ACCP-9抗栓指南中文版

合集下载

ACCP指南-静脉血栓栓塞性疾病抗栓治疗

ACCP指南静脉血栓栓塞性疾病抗栓治疗1.0深静脉血栓的初始治疗1.1下肢急性深静脉血栓形成的初始治疗1.1.1对于有客观依据证实为深静脉血栓的患者，我们推荐短期进行皮下低分子量肝素或静脉或皮下肝素治疗（1A级）。

1.1.2对于临床高度怀疑深静脉血栓的患者，医学教|育网搜集整理在等待诊断检查结果期间，推荐进行抗凝治疗（1C+级）。

1.1.3对于急性深静脉血栓，我们推荐首先进行肝素或低分子量肝素治疗至少5天（1C级）。

1.1.4我们推荐在治疗的第1天开始联合应用维生素K拮抗剂和低分子量肝素或肝素，在国际标准化比值（INR）稳定并大于2.0后，停用肝素（1A级）。

1.2下肢急性深静脉血栓形成初始治疗中静脉普通肝素的应用1.2.1如果采用静脉肝素治疗，我们推荐持续静脉给药并调节剂量，达到并维持部分凝血活酶时间（aPTT）延长至相当于血浆肝素水平从0.3-0.7IU/ml的抗因子Xa活性水平（酰胺水解法测定）（1C+级）。

1.2.2对于每天需要大剂量肝素治疗而又达不到aPTT治疗水平的患者，我们推荐通过测定抗因子Ⅹa的水平来指导用药剂量（1B级）。

1.3下肢急性深静脉血栓形成初始治疗中皮下普通肝素的应用1.3.1对于急性深静脉血栓形成的患者，我们推荐皮下普通肝素足可以替代静脉普通肝素的治疗（1A级）。

1.3.2对于接受皮下普通肝素治疗的患者，我们推荐初始剂量为3.5万U/24小时，随后维持aPTT至治疗范围（1C+级）。

1.4低分子量肝素在下肢急性深静脉血栓形成初始治疗中的应用1.4.1对于急性深静脉血栓患者，如住院患者有必要（1A级），或门诊患者如果有可能（1C级），我们推荐1-2次/天的皮下低分子量肝素优于普通肝素。

1.4.2对于接受低分子量肝素治疗的急性深静脉血栓患者，我们推荐不要常规进行抗因子Xa水平的测定（1A级）。

1.4.3对于严重肾功能衰竭的患者，我们建议静脉普通肝素优于低分子量肝素（2C级）。

2012ACCP抗栓治疗与血栓预防临床实践指南

2012 ACCP 抗栓治疗与血栓预防临床实践指南（第9 版）美国胸科医师协会（ACCP ）于2012 年 2 月7 日公布了第9 版《抗栓与血栓预防》临床实践指南，发表于《胸》杂志的增刊：Chest 2012, 141 （ 2 Suppl ）。

与上一版指南（2008 年发布）相比，新版指南更为简洁明了，首次加入了关于深静脉血栓形成（DVT）的诊断章节。

指南目录1、Disclaimer2、Panel List3、Executive Summary （执行摘要）4、Introduction to the Ninth Edition （第九版简介）点击下载全文5、Methodology for the Development of AntithromboticTherapy and Prevention of Thrombosis Guidelines （抗栓和溶栓治疗指南制定方法）点击下载全文6、Patient Values and Preferences in DecisionMaking for Antithrombotic Therapy （抗凝治疗决策中的患者评估和参数）点击下载全文7、Parenteral Anticoagulants （肠外抗凝治疗）点击下载全文8、Oral Anticoagulant Therapy （口服抗凝药的使用）点击下载全文9、Antiplatelet Drugs（抗血小板药物）点击下载全文10、New Antithrombotic Drugs （抗栓新药）点击下载全文11、Evidence-Based Management of AnticoagulantTherapy（抗栓治疗管理的循证基础）点击下载全文12、Approach to Outcome Measurement in thePrevention of Thrombosis in Surgical and MedicalPatients （外科治疗患者预防血栓形成预后管理措施）点击下载全文13、Prevention of VTE in Nonsurgical Patients（非手术患者的VTE 预防）点击下载全文14、Prevention of VTE in Nonorthopedic SurgicalPatients（非骨科手术的VTE 预防）点击下载全文15、Prevention of VTE in Orthopedic Surgery Patients （骨科手术患者的VTE 预防）点击下载全文16、Perioperative Management of Antithrombotic Therapy （围手术期的抗栓治疗管理）点击下载全文17 、Diagnosis of DVT （深静脉血栓形成的诊断）点击下载全文18、Antithrombotic Therapy for VTE Disease （静脉血栓栓塞性疾病的抗栓治疗）点击下载全文19、Treatment and Prevention of Heparin-Induced Thrombocytopenia（肝素诱导的血小板减少症的治疗与预防）点击下载全文20、Antithrombotic Therapy for AtrialFibrillation（房颤的抗栓治疗）点击下载全文21、Antithrombotic and Thrombolytic Therapy for Valvular Disease（心瓣膜病的抗栓和溶栓治疗）点击下载全文22、Antithrombotic and Thrombolytic Therapy for Ischemic Stroke（缺血性卒中的抗栓和溶栓治疗）点击下载全文23、Primary and Secondary Prevention of Cardiovascular Disease（心血管疾病的一级和二级预防）点击下载全文24 、Antithrombotic Therapy in Peripheral Artery Disease（周围动脉疾病的抗栓治疗）点击下载全文25、VTE, Thrombophilia, Antithrombotic Therapy, andPregnancy（静脉血栓栓塞、血栓形成倾向、抗栓治疗与妊娠）点击下载全文26 、Antithrombotic Therapy in Neonates and Children（新生儿和儿童的抗栓治疗）点击下载全文更多内容请点击：DVT 病因新指南:经济舱综合征缺乏证据ACCP 新指南:并非所有患者适用DVT 预防另外，非常感谢fxjj 医友为大家提供该指南的部分内容，期待在大家共同努力下，能在该频道分享到更多更新的指南温馨提示：由于该指南的内容较为丰富，文档较多（共26 个文档），所以，完整指南内容包括了附件中的 3 个压缩包和2 个pdf 文档。

ACCP9美国胸科医师协会抗栓与血栓预防指南

7.1 对于无症状血栓形成者（不包括既往VTE史）我们不推荐长期每天使用器械或药物进行血栓预防（推荐级别：1C 级）。
3.6.1. 对于接受腹腔-盆腔普通外科手术、且VTE发生风险极低（<0.5%；Rogers评分，<7；Caprini评分，0 ）的患者，除尽早下床活动外，我们不推荐给予特殊的药物（1B级）或机械（2C级）性预防措施。 3.6.2. 对于接受腹腔-盆腔普通外科手术、且VTE发生风险较低（～1.5%；Rogers评分，7-10； Caprini评分，1-2 ）的患者，我们建议给予机械预防措施，首选间歇充气加压（IPC ），优于不给予预防（2C级）。
2.2 对于接受骨科大手术（THA 、TKA 、HFS）且接受LMWH作为药物预防措施的患者，我们建议在术前 12小时或以上开始用药，或在术后12小时或以上开始用药，而不是在术前4小时内或术后4小时内（1B 级）。 2.3.1. 对于接受THA或TKA手术的患者，不论是否同时使用IPCD或治疗时间多长，我们建议优先选用 LMWH，可选其他替代方法：磺达肝癸钠、阿哌沙班、达比加群、利伐沙班、 LDUH （均为2B级）、调整剂量VKA或阿司匹林（均为2C级）。
2.7. 对于接受大型骨科手术且拒绝或不配合药物注射或使用IPCD的患者，我们建议使用阿哌沙班或达比加群（如果没有阿哌沙班或达比加群，可以用利伐沙班或剂量调整VKA代替），而不是其他形式的预防措施（均为1B级）。 2.8. 对于接受大型骨科手术伴出血风险升高或对于药物和机械抗栓预防都有禁忌症的患者，我们不建议植入下腔静脉过滤器（IVC）作为初级预防（2C 级）。。
4.2.1 对于无其他VTE 危险因素的门诊肿瘤患者，不建议使用低分子量肝素（LMWH）或低剂量普通肝素（LDUH）进行血栓预防（推荐级别：2B 级），也不推荐预防性使用维生素 K 拮抗剂（推荐级别： 1B 级）。

ACCP9th的指南解读(简版)

高危中危低危
分值
>6 2－6 <2
European Heart Journal (2008) 29, 2276–2315
肺栓塞的风险
65％ 30％ 10％
分值 ≥4 <4
分值
1.5 1.5 1
1
1.5 3
3
肺栓塞的风险 likely
unlikely
ACCP 9指南 —— VTE的治疗低分子肝素仍然为初始治疗一线推荐
所有致死性PE病例在死亡前得到诊断的仅30％
大约80％的VTE没有明显的症状（无症状型）
致死性PE VTE
怀疑DVT的病例用客观检查得到证实的比例<30%
1. Goldhaber SZ, et al. American Journal of Medicine 1982;73:822-826. 2. Lethen H, et al. American Journal of Cardiology 1997;80:1066-1069.
与普通肝素相比，依诺肝素显著降低TKA患者的DVT 发生率达28％，且不增加出血发生率
所有接受治疗的患者
40
P=0.02
35
30
34.2 RRR=2
25
20
8% 24.6
15
10
5
0
普通肝素（225）
依诺肝素（228）
行静脉造影的患者
60
P=0.02
50 51.7
40
30
37.2
20
10
0
普通肝素（143）
低
LDUH
建议联用机械预防（ES或IPC）
高
机械预防（IPC）

ACCP9指南

Chest 2012;141;7S-47S.
有房颤史的缺血性卒中抗栓建议
对于有房颤（包括阵发性房颤）史的缺血性卒中或短暂性脑缺
血发作患者，我们推荐予以抗栓治疗（1A）。推荐口服抗凝治疗（1A），阿司匹林（1B），或阿司匹林联合氯吡格雷
（1B）。
Chest 2012;141;7S-47S.
有房颤史的缺血性卒中抗栓建议
雷75mg/d+小剂量阿司匹林（2B）
Chest 2012;141;7S-47S.
急性冠脉综合征后一年内接受经皮冠状动脉介入治疗的患者抗栓建议
• 我们推荐双联抗血小板治疗：替卡格雷90mg/d每日2次+小
剂量阿司匹林75-100mg/d或者氯吡格雷75mg/d+小剂量阿司匹林或者普拉格雷10mg/d +小剂量阿司匹林（1B）。
PAD患者的抗栓建议
阿司匹林一级预防使用推荐
对于年龄大于或等于50岁的无症状心血管疾病人群，我们建议使用低剂量阿司匹林75-100mg/d（2B）。
Chest 2012;141;7S-47S.
目
ACCP9简介
录
冠心病一级预防的抗栓建议冠心病患者的抗栓建议肺栓塞患者的抗栓建议
Chest 2012;141;7S-47S.
静脉血栓栓塞高风险患者抗栓建议
对于有静脉血栓栓塞高风险且无高出血风险的普通患者和腹部盆腔
手术患者（6%;Caprini评分,≥5）,应予以抗凝治疗。
若存在低分子肝素和普通肝素使用禁忌或无条件应用这些药,我们建议低剂量阿司匹林（2C）,磺达肝葵钠（2C）, 或机械性预防--首选
Chest 2012;141;7S-47S.
非心源性卒中抗栓建议

房颤抗栓治疗ACCP9

▪ 建议2：CHADS2评分为0分者无需抗凝。 CHADS2评分为1分者，建议口服抗凝药物，不适于抗凝药物者（如具有出血的高危因
素）建议联合应用阿司匹林和氯吡格雷。若无禁忌证，所有CHADS2评分≥2分者均应接受口服抗凝药物。不适于抗凝药物者
（如具有出血的高危因素）需联合应用阿司匹林和氯吡格雷。
▪ 解读：CHADS2评分内容包括慢性心力衰竭（1分）、高血压（1分）、年龄＞75岁（1 分）、糖尿病（1分）、卒中或短暂脑缺血发作病史（2分）。随着CHADS2评分的增高，房颤患者未来发生缺血性卒中的风险逐渐增高。在临床实践中，应对每例房颤患者进行血栓栓塞事件风险评估，并制定相应的抗栓治疗方案.
力衰竭、肝脏疾病、近期曾进行手术治疗或正在服用可增强华法林作用的药物INR的监测频度应视患者具体情况而定。应用华法林治疗初期，至少应每3~5 d检测1次INR。当INR达到目标值、华法林剂量相对固定后，每4周检测1次。如患者在接受华法林治疗过程中应用了可能影响华法林作用的药物、食物或发生其他疾患，则应增加监测频度。
越来越多的研究证实对卒中风险增高的患者合理应用以维生素k拮抗剂华法林为代表的抗凝药物有助于显著降低缺血性卒中的发生率然而我国大多数房颤患者并未得到抗凝治疗因此进一步增强对房颤及其并发症的认识加强血栓栓塞并发症特别是卒中的预防对于改善患者预后进而减轻与之相关的社会经济和家庭负担具有重要意义
解读2012ACCP血栓治疗预防指南
▪ 解读：未接受介入治疗的急性冠状动脉综合征患者再发急性冠状动脉事件的风险很高，
应加强二级预防。由于未行支架治疗，故伴
房颤的患者无需三联抗栓药物治疗，应用剂
量调整的华法林与阿司匹林或氯吡格雷联合治疗，可以显著降低不良事件的风险。

ACCP9第9版指南摘要翻译

—实施概要美国胸科医师学院循证医学临床实践指南：—抗栓治疗与血栓预防(第9版)Gordon H. Guyatt , MD, FCCP ; Elie A. Akl , MD, PhD, MPH ; Mark Crowther , MD ;David D. Gutterman, MD, FCCP; Holger J. Schünemann, MD, PhD, FCCP; for the American College of Chest Physicians Antithrombotic Therapy and Prevention of Thrombosis Panel*缩略语ACS=急性冠脉综合征; AF=心房颤动; AIS=动脉缺血性卒中; APLA=抗磷脂抗体；ASA =阿司匹林；AT9 = 抗栓治疗与血栓预防(第9版)，美国胸科医师学院循证医学临床实践指南；BMS=裸金属支架；CABG=冠状动脉搭桥术; GAD=冠状动脉疾病;CDT=导管溶栓；CHADS2 =充血性心力衰竭，高血压，年龄≥75岁，糖尿病，卒中或短暂脑缺血发作；CSVT=大脑窦静脉血栓形成; CTPH=慢性血栓栓塞性肺动脉高压；CUS=压缩超声；CVAD=中心静脉植入装置；DES=药物洗脱支架；GCS=分级加压弹力袜;；HFS=髋骨骨折手术；HIT =肝素诱导的血小板减少症；HITT=肝素诱导的血小板减少症合并血栓形成；IA=动脉内的；ICH=颅内出血；IE=感染性心内膜炎; INR=国际标准化比率；IPCD=间歇充气加压装置；IVC=下腔静脉；LDUH=低剂量普通肝素；LMWH=低分子肝素；LV=左心室；MBTS=改良Blalock-Taussig分流术；MR=核磁共振成像；PAD=-外周动脉疾病；PCI=经皮冠状动脉介入治疗；PE=肺栓塞；PFO=卵圆孔未闭; PMBV=经皮二尖瓣球囊成形术; PTS=栓塞后综合征; PVT=人工瓣膜血栓形成; r-tPA=重组组织型纤溶酶原活化剂；RVT=肾静脉血栓形成；SC=皮下；TEE=经食管超声心动图; THA=全髋关节置换术；TIA=短暂性缺血发作；TKA=全膝关节置换术；UAC=脐动脉导管; UEDVT=上肢深静脉血栓形成；UFH=普通肝素;US=超声；UVC=脐静脉导管；VAD=心室辅助装置；VKA=维生素k拮抗剂前言已发表的ACCP第8版抗栓指南，以文章的形式，叙事性的证据总结和原则作为推荐，一小部分从循证得出的证据资料总结，一些项目来自于原始研究的广泛汇总表。

VTE防治和ACCP9th规范解读

KPHI 2009
专题性指南
血栓预防指南
ASSO 2007（骨科）
相关专业的治疗指南
ASCO 2007（肿瘤） NCCN 2009（肿瘤） RCOG 2010（妇科内分泌） CHR 2006（妊娠） CEM 2009（急诊）
血栓治疗中的指南
BJH 2006（肝素） NHS QIS2009（华法林）
17-57% 84%
髋置换术 V
30-65%
产后
LS/V
1-3%
DVT 发生率
10-38% 25%
33-53% 59-89% 13-29%
VTE所致死亡－－怵目惊心
VTE所导致的死亡例数: 543,4541
VTE所致死亡超过了以下原因所致死亡的总数:
– AIDS
5,8602
– 乳腺癌
86,8312
IPC机械预防（2C）
中危(~3%；Rogers score>10， Caprini score 3~4) 无大出血风险
中危(~3%；Rogers score>10， Caprini score 3~4) 有大出血风险
LMWH（2B） LDUH（2B） IPC机械预防（2C）
IPC机械预防（2C）
手术类型
VTE risk 极低危低危
药物预防 NO NO
证据等级 1B
中危
LDUH
2B
且非出血 LMWH
2B
高危人群
Hale Waihona Puke 中危且伴出血高危风险
高危
LDUH
1B
且非出血高 LMWH
1B
危人群
高危
直到出血风
且为出血高危人群
险消失，再开始药物

ACCP第9版血栓预防指南(原文)

B ackground: A ntithrombotic therapy in valvular disease is important to mitigate thromboembo-lism, but the hemorrhagic risk imposed must be considered. M ethods: T he methods of this guideline follow those described in Methodology for the Develop-ment of Antithrombotic Therapy and Prevention of Thrombosis Guidelines. Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines in this supplement. R esults: I n rheumatic mitral disease, we recommend vitamin K antagonist (VKA) therapy when the left atrial diameter is . 55 mm (Grade 2C) or when complicated by left atrial thrombus (Grade 1A). In candidates for percutaneous mitral valvotomy with left atrial thrombus, we recom-mend VKA therapy until thrombus resolution, and we recommend abandoning valvotomy if the thrombus fails to resolve (Grade 1A). In patients with patent foramen ovale (PFO) and stroke or transient ischemic attack, we recommend initial aspirin therapy (Grade 1B) and suggest substitu-tion of VKA if recurrence (Grade 2C). In patients with cryptogenic stroke and DVT and a PFO, we recommend VKA therapy for 3 months (Grade 1B) and consideration of PFO closure (Grade 2C). We recommend against the use of anticoagulant (Grade 1C) and antiplatelet therapy (Grade 1B) for native valve endocarditis. We suggest holding VKA therapy until the patient is stabilized without neurologic complications for infective endocarditis of a prosthetic valve (Grade 2C). In the ﬁ rst 3 months after bioprosthetic valve implantation, we recommend aspirin for aortic valves (Grade 2C), the addition of clopidogrel to aspirin if the aortic valve is transcatheter (Grade 2C), and VKA therapy with a target international normalized ratio (INR) of 2.5 for mitral valves (Grade 2C). After 3 months, we suggest aspirin therapy (Grade 2C). We recommend early bridging of mechanical valve patients to VKA therapy with unfractionated heparin (DVT dosing) or low-molecular-weight heparin (Grade 2C). We recommend long-term VKA therapy for all mechanical valves (Grade 1B): target INR 2.5 for aortic (Grade 1B) and 3.0 for mitral or double valve (Grade 2C). In patients with mechanical valves at low bleeding risk, we suggest the addition of low-dose aspi-rin (50-100 mg/d) (Grade 1B). In valve repair patients, we suggest aspirin therapy (Grade 2C). In patients with thrombosed prosthetic valve, we recommend ﬁ brinolysis for right-sided valves andleft-sided valves with thrombus area , 0.8 cm 2 (Grade 2C). For patients with left-sided prosthetic valve thrombosis and thrombus area Ն 0.8 cm 2, we recommend early surgery (Grade 2C). C onclusions: T hese antithrombotic guidelines provide recommendations based on the optimal balance of thrombotic and hemorrhagic risk. C HEST 2012; 141(2)(Suppl):e576S–e600SA bbreviations: A F 5 atrial ﬁ brillation; APA 5 antiplatelet agent; AVR 5 aortic valve replacement; GRADE 5 Grades of Recommendations, Assessment, Development, and Evaluation; ICH 5 intracerebral hemorrhage; IE 5 infective endocarditis; INR 5 international normalized ratio; LMWH 5 low-molecular-weight heparin; MAC 5 mitral annular calciﬁ cation; MVP 5 mitral valve prolapse; NBTE 5 nonbacterial thrombotic endocarditis; NYH A 5 New York H eart Association; OAC 5 oral anticoagulation; PFO 5 patent foramen ovale; PICO 5 population, intervention, comparator, and outcome; PMBV 5 percutaneous mitral balloon valvotomy; PVE 5 prosthetic valve endocarditis; PVT 5 prosthetic valve thrombosis; RCT 5 randomized controlled trial; RR 5 relative risk; TEE 5 transesophageal echocardiography; TIA 5 transient ischemic attack; UFH 5 unfractionated heparin; VKA 5 vitamin K antagonistfor Valvular DiseaseAntithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice GuidelinesR ichard P . W hitlock ,M D ;J ack C. S un ,M D ;S tephen E. F remes ,M D ,F CCP ;F raser D. R ubens ,M D ;and K evin H. T eoh ,M Dthe presence of atrial ﬁ brillation or previoussystemic embolism, we recommend VKA therapy (target IN R, 2.5; range, 2.0-3.0) over no VKA therapy (Grade 1A) .2.1.1. For patients being considered for percu-taneous mitral balloon valvotomy (PMBV) with preprocedural transesophageal echocardiog-raphy (TEE) showing left atrial thrombus, we recommend postponement of PMBV and that VKA therapy (target INR,3.0; range, 2.5-3.5) be administered until thrombus resolution is docu-mented by repeat TEE over no VKA therapy (Grade 1A) .2.1.2. For patients being considered for PMBV with preprocedural TEE showing left atrial thrombus, if the left atrial thrombus does not resolve with VKA therapy, we recommend that PMBV not be performed (Grade 1A) .6.2.1. In patients with asymptomatic patent fora-men ovale (PFO) or atrial septal aneurysm, we suggest against antithrombotic therapy (Grade 2C) .6.2.2. In patients with cryptogenic stroke and PFO or atrial septal aneurysm, we recommend aspirin (50-100 mg/d) over no aspirin (Grade 1A) .6.2.3. In patients with cryptogenic stroke and PFO or atrial septal aneurysm, who experience recurrent events despite aspirin therapy, we suggest treatment with VKA therapy (target IN R, 2.5; range, 2.0-3.0) and consideration of device closure over aspirin therapy (Grade 2C) .6.2.4. In patients with cryptogenic stroke and PFO, with evidence of DVT, we recommend VKA therapy for 3 months (target IN R, 2.5; range, 2.0-3.0) (Grade 1B) and consideration of device closure over no VKA therapy or aspirin therapy (Grade 2C) .7.1.1. In patients with infective endocarditis (IE), we recommend against routine anticoagu-lant therapy, unless a separate indication exists (Grade 1C) .7.1.2. In patients with IE, we recommend against routine antiplatelet therapy, unless a separate indication exists (Grade 1B) .7.2. In patients on VKA for a prosthetic valve who develop IE, we suggest VKA be discontin-ued at the time of initial presentation until it is clear that invasive procedures will not be required and the patient has stabilized without signs of CNS involvement. When the patient isR evision accepted August 31, 2011 . A fﬁ liations: From McMaster University (Drs Whitlock and Teoh), H amilton, ON, Canada; the University of Washington School of Medicine (Dr Sun), Seattle, WA; the Sunnybrook Hos-pital (Dr Fremes), University of Toronto, Toronto, ON, Canada; and the Ottawa H eart Institute (Dr Rubens), Ottawa, ON, Canada .F unding/Support: The Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines received support from the National Heart, Lung, and Blood Institute [R13 HL104758] and Bayer Schering Pharma AG. Support in the form of educational grants was also provided by Bristol-Myers Squibb; Pﬁ zer, Inc; Canyon Pharmaceuticals; and sanoﬁ -aventis US.D isclaimer: American College of Chest Physician guidelines are intended for general information only, are not medical advice, and do not replace professional medical care and physician advice, which always should be sought for any medical condition. The complete disclaimer for this guideline can be accessed at /content/141/2_suppl/1S.C orrespondence to: Richard P. Whitlock, MD, Population Health Research Institute, McMaster University, David Braley Cardiac, Vascular, and Stroke Research Institute, 237 Barton St East, Room C1-114, Hamilton, ON, L8L 2X2, Canada; e-mail: richard.whitlock@phri.ca© 2012 American College of Chest Physicians.Reproduction of this article is prohibited without written permission from the American College of Chest Physicians ( h ttp:///site/misc/reprints.xhtml ).D OI: 10.1378/chest.11-2305 S ummary of Recommendat ionsNote on Shaded Text: Throughout this guideline,shading is used within the summary of recommenda-tions sections to indicate recommendations that are newly added or have been changed since the pub-lication of Antithrombotic and Thrombolytic Therapy: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Recommendations that remain unchanged are not shaded.2.0.1. In patients with rheumatic mitral valve disease and normal sinus rhythm with a left atrial diameter , 55 mm we suggest not using anti-platelet or vitamin K antagonist (VKA) therapy (Grade 2C).2.0.2. In patients with rheumatic mitral valve disease and normal sinus rhythm with a left atrial diameter . 55 mm, we suggest VKA therapy (target international normalized ratio [IN R], 2.5; range, 2.0-3.0) over no VKA therapy or anti-platelet (Grade 2C) .2.0.3. For patients with rheumatic mitral valve disease complicated by the presence of left atrial thrombus, we recommend VKA therapy (target INR, 2.5; range, 2.0-3.0) over no VKA therapy (Grade 1A).2.0.4. For patients with rheumatic mitral valve disease complicated singly or in combination bygest target INR 3.0 (range 2.5-3.5) over target INR 2.5 (range 2.0-3.0) (Grade 2C) .9.6. In patients with a mechanical mitral or aor-tic valve at low risk of bleeding, we suggest add-ing over not adding an antiplatelet agent such as low-dose aspirin (50-100 mg/d) to the VKA therapy (Grade 1B) .R emarks: Caution should be used in patients at increased bleeding risk, such as history of GI bleeding.9.7. For patients with mechanical aortic or mitral valves we recommend VKA over anti-platelet agents (Grade 1B) .10.1. In patients undergoing mitral valve repair with a prosthetic band in normal sinus rhythm, we suggest the use of antiplatelet therapy for the ﬁ rst 3 months over VKA therapy (Grade 2C) .10.2. In patients undergoing aortic valve repair, we suggest aspirin at 50 to 100 mg/d over VKA therapy (Grade 2C) .11.1. For patients with right-sided prosthetic valve thrombosis (PVT), in the absence of contraindications we suggest administration of ﬁ brinolytic therapy over surgical intervention (Grade 2C) .11.2.1. For patients with left-sided PVT and large thrombus area ( Ն 0.8 cm 2), we suggest early surgery over ﬁ brinolytic therapy (Grade 2C) . If contraindications to surgery exist, we suggest the use of ﬁ brinolytic therapy (Grade 2C) .11.2.2. For patients with left-sided PVT and small thrombus area ( , 0.8 cm 2), we suggest administration of ﬁ brinolytic therapy over sur-gery. For very small, nonobstructive throm-bus we suggest IV UFH accompanied by serial Doppler echocardiography to document throm-bus resolution or improvement over other alter-natives (Grade 2C) .T hromboembolic complications of valvular heart disease are often devastating. Antithrombotic therapy can reduce the risk of thromboembolism, but at the cost of increased bleeding. This article seeks to provide recommendations based on the optimal bal-ance of these competing factors. T able 1 describes the population, intervention, comparator, and outcome (PICO) elements for the questions addressed in this article and the design of the studies used to address them. We deﬁ ne onlydeemed stable without contraindications or neurologic complications, we suggest reinsti-tution of VKA therapy (Grade 2C).7.3. In patients with nonbacterial thrombotic endocarditis and systemic or pulmonary emboli, we suggest treatment with full-dose IV unfrac-tionated heparin (UFH) or subcutaneous low-molecular-weight heparin (LMWH) over no anticoagulation (Grade 2C) .8.2.1. In patients with aortic bioprosthetic valves, who are in sinus rhythm and have no other indication for VKA therapy, we suggest aspirin (50-100 mg/d) over VKA therapy in the ﬁ rst 3 months (Grade 2C) .8.2.2. In patients with transcatheter aortic bio-prosthetic valves, we suggest aspirin (50-100 mg/d) plus clopidogrel (75 mg/d) over VKA therapy and over no antiplatelet therapy in the ﬁ rst 3 months (Grade 2C) .8.2.3. In patients with a bioprosthetic valve in the mitral position, we suggest VKA therapy (target IN R, 2.5; range, 2.0-3.0) over no VKA therapy for the ﬁ rst 3 months after valve inser-tion (Grade 2C) .8.3. In patients with bioprosthetic valves in nor-mal sinus rhythm, we suggest aspirin therapy over no aspirin therapy after 3 months postop-erative (Grade 2C) .9.1. In patients with mechanical heart valves, we suggest bridging with unfractionated heparin (UFH, prophylactic dose) or LMWH (prophylac-tic or therapeutic dose) over IV therapeutic UFH until stable on VKA therapy (Grade 2C) .9.2. In patients with mechanical heart valves, we recommend VKA therapy over no VKA therapy for long-term management (Grade 1B) .9.3.1 In patients with a mechanical aortic valve, we suggest VKA therapy with a target of 2.5 (range, 2.0-3.0) over lower targets (Grade 2C) .9.3.2. In patients with a mechanical aortic valve, we recommend VKA therapy with a tar-get of 2.5 (range 2.0-3.0) over higher targets (Grade 1B) .9.4. In patients with a mechanical mitral valve, we suggest VKA therapy with a target of 3.0 (range, 2.5-3.5) over lower INR targets (Grade 2C) .9.5. In patients with mechanical heart valves in both the aortic and mitral position, we sug-T able 1— S tructured Clinical QuestionsSectionPICO QuestionMethodology Population Interventions Comparator Outcome2.0 Rheumatic mitral valve2.0.1Normal sinus rhythmand left atrialdiameter ,55 mm Anticoagulationor antiplateletNo anticoagulationor antiplateletThromboembolism Observational studies2.0.2Normal sinus rhythmand left atrialdiameter .55 mmAnticoagulation No anticoagulation Thromboembolism Observational studies2.0.3Presence of leftatrial thrombusAnticoagulation No anticoagulation Thromboembolism Observational studies2.0.4Atrial ﬁ brillation orprevious systemicembolism Anticoagulation No anticoagulation Total mortality,stroke, majorbleeding eventRCT observationalstudies2.1.1Percutaneous mitralballoon valvotomyin presence of leftatrial thrombus Anticoagulationprior toprocedureNo anticoagulationprior toprocedureThromboembolism Observational studies2.1.2Percutaneous mitralballoon valvotomywith nonresolvingleft atrial thrombusPMBV No PMBV Thromboembolism Expert consensus6.0 Aortic atheroma and PFO6.2.1AsymptomaticPFO or atrialseptum aneurysm Anticoagulationor antiplateletNo anticoagulationor antiplateletStroke Observational studies6.2.2Stroke in the presenceof PFO Antiplatelet No antiplatelet Recurrent strokeor deathRCT subgroup data6.2.3Recurrent strokeand PFOAnticoagulation Antiplatelet Recurrent stroke Observational studies6.2.4PFO in presenceof DVT Anticoagulation No anticoagulation Recurrent stoke,pulmonaryembolism, mortalityRCT (indirect)7.0 Endocarditis7.1.1Infectiveendocarditis Anticoagulation No anticoagulation Thromboembolism,intracerebral bleedObservational studies7.1.2Infectiveendocarditis Antiplatelet No antiplatelet Thromboembolism,mortality,major bleedRCT7.2Prosthetic valveendocarditis Anticoagulation No anticoagulation Thromboembolism,bleedingObservational studies7.3Nonbacterialthromboticendocarditis withprior embolismAnticoagulation No anticoagulation Recurrent embolism Observational studies8.0 Bioprosthetic heart valves8.2.1Aortic bioprosthesiswith normalsinus rhythm Anticoagulationfor ﬁ rst 3 moAntiplatelet forﬁ rst 3 moThromboembolism,mortality, majorbleeding eventRCT8.2.2Transcatheteraortic bioprosthesiswith normalsinus rhythm Anticoagulationin ﬁ rst 3 moAntiplatelet forﬁ rst 3 moThromboembolism,major bleeding eventObservational studies8.2.3Mitral bioprosthesiswith normalsinus rhythm Anticoagulationin ﬁ rst 3 moNo anticoagulationfor ﬁ rst 3 moThromboembolism,major bleeding eventObservational studies(Continued)continues to consider vitamin K antagonists (VKAs) as the ﬁ rst-line oral anticoagulant until evidence of efﬁ cacy and safety within the valve population is generated. For recommendations on the manage-ment of parenteral anticoagulation (dosing and monitoring), oral anticoagulation (dosing and mon-itoring), and bleeding complications, please referto the article by Holbrook et al2 about management of anticoagulation in this guideline. Finally, therepatient characteristics relevant to our questions. This article does not make recommendations spe-ciﬁ c to atrial ﬁ brillation (AF); for this issue, wedirect you to the article by You et al1on AF in this supplement. In areas of overlap with the AF article, where newer anticoagulants such as dabigatran may be considered for nonvalvular AF, caution must be used when extrapolating their use to the populations described in this article. This articleSection PICO QuestionMethodology Population InterventionsComparatorOutcome9.0 Mechanical heart valves9.1Mechanicalheart valves early postoperative (day 0-5)UFH or LMWH (DVT dosing)IV therapeutic UFHThromboembolism, bleedingObservational studies9.2Mechanical heart valves Long-termanticoagulation No long-term anticoagulation Thromboembolism, valve thrombosis Meta-analysis of observational data 9.3.1Mechanical aortic valve Conventional INR target (2.0-3.0)Lower INR targets Thromboembolism, bleedingRCT 9.3.2Mechanical aortic valve Conventional INR target (2.0-3.0)Higher INR targets Thromboembolism, major bleeding event, mortalityRCT9.4Mechanical mitral valve Conventional INR target (2.5-3.5)Lower INR targets Thromboembolism, major bleeding event, mortality RCT9.5Mechanical aortic and mitral valve INR target 2.5-3.5INR target 2.0 to 3.0MortalityRCT9.6Mechanical heart valvesAntiplatelet in addition to anticoagulationAnticoagulation aloneThromboembolism, mortality, valve thrombosis, major bleeding event Meta-analysis of RCTs10.0 Heart valve repair10.1Mitral valve repair with prosthetic band AntiplateletAnticoagulationThromboembolism, valve thrombosis Observational studies10.2Aortic valve repairAntiplatelet Anticoagulation Thromboembolism, bleedingObservational studies11.0 Prosthetic valve thrombosis11.1Right-sidedprosthetic valve thrombosisFibrinolytic therapy Surgical interventionMortality,hemodynamic success,thromboembolism, bleeding, recurrence of obstruction Observational studies11.2.1Left-sided prostheticvalve thrombosis with thrombus Ն0.8 cm 2Fibrinolytic therapy Surgical intervention Mortality,hemodynamic success,thromboembolism, bleeding, recurrence of obstruction Observational studies11.2.2Left-sided prosthetic valve thrombosis with thrombus ,0.8 cm 2Fibrinolytic therapy Surgical intervention Mortality,hemodynamic success,thromboembolism, bleeding, recurrence of obstructionObservational studiesI NR 5 international normalized ratio; LMWH 5 low-molecular-weight heparin; PFO 5 patent foramen ovale; PICO 5 population, intervention, comparator, and outcome; PMBV 5 percutaneous mitral balloon valvotomy; RCT 5 randomized controlled trial; UFH 5 unfractionated heparin.Table 1—ContinuedThe relationship between thromboembolism and left atrial size remains unclear. Early studies 5,13,14ofrheumatic mitral valve disease reported a weak corre-lation. H owever, several studies have now demon-strated an association between larger left atrial size and left atrial thrombus or spontaneous echocardio-graphic contrast. 15-17I n those patients with rheumatic mitral valve disease who suffer a ﬁ rst embolus, recurrent emboli occur frequently (one-third to two-thirds of cases)and early (two-thirds within the ﬁ rst year).5,23-25 A hypercoagulable state in mitral stenosis mightcontribute to the risk of thromboembolism. 26,27 Norandomized trial has been completed in this popu-lation, but observational data suggest that the risk of recurrent emboli may be reduced by VKA therapy. Szekely 7 found a recurrence rate of 9.6%/y with no anticoagulation and 3.4%/y with warfarin (relative risk [RR], 0.36; 95% CI, 0.08-1.6). Similar estimateshave been reported by others. 14,28Among patients with mitral stenosis and left atrial thrombus on transesophageal echocardiography (TEE), VKA therapy results in a 62% thrombus disappearance over anaverage of 34 months. 29T he onset of AF increases the risk of systemic embolization in patients with rheumatic mitral valve disease.7,13 As in those with recurrent embolism, observational studies suggest a large decrease in riskwith warfarin administration. 13,30Indirect evidencefrom randomized trials in nonvalvular AF provide further support for the impact of warfarin in the pre-vention of thromboembolism in patients with rheu-matic mitral valve with AF. R ecommendations2.0.1. In patients with rheumatic mitral valve disease and normal sinus rhythm with a left atrial diameter , 55 mm, we suggest not using anti-platelet or VKA therapy (Grade 2C) .2.0.2. In patients with rheumatic mitral valve disease and normal sinus rhythm with a left atrial diameter . 55 mm, we suggest VKA ther-apy (target IN R, 2.5; range, 2.0-3.0) over no VKA therapy or antiplatelet (Grade 2C) .2.0.3. For patients with rheumatic mitral valve disease complicated singly or in combination by the presence of left atrial thrombus, we recom-mend VKA therapy (target IN R, 2.5; range, 2.0-3.0) over no VKA therapy (Grade 1A) .2.0.4. For patients with rheumatic mitral valve disease complicated singly or in combination by the presence of AF or previous systemic embolism, we recommend VKA therapy (targetare very few data directly addressing the antithrom-botic management of right-sided prosthetic valves. Indirect evidence from mitral and aortic valves pro-vides the best evidence and the basis for recommen-dations regarding tricuspid and pulmonic prostheses.1.0 M ethodsT he development of the current recommendations followed the general approach of Methodology for the Development of Antithrombotic Therapy and Prevention of Thrombosis Guide-lines. Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-BasedClinical Practice Guidelines. 3 In brief, literature searches to updatethe existing database from the AT8 guidelines were performed (January 1, 2005 to October 2009). The literature was rated according to the Grades of Recommendations, Assessment, Development, and Evaluation (GRADE) framework. The panel considered quality of information, balance of risk and harm, and patients’ values and preferences to determine the strength of recommendation.I n making recommendations, we have taken a p rimum non nocere approach, placing the burden of proof with those who would claim a beneﬁ t of treatment. In other words, when there is uncertain beneﬁ t and an appreciable probability of important harm associated with treatment, we recommend against such treatments.T he value given to the harmful effect of an extracranial bleeding event (as compared with that of valve thrombosis, peripheral thromboembolism, or stroke) greatly impacts the balance of ben-eﬁ ts and harms of a given therapy. There are limited data to guide us with respect to the relative value of these outcomes. For this article, we used the result of the preference-weighting exercisecarried out by MacLean et al4 as part of these guidelines, which attributes approximately three times the disutility (aversiveness, negative weight) to a stroke vs an extracranial bleeding event; a valve thrombosis carries slightly greater disutility than an extra-cranial bleeding event.2.0 R heumatic M itral V alve D isease Rheumatic mitral valve disease carries the great-est risk of systemic thromboembolism of any com-mon form of acquired valvular disease. Wood 5citeda prevalence of systemic emboli of 9% to 14% in several large early series of patients with mitralstenosis. In 1961, Ellis and H arken 6reported that27% of 1,500 patients undergoing surgical mitral valvotomy had a history of clinically detectable sys-temic emboli. Among 754 patients followed up for5,833 patient-years, Szekely 7observed an incidenceof emboli of 1.5% per year, whereas the number was found to vary from 1.5% to 4.7% per year preopera-tively in six reports of rheumatic mitral valve disease. 8Although the risk may increase in the elderly andthose with lower cardiac indices, 9-12these ﬁndings have been inconsistent across studies. 5,13-21Other characteristics that may increase the risk of systemic embolism include the presence of a left atrial throm-bus and signiﬁ cant aortic regurgitation. 22people with MVP had an excess lifetime risk of stroke or transient ischemic attack (TIA) (RR, 2.2; P , .001). Thus, it is as yet unclear whether MVP truly increased the risk of thromboembolic process. Mitral valve strands, also known as Lambl’s excres-cences, have also been implicated as a potential embolic source, but they do not seem to increasethe risk of stroke recurrence.44We therefore sug-gest that patients with MVP or strands who have not experienced systemic embolism, unexplained TIAs, or ischemic stroke, and do not have evident vascular disease should be managed as other patients considering primary prevention of vascular events. Given the risk of bleeding complications with anticoagulation and the lack of data to demon-strate a beneﬁ t in terms of reducing (recurrent) thromboembolic events, patients with MVP or strands and a history of ischemic stroke or TIA should be treated with antiplatelet agents follow-ing the recommendations by Landsberg et al 45 forpatients with noncardioembolic stroke. In those patients with MVP or strands who have recurrent thromboembolic events despite antiplatelet agent (APA) therapy, the likelihood of a cardiac source increases.4.0 Mitral Annular Calcification M itral annular calciﬁ cation (MAC), like MVP , may be a source of cardioembolic stroke. The best esti-mate of the embolic potential of MAC comes fromthe Framingham H eart Study. 46 Among 1,159 indi-viduals with no history of stroke at the index echo-cardiographic examination, the risk of stroke inthose with MAC was 2.1 times greater than those without MAC (5.1% without MAC vs 13.8% with MAC, P 5 .006), independent of traditional risk factors for stroke. There was a continuous relation-ship between the risk of stroke and the severity of the MAC. A major issue in this condition is that emboli may represent thrombus or calciﬁ c spic-ules, the latter of which antithrombotic therapywill not prevent. 46-48From the available literature,we suggest that patients with MAC who have not experienced systemic embolism, unexplained TIAs, or ischemic stroke, and do not have evident vas-cular disease should be managed as other patients considering primary prevention of vascular events. It would be reasonable to manage patients with MAC and evidence of thromboembolic process with no other identiﬁ able source as patients withTIAs without MAC. 45 Failure of this antithrombotictherapy or evidence of multiple calciﬁ c emboli should prompt consideration of valve replacement.INR, 2.5; range, 2.0-3.0) over no VKA therapy (Grade 1A) . 2.1 Patients With Rheumatic Mitral Valve Disease Undergoing Percutaneous Mitral Balloon Valvotomy During the percutaneous mitral balloon valvot-omy (PMBV) procedure, when the catheter is pushed through the septum it often goes into the left atrial appendage, the usual site of thrombus. Thus, the presence of left atrial thrombus precludes PMBV. Accurate detection of thrombus requires atransesophageal echocardiogram (TEE). Silaruks et al 31have demonstrated that 24.2% of left atrial thrombi will resolve within 6 months of anticoagulation. Further,Kang et al 32 have demonstrated that after thrombusresolution, PMBV can be safely performed. Predic-tors of thrombus resolution are New York H eart Association (NYHA) functional class II or better, leftatrial appendage thrombus size Յ1.6 cm 2, less dense spontaneous echocardiographic contrast, and an INR Ն 2.5. Patients with all of these predictors had a 94.4% chance of complete thrombus resolutionat 6 months. 31I n those patients without left atrial thrombus and no other indication for anticoagulation, Abraham et al 33demonstrated PMBV can be performed in the absence of anticoagulation, with no patients in 629 procedures performed having an embolism within 3 months post procedure. R ecommendations 2.1.1. For patients being considered for PMBV with preprocedural TEE showing left atrial thrombus, we recommend postponement of PMBV and that VKA therapy (target INR, 3.0; range, 2.5-3.5) be administered until thrombus resolution is documented by repeat TEE over no VKA therapy (Grade 1A) .2.1.2. For patients being considered for PMBV with preprocedural TEE showing left atrial thrombus, if the left atrial thrombus does not resolve with VKA therapy, we recommend that PMBV not be performed (Grade 1A ).3.0 Mitral Valve Prolapse and Mitral Valve StrandsMitral valve prolapse (MVP) is a common con-genital form of valve disease. Although early evi-dence from case series and control studies suggestedan association with stroke, 34-40 Gilon et al 41and the Framingham Heart Study 42 failed to replicate theresults. More recently, Avierinos et al 43found that。

ACCP-9抗栓指南中文版

近日，美国胸内科医师学会（ACCP）在《胸》（Chest 2012，141：7S-47S）杂志公布了第9版《抗栓治疗及预防血栓形成指南》（ACCP-9）。

此版指南在第8版基础上，结合最新循证医学证据，对抗栓治疗进行了全面细致的推荐。

阿司匹林一级预防再受推荐ACCP-9最新推荐：对于心血管病一级预防，年龄>50岁且无心血管疾病症状的人群应用小剂量阿司匹林75~100 mg/d 优于不用（推荐级别：2B）。

新指南指出，阿司匹林服用10年可以轻度降低各类心血管风险的全因死亡率。

对于心血管风险中高危患者来说，心肌梗死发生率降低的同时伴随严重出血的增加。

不论何种风险患者，如果不愿长期服药以换取很小的获益，可以不用阿司匹林进行一级预防。

心血管风险中高危患者，若心肌梗死预防获益大于胃肠道出血风险，应当应用阿司匹林。

阿司匹林用于心血管疾病一级预防疗效确切对于心血管疾病来说，推行健康的生活方式、有效控制危险因素、合理使用循证药物，才能真正发挥预防的作用。

作为防治心脑血管疾病的基石，阿司匹林的心血管益处已得到大量循证医学证据的证明，适用于动脉粥样硬化疾病的一级、二级预防和急性期治疗。

既往基于6项大规模随机临床试验[英国医师研究（BMD）、美国医师研究（PHS）、血栓形成预防试验（TPT）、高血压最佳治疗研究（HOT）、一级预防研究（PPP）和妇女健康研究（WHS）]的荟萃分析表明，未来10年心血管事件风险>6%的个体服用阿司匹林的获益大于风险。

最近，英国学者在《内科学年鉴》（Ann Intern Med）杂志发表了一项荟萃分析，对应用阿司匹林进行常规一级预防提出质疑。

然而，在ACCP-9中，采用包含最新临床试验的高质量系统性评估和荟萃分析对阿司匹林相对作用进行评估的结果显示，每治疗1000例患者，阿司匹林使低危人群心肌梗死减少6例，总死亡减少6例。

其中，应用阿司匹林分别使中、高危人群非致死性心肌梗死减少19/1000例和31/1000例，同时增加严重出血发生率（RR=1.54，95%CI 1.30~1.82）。

美国胸科医师协会第九版抗栓治疗及血栓预防指南静脉血栓栓塞性疾病最新进展

美国胸科医师协会第九版抗栓治疗及血栓预防指南静脉血栓栓塞性疾病最新进展周玉杰，杨士伟（首都医科大学附属北京安贞医院　心内科12病房，北京　100029）通讯作者：周玉杰　E-mail：jackydang@静脉血栓栓塞性疾病（venous thromboembolism ，VTE ）包括深静脉血栓（deep venous thrombosis ，DVT ）和肺栓塞（pulmonary embolism ，PE ）。

近日，美国胸科医师协会（American College of Chest Physicians ，ACCP ）在Chest 杂志上公布了第9版《抗栓治疗及血栓预防指南》（ACCP-9）[1-4]。

此版指南在第8版基础上，结合最新循证医学证据，对抗栓治疗进行了全面细致的推荐。

本文将结合ACCP-9对VTE 的最新进展进行阐述。

1　病因与诱因Virchow 于1856年提出了导致静脉血栓形成的三因素假说：静脉血流淤滞、血管损伤和高凝状态。

经过大量试验证实，该假说目前已得到了公认。

许多参与上述过程的临床情况均可诱发静脉血栓形成，主要包括：（1）肢体制动：各种疾病导致的长时间卧床或肢体制动，如急性心肌梗死、主要脏器功能衰竭、脑卒中、大型手术后等；（2）静脉受压：如股动脉或静脉穿刺术后压迫止血导致下肢静脉回流受阻，妊娠、腹腔巨大肿瘤或大量腹水导致盆腔静脉或下腔静脉回流受阻等；（3）静脉曲张：主要是指深静脉曲张，浅静脉曲张一般不会导致血栓形成；（4）静脉损伤：如外伤或手术累及静脉、静脉穿刺、静脉炎等；（5）高凝状态：各种遗传性或获得性血栓形成倾向，如抗凝因子缺乏（抗凝血酶Ⅲ、C 蛋白或S 蛋白最常见）、弥漫性血管内凝血（disseminated intravascular coagulation ，DIC ）、抗磷脂综合征、肾病综合征、恶性肿瘤、大量呕吐或腹泻导致的脱水、药物因素（长期口服避孕药、激素或抗肿瘤药物）等；（6）其他：如高龄、吸烟、肥胖等。

ACCP心房颤动抗栓治疗简明指南

ACCP心房颤动抗栓治疗简明指南心房颤动（atrial fibrillation, 房颤）是最常见的一种心律失常，它也是脑卒中的一个非常重要的独立危险因素。

在美国有近250万房颤患者。

房颤的发生受年龄因素的影响，50岁以下人群发病率很低，从60岁开始房颤的发病率迅速增高，80岁以上发病率可接近10％。

房颤的平均发病年龄在72岁左右。

在所有的年龄段中，男性房颤的发病率明显高于女性。

随着人口的老龄化，在未来十年中房颤的发病率似乎有增高的趋势。

一级预防临床试验中和无抗血栓治疗的房颤患者脑卒中的发病率平均每年％。

与Framingham研究中所估计的脑卒中发病率相近。

房颤可使各年龄段脑卒中的危险增加4-5倍。

随着患病率的增加，房颤已成为发生脑卒中的一个重要原因。

Framingham研究中，房颤导致的脑卒中危险由50-59岁时％增加到80-89岁时％。

在美国，大约有15％的脑卒中继发于房颤。

房颤患者脑卒中主要是心源性栓塞的结果，主要的证据是手术发现风湿性二尖瓣疾病患者心腔内血栓，食管超声发现房颤患者有左心房附壁血栓主要在左心耳。

一、慢性房颤或心房扑动长期抗栓治疗: 抗凝和抗血小板制剂（一）慢性房颤1．口服抗凝治疗5个一级预防试验对比口服维生素K拮抗剂(Vitamin K antagonist, VKA) 与安慰剂。

入选的病例包括有慢性持续性房颤(包括持续的和永久的房颤)或阵发性房颤。

大多数病例房颤持续数月到数年。

由于口服抗凝剂对预防脑卒中和系统栓塞作用明显(CAFA由于其他试验发现抗凝的优势而早期停止)，所有试验均提前中止。

但这些研究终点事件数量相对较少, 很大程度上影响了疗效估测的可信度。

汇总分析结果显示脑卒中的年发生率从对照组的％减少到调整剂量华法林治疗的％，相对危险降低(RRR) 68％[95％CI，50-79％]。

绝对危险降低为每1,000例患者治疗1年可预防31例脑卒中(或治疗1年预防1例脑卒中需要治疗32例) 。