcal prosthetic valve IE is more frequently due to coagulase-negative staphylococci (CNS)with oxacillin resistance.However,in a recent study of 1779cases of IE collected prospectively in16countries,S.aureus was the most frequent cause not only of IE but also of prosthetic valve IE.22Conversely,CNS can also cause native valve IE,29–31 especially S.lugdunensis,which frequently has an aggressive clinical course.2.Infective endocarditis with negative blood cultures because of prior antibiotic treatmentThis situation arises in patients who received antibiotics for unexplained fever before any blood cultures were performed and in whom the diagnosis of IE was not considered;usually the diagnosis is eventually considered in the face of relapsing febrile episodes following antibiotic discontinuation.Blood cul-tures may remain negative for many days after antibiotic discon-tinuation,and causative organisms are most often oral streptococci or CNS.3.Infective endocarditis frequently associated with negative blood culturesThey are usually due to fastidious organisms such as nutritionally variant streptococci,fastidious Gram-negative bacilli of the HACEK group(Haemophilus parainfluenzae,H.aphrophilus, H.paraphrophilus,H.influenzae,Actinobacillus actinomycetemcomi-tans,Cardiobacterium hominis,Eikenella corrodens,Kingella kingae, and K.denitrificans),Brucella,and fungi.4.Infective endocarditis associated with constantly negative blood culturesThey are caused by intracellular bacteria such as Coxiella burnetii, Bartonella,Chlamydia,and,as recently demonstrated,Tropheryma whipplei,the agent of Whipple’s disease.32Overall,these account for up to5%of all IE.Diagnosis in such cases relies on serological testing,cell culture or gene amplification.infection by circulating bacteria.However,mechanical disruption of the endothelium results in exposure of underlying extracellular matrix proteins,the production of tissue factor,and the deposition offibrin and platelets as a normal healing process.Such non-bacterial thrombotic endocarditis(NBTE)facilitates bacterial adherence and infection.Endothelial damage may result from mechanical lesions provoked by turbulent bloodflow,electrodes or catheters,inflammation,as in rheumatic carditis,or degenerative changes in elderly individuals,which are associated with inflam-mation,microulcers,and microthrombi.Degenerative valve lesions are detected by echocardiography in up to50%of asymp-tomatic patients over60years,33and in a similar proportion of elderly patients with IE.This might account for the increased risk of IE in the elderly.Endothelial inflammation without valve lesions may also promote IE.Local inflammation triggers endothelial cells to express integrins of the b1family(very late antigen).Integrins are transmembrane proteins that can connect extracellular deter-minants to the cellular cytoskeleton.Integrins of the b1family bind circulatingfibronectin to the endothelial surface while S.aureus and some other IE pathogens carryfibronectin-binding proteins on their surface.Hence,when activated endothelial cells bindfibro-nectin they provide an adhesive surface to circulating staphylo-cocci.Once adherent,S.aureus trigger their active internalization into valve endothelial cells,where they can either persist and escape host defences and antibiotics,or multiply and spread to distant organs.34Thus,there are at least two scenarios for primary valve infection:one involving a physically damaged endo-thelium,favouring infection by most types of organism,and one occurring on physically undamaged endothelium,promoting IE due to S.aureus and other potential intracellular pathogens. Transient bacteraemiaThe role of bacteraemia has been studied in animals with catheter-induced NBTE.Both the magnitude of bacteraemia and the ability of the pathogen to attach to damaged valves are important.35Of note,bacteraemia does not occur only after invasive procedures, but also as a consequence of chewing and tooth brushing.Such spontaneous bacteraemia is of low grade and short duration[1–100colony-forming units(cfu)/ml of blood for,10min],but its high incidence may explain why most cases of IE are unrelated to invasive procedures.26,36Microbial pathogens and host defences Classical IE pathogens(S.aureus,Streptococcus spp.,and Enterococ-cus spp.)share the ability to adhere to damaged valves,trigger local procoagulant activity,and nurture infected vegetations in which they can survive.37They are equipped with numerous surface determinants that mediate adherence to host matrix mol-ecules present on damaged valves(e.g.fibrinogen,fibronectin, platelet proteins)and trigger platelet activation.Following coloni-zation,adherent bacteria must escape host defences.Gram-be the target of platelet microbicidal proteins(PMPs),which are produced by activated platelets and kill microbes by disturbing their plasma membrane.Bacteria recovered from patients with IE are consistently resistant to PMP-induced killing,whereas similar bacteria recovered from patients with other types of infection are susceptible.38Thus,escaping PMP-induced killing is a typical characteristic of IE-causing pathogens.E.Preventive measuresEvidence justifying the use of antibiotic prophylaxis for infective endocarditis in previous ESC recommendationsThe principle of prophylaxis for IE was developed on the basis of observational studies in the early20th century.39The basic hypoth-esis is based on the assumption that bacteraemia subsequent to medical procedures can cause IE,particularly in patients with pre-disposing factors,and that prophylactic antibiotics can prevent IE in these patients by minimizing or preventing bacteraemia,or by altering bacterial properties leading to reduced bacterial adherence on the endothelial surface.The recommendations for prophylaxis are based in part on the results of animal studies showing that anti-biotics could prevent the development of experimental IE after inoculation of bacteria.40Reasons justifying revision of previous ESC GuidelinesWithin these guidelines,the Task Force aimed to avoid extensive, non-evidence-based use of antibiotics for all at-risk patients under-going interventional procedures,but to limit prophylaxis to the highest risk patients.The main reasons justifying the revision of previous recommendations are the following:1.Incidence of bacteraemia after dental procedures and during daily routine activitiesThe reported incidence of transient bacteraemia after dental pro-cedures is highly variable and ranges from10to100%.41This may be a result of different analytical methods and sampling pro-cedures,and these results should be interpreted with caution. The incidence after other types of medical procedures is even less well established.In contrast,transient bacteraemia is reported to occur frequently in the context of daily routine activities such as tooth brushing,flossing,or chewing.42,43It therefore appears plaus-ible that a large proportion of IE-causing bacteraemia may derive from these daily routine activities.In addition,in patients with poor dental health,bacteraemia can be observed independently of dental procedures,and rates of post-procedural bacteraemia are higher in this group.Thesefindings emphasize the importance of good oral hygiene and regular dental review to prevent IE.44 2.Risks and benefits of prophylaxisThe following considerations are critical with respect to the assumption that antibiotic prophylaxis can efficiently prevent IE in patients who are at increased lifetime risk of the disease:extent to which a patient may benefit from antibiotic prophy-laxis for distinct procedures.A better parameter,the procedure-related risk,ranges from1:14000000for dental procedures in the average population to1:95000in patients with previous IE.45,46These estimations demonstrate the huge number of patients that will require treatment to prevent one single case of IE.(b)In the majority of patients,no potential index procedure pre-ceding thefirst clinical appearance of IE can be identified.26 Even if effectiveness and compliance are assumed to approxi-mate100%,this observation leads to two conclusions:(i)IE prophylaxis can at best only protect a small proportion of patients;47and(ii)the bacteraemia that causes IE in the majority of patients appears to derive from another source.(c)Antibiotic administration carries a small risk of anaphylaxis.However,no case of fatal anaphylaxis has been reported in the literature after oral amoxicillin administration for prophy-laxis of IE.48(d)Widespread and often inappropriate use of antibiotics mayresult in the emergence of resistant microorganisms.However,the extent to which antiobiotic use for IE prophy-laxis could be implicated in the general problem of resistance is unknown.44ck of scientific evidence for the efficacy of infective endocarditis prophylaxisStudies reporting on the efficacy of antibiotic prophylaxis to prevent or alter bacteraemia in humans after dental procedures are contradictory,49,50and so far there are no data demonstrating that reduced duration or frequency of bacteraemia after any medical procedure leads to a reduced procedure-related risk of IE. Similarly,no sufficient evidence exists from case–control studies36,51,52to support the necessity of IE prophylaxis.Even strict adherence to generally accepted recommendations for pro-phylaxis might have little impact on the total number of patients with IE in the community.52Finally,the concept of antibiotic prophylaxis efficacy itself has never been investigated in a prospective randomized controlled trial,53and assumptions on efficacy are based on non-uniform expert opinion,data from animal experiments,case reports, studies on isolated aspects of the hypothesis,and contradictory observational studies.Recent guideline committees of national cardiovascular societies have re-evaluated the existing scientific evidence in thisfield.6,9–11 Although the individual recommendations of these committees differ in some aspects,they did uniformly and independently draw four conclusions:(1)The existing evidence does not support the extensive use ofantibiotic prophylaxis recommended in previous guidelines.(2)Prophylaxis should be limited to the highest risk patients(patients with the highest incidence of IE and/or highest risk of adverse outcome from IE).(3)The indications for antibiotic prophylaxis for IE should bereduced in comparison with previous recommendations.。
2019欧洲心房纤颤指南(解读)欧洲 ESC(201 0)房颤管理指南解读 201 0 年 9 月在瑞典召开的欧洲心脏病学大会公布了最新房颤管理指南(以下简称新版指南) [1 ] ,该指南是欧洲心脏病学会单独发布的指南,之前他们均与 AHA/ACC联合发布指南,可能今后世界上只有一个指南的格局将发生改变。
新版指南较 2006 年 AHA/ACC/ESC联合公布的房颤指南(以下简称 2006 版指南) [2]相比,流行病学、抗凝、室率控制等方面发生了很大变化,下面笔者简要解读如下:第一部分流行病学 1 .1 降低再住院率-房颤管理的新目标指南将降低死亡率、再住院率、卒中、提高生活质量和活动耐量及改善左室功能作为房颤管理的主要目标。
与 2006 版指南相比,首次把降低再住院率作为房颤管理的目标。
指南提出:房颤占所有再住院原因的 1 /3,急性冠脉综合征、心衰加重、血栓栓塞并发症是其主要原因。
对房颤的管理提出了更高的要求,而不是简单的抗凝和控制室率。
1 .2 遗传因素-房颤发生发展的新机制指南首次将遗传因素作为房颤发生发展的新机制。
文中指出:房颤,尤其是特发性房颤具有一定的遗传背景, ANP、 PITX2、SCN5A等[3-5]基因均与房颤的发生发展相关,但是具体机制尚待进一步阐明。
第二部分房颤的分类及分级 2.1 房颤的分类目前国际上房颤的分类很多,新版指南根据房颤持续时间将房颤分为 5 类:首发房颤(首次发现房颤)、阵发性房颤(持续时间小于 48 小时,可以自行终止)、持续性房颤(持续时间超过 7 天)、持久性房颤(持续超过 1 年)、慢性房颤(患者已处于适应状态)。
除此之外,因脑血栓或其他原因住院而发现房颤,患者无明显症状的房颤定义为沉默性房颤。
与 2006 版指南相比,增加了持久性房颤和慢性房颤,分类更加细致,便于临床管理。
2.2 EHRA score-房颤危险度分级,房颤中的NYAH 分级指南中指出:房颤的急性期管理应该包括缓解症状,评价相关危险因素。
正确解读感染性心内膜炎感染性心内膜炎是一种较为常见的危重疾病,通常为心脏内的心内膜结构出现感染,一旦感染严重会直接导致患者出现左心衰和死亡。
因此,要高度重视此种疾病,倘若出现感染性心内膜炎需及时进行就医,否则会危及患者的生命安全。
以下通过科普一些感染性心内膜炎的方法,让更多人正确认识与解读感染性心内膜炎,保护自身的生命安全。
1.感染性心内膜炎的分类(1)什么是感染性心内膜炎感染性心内膜炎是由于细菌、真菌或是其他病菌感染了心脏内膜、心室壁内膜或邻近大动脉内膜所造成的全身炎症反应。
发病率在临床上较低,多见于老年人,老龄化的加重及老年人需要进行特殊检查,较易诱发菌血症感染,在治疗后虽能痊愈,但有部分病人会出现再次发热、心脏损害等现象。
(2)感染性心内膜炎分类感染性心内膜炎可以划分成急性与亚急性感染性心内膜炎两类。
急性感染性心内膜炎具有起病剧,多由较强的化脓菌所引起的,其中多为金黄色葡萄球菌,随后则为化脓性链球菌。
病原菌通常是在机体的某局部引发化脓性炎症,一旦机体的抵抗力降低,病原菌就会进入血液,引发败血症,并侵犯心内膜。
此种急性感染性心内膜炎通常是在正常的心内膜上,单独侵犯主动脉瓣、或侵犯二尖瓣。
其病具有突然、迅速,且伴随着高热、寒战,全身毒血症状明显的症状,并且是全身严重感染的一部分,感染迁徙较多见,病程凶险,死亡率比较高。
亚急性感染性心内膜炎,通常是发生在器质性心脏病,包含了心脏瓣膜病、先天性血管病等。
与急性感染性心内膜炎相比之下,亚急性染性心内膜炎起病比较缓慢,病程通常为数周到数学,感染迁徙的情况少见。
通常会出现全身不适、疲倦、低热、体重减轻等症状,也有少数是以并发症的形式发病的,如栓塞、无法解释的卒中、肾小球肾炎等。
1.感染性心内膜炎的高危人群染性心内膜炎的重症率较高,致死率也比较高,需要对该疾病高度警惕,尤其是高危人群,更应该加重预防,通过预防来有效避免此种疾病的产生。
(1)瓣膜异常者。
瓣膜异常者作为较为高发人群之一,包含了天性瓣膜异常,如二叶式主动脉搏、风湿性瓣膜病、先天性心脏病以及二尖瓣脱垂、退行性心瓣膜病等相关人群,是该疾病的高危人群。