ACCP9美国胸科医师协会抗栓与血栓预防指南

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ACCP新指南并非所有患者适用DVT预防

ACCP新指南:并非所有患者适用DVT预防美国胸科医师学会（ACCP）最新指南《抗栓治疗和血栓形成预防临床实践指南（第9版）》推荐，决定使用或不使用深静脉血栓（DVT）和静脉血栓栓塞（VTE）预防性治疗时要考虑个别患者血栓形成风险。

该指南对患者风险进行分类，这提示临床医师在进行预防性治疗前应考虑患者DVT/VTE风险。

长途旅行的DVT/VTE风险因素研究虽然大多数患者不易出现旅行相关性深静脉血栓形成/静脉血栓栓塞，但指南支出，长途航班后，几种因素可能会增加个体DVT/VTE风险，包括既往DVT/VTE或已知的血栓形成性疾病；恶性肿瘤；近期手术或创伤;不活动；使用雌激素或怀孕；坐在靠窗的座位。

由于旅客的旅游相关性DVT / VTE风险升高，该指南建议应经常行走，拉伸小腿肌肉，如果可能的话坐在靠过道的座位，或使用膝盖下渐进性压力弹性袜即静脉曲张袜。

相反，该指南建议称，尚无确切证据显示脱水，饮酒，或坐经济舱可增加长途飞行对患者造成的DVT / VTE风险。

阿司匹林及新疗法预防DVT / VTE该指南还还对提出了有关使用新疗法或潜在疗法用于DVT / VTE预防和治疗的建议。

虽然阿司匹林用于DVT/VTE预防并不是什么新方法，但以前的ACCP指南反对在任何手术人群中使用阿司匹林单药进行预防性治疗。

最新版的治疗指南中，ACCP已对此进行了修订，并表示在大多数矫形手术中，阿司匹林也是预防DVT/VTE的一种选择，尽管其不是首选药物。

抗栓指南的创新《抗栓治疗和血栓形成预防临床实践指南（第9版）》包括显著影响血栓形成的预防，诊断和治疗的600多条建议的创新。

两个关键的进步是更加明确和定量的考虑对患者重要的指标和预后限定因素。

后者的创新引起血栓形成预防中对机体指标不同的解释，而以前曾重点监测无症状血栓。

资料来源：New Guidelines Suggest DVT Prophylaxis not Appropriate for All Patients.美国胸科医师学会，2012/02/07全文：New Guidelines Suggest DVT Prophylaxis not Appropriate for All PatientsArticle | 02.07.12(NORTHBROOK, IL, FEBRUARY 7, 2012) — New evidence-based guidelines from the American College of Chest Physicians (ACCP) recommend considering individual patients’risk of thrombosis when deciding for or against the use of preventive therapies for deep vein thrombosis (DVT) and venous thromboembolism (VTE). Specifically, the Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines, published in the February issue of the journal CHEST, focus on risk stratification of patients, suggesting clinicians should consider a patient’s risk for DVT/VTE and risk for bleeding before administering or prescribing a prevention therapy.“There has been a significant push in health care to administer DVT prevention for every patient, regardless of risk. As a result, many patients are receiving unnecessary therapies that provide little benefit and could have adverse effects,”said Guidelines Panel Chair Gordon Guyatt, MD, FCCP, Department of Medicine, McMaster University Faculty of Health Sciences, Hamilton, Ontario, Canada. “The decision to administer DVT prevention therapy should be based on the patients’risk and the benefits of prevention or treatment.” To address this, the ACCP guidelines provide comprehensive risk stratification recommendations for most major clinical areas, including medical, nonorthopedic surgery, orthopedic surgery, pregnancy, cardiovascular disease, atrial fibrillation, stroke, pediatrics, and long-distance travel.DVT/VTE Risk Factors for Long-distance TravelAlthough developing a travel-related DVT/VTE is unlikely in most cases, the guidelines note that for long-distance flights, several factors may increase an individual’s risk of developing a DVT/VTE, including previous DVT/VTE or known thrombophilic disorder; malignancy; recent surgery or trauma; immobility; estrogen use or pregnancy; and sitting in a window seat. For travelers with an increased risk for travel-related DVT/VTE, the guidelines recommend frequent ambulation, calf muscle stretching, sitting in an aisle seat if possible, or the use of below-knee graduated compression stockings. Conversely, the guidelines suggest there is no definitive evidence to support that dehydration, alcohol intake, or sitting in economy class increases a patient’s risk for developing a DVT/VTE resulting from long-distance flights. Aspirin and New Therapies for DVT/VTE PreventionThe guidelines also provide recommendations related to the use of new or potential therapies for the prevention and treatment of DVT/VTE. Although aspirin is not a new therapy for the prevention of DVT/VTE, previous ACCP guidelines recommended against using aspirin as the single agent for prophylaxis in any surgical population. In the current edition, the ACCP has revised this recommendation and indicates aspirin is an option—although not typically the agent of choice—for the prevention of DVT/VTE in major orthopedic surgery.“Although we are not recommending aspirin as the optimal DVT/VTE prophylaxis, we have reviewed the existing evidence and concluded that aspirin is an acceptable option in some instances where preventive therapy is needed,”said guideline co-author Mark Crowther, MD, Department of Medicine, McMaster University, Hamilton, Ontario, Canada. In regard to new oral anticoagulants, guideline authors recognize the recent clinical trials of apixaban and rivaroxaban, both direct factor Xa inhibitors, and dabigatran etexilate, a direct thrombin inhibitor, and offer recommendations for the new agents for select clinical conditions, including atrial fibrillation and orthopedic surgery.Innovations in Antithrombotic GuidelinesThe Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines include innovations that have significantly impacted the more than 600 recommendations for the prevention, diagnosis, and treatment of thrombosis. Two key advances are the more explicit and quantitative consideration of patient values and preferences and restriction of outcomes to only those deemed to be important for the patient. The latter innovation results in different interpretation of the body of evidence in thrombosis prevention that has previously focused on the detection of asymptomatic thrombosis by surveillance methods.Guideline authors also took a more critical look at the overall process of guideline development, providing more methodologically sophisticated scrutiny of all available evidence. “The evidence review for the new guidelines was more rigorous than ever before, and our method for grading research studies has become even more stringent,”said guideline co-author David Gutterman, MD, FCCP, ACCP Immediate Past President, Cardiovascular Research Center, Medical College of Wisconsin, Milwaukee, Wisconsin. “We believe that the objective rigorous application of the science of guideline development will ultimately best serve our patients.”The guidelines are endorsed by the following medical associations: the American Association for Clinical Chemistry, American College of Clinical Pharmacy, American Society of Health-System Pharmacists, American Society of Hematology, International Society of Thrombosis and Hemostasis, and the American College of Obstetrics and Gynecology (pregnancy article only).For more information about the guidelines and accompanying clinician resources, visit and follow #AT9 on Twitter. Patient resources related to the guidelines are available through OneBreath®, an initiative of The CHEST Foundation, the philanthropic arm of the ACCP.About the American College of Chest PhysiciansThe ACCP represents 18,400 members who provide patient care in the areas of pulmonary, critical care, and sleep medicine in the United States and more than 100 countries throughout the world. The mission of the ACCP is to promote the prevention, diagnosis, and treatment of chest diseases through education, communication, and research. CHEST is the official peer-reviewed publication of the ACCP. More than 30,000 readers worldwide turn to CHEST in print and 400,000 people view CHEST online each month for the latest in chest-related medicine. For more information about the ACCP, visit or follow the ACCP via social media at /accpchest and @accpchest.。

最新ACCP-9抗栓治疗和预防指南英文全文版

DOI 10.1378/chest.1412S3 2012;141;7S-47S ChestPhysicians Antithrombotic Therapy and Prevention of Thrombosis Panel Holger J. Schuünemann and for the American College of ChestGordon H. Guyatt, Elie A. Akl, Mark Crowther, David D. Gutterman,Evidence-Based Clinical Practice Guidelinesed: American College of Chest Physicians Therapy and Prevention of Thrombosis, 9th Executive Summary : Antithrombotic/content/141/2_suppl/7S.full.html services can be found online on the World Wide Web at:The online version of this article, along with updated information and7S.DC1.html/content/suppl/2012/02/06/141.2_suppl.Supplemental material related to this article is available at:ISSN:0012-3692)/site/misc/reprints.xhtml (written permission of the copyright holder.this article or PDF may be reproduced or distributed without the prior Dundee Road, Northbrook, IL 60062. All rights reserved. No part of Copyright2012by the American College of Chest Physicians, 3300Physicians. It has been published monthly since 1935.is the official journal of the American College of Chest ChestCHEST / 141 / 2 / FEBRUARY , 2012 SUPPLEMENT 7ST he eighth iteration of the American College of Chest Physicians Antithrombotic Guidelines pre-sented, in a paper version, a narrative evidence sum-mary and rationale for the recommendations, a small number of evidence proﬁ les summarizing bodies ofevidence, and some articles with quite extensivesummary tables of primary studies. In total, this represented 600 recommendations summarized in 968 pages of text. Many readers responded that the result was too voluminous for their liking or prac-tical use. C ognizant of this feedback, we worked hard to minimize the length of the text for the ninth iteration of the guidelines Antithrombotic Therapy and Pre-vention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (AT9) without sacriﬁ cing key content. A number of topic editors found our shortening edits draconian, but we were determined to produce the leanest product possible.T here were, however, a number of obstacles. In what we believe is a key advance in AT9, we con-ducted a systematic review of what is known about patients’ values and preferences regarding antithrom-botic therapy and included the results as an article in AT9. In another forward step, we recognized the problems with asymptomatic thrombosis as a surro-gate outcome, and devised strategies to estimate reductions in symptomatic DVT and pulmonary embolism with antithrombotic prophylaxis. We felt it important to explain this innovation to users of AT9, and this meant another article. W e included, for the ﬁ rst time, an article on diag-nosis addressing patients with symptoms and signs suggesting DVT. We increased the range of interven-tions we have covered, resulting in additional recom-mendations. Finally, we produced many summary of ﬁ ndings tables, which offer extremely succinct and informative presentations of best estimates of effect and the conﬁ dence associated with those estimates.I f published in the same fashion as the Antithrom-botic and Thrombolytic Therapy, 8th ed: AmericanA bbreviations:ACS 5 acute coronary syndrome; AF 5 atrialﬁ brillation; AIS 5 arterial ischemic stroke; APLA 5antiphospolipidantibodies; ASA 5 acetylsalicylic acid; AT9 5 Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines; BMS 5 bare-metal stent; CABG 5 coronary artery bypass graft; CAD 5coronary artery disease; CDT 5catheter-directed thrombosis; CHADS 2 5 congestive heart failure, hyperten-sion, age Ն 75 years, diabetes mellitus, prior stroke or transient ischemic attack; CSVT 5 cerebral sinovenous thrombosis; CTPH 5 chronic thromboembolic pulmonary hypertension; CUS 5 com-pression ultrasound; CVAD 5 central venous access device; DES 5 d rug-eluting stent; GCS 5 g raduated compression stockings; H FS 5 hip fracture surgery; HIT 5 heparin-induced thrombocy-topenia; HITT 5 heparin-induced thrombocytopenia complicated by thrombosis; IA 5 intraarterial; ICH 5intracerebral hemor-rhage; IE 5 infective endocarditis; INR 5 international normalized ratio; IPC 5 intermittent pneumatic compression; IPCD 5 inter-mittent pneumatic compression device; IVC 5 inferior vena cava; LDUH 5 low-dose unfractionated heparin; LMWH 5 low-molecular-weight heparin; LV 5 left ventricular; MBTS 5 modiﬁ ed Blalock-Taussig shunt; MR 5 magnetic resonance; PAD 5peripheral artery disease; PCI 5 percutaneous coronary inter v ention; PE 5 pul-monary embolism; PFO 5 patent foramen ovale; PMBV 5 p ercuta-neous mitral balloon valvotomy; PTS 5postthrombotic syndrome; PVT 5 prosthetic valve thrombosis; r-tPA 5 recombinant tissue plas-minogen activator; RVT 5 renal vein thrombosis; SC 5 subcuta-neous; TEE 5 transesophageal echocardiography; THA 5 total hip arthroplasty; TIA 5 transient ischemic attack; TKA 5 total knee arthroplasty; UAC 5umbilical arterial catheter; UEDVT 5 upper-extremity DVT; UFH 5 unfractionated heparin; US 5 ultrasound; UVC 5 umbilical venous catheter; VAD 5 ventricular assist device; VKA 5 vitamin K antagonistAntithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice GuidelinesG ordon H. G uyatt ,M D, FCCP ;E lie A. A kl ,M D, PhD, M PH ;M ark C rowther ,M D ;D avid D. G utterman ,M D, FCCP ;H olger J. S chü n emann ,M D, PhD, FCCP ;f or the American College of Chest Physicians Antithrombotic Therapy and Prevention of Thrombosis Panel *CHEST 2012; 141(2)(Suppl):7S–47S8SExecutive Summarytables) and some tables summarizing the methodsand results, and the risk of bias, associated with the individual studies that contributed to the evidence proﬁ les and summary of ﬁ ndings tables.T he world of medical information is rapidly becom-ing a world of electronic storage and presentation of primary studies, recommendations, and a wide variety of other information of interest to health care prac t itioners. Although our abbreviated paper copy presentation represents a necessary response to a challenging situation, it is also a harbinger of the increasingly electronic world of medical information into which future editions of guidelines are destined to move.S ummary of Recommendations Note 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 publica-tion of Antithrombotic and Thrombolytic Therapy: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Rec-ommendations that remain unchanged are not shaded.E vidence-Based Management of Anticoagulant TherapyF or further details, see Holbrook et al. 1 2.1 Loading Dose for Initiation of Vitamin K Antagonist(VKA) Therapy2.1. For patients sufﬁ ciently healthy to be treated as outpatients, we suggest initiating VKA therapy with warfarin 10 mg daily for the ﬁ rst 2 days followed by dosing based on international normalized ratio (INR) measurements rather than starting with the estimated maintenance dose (Grade 2C) .2.2 Initial Dose Selection and Pharmacogenetic Testing2.2. For patients initiating VKA therapy, we recommend against the routine use of pharma-cogenetic testing for guiding doses of VKA (Grade 1B) . 2.3 Initiation Overlap for Heparin and VKA2.3. For patients with acute VTE, we suggest that VKA therapy be started on day 1 or 2 of low-molecular-weight heparin (LMWH) or low-dose unfractionated heparin (UFH) therapy rather than waiting for several days to start (Grade 2C) .College of Chest Physicians Antithrombotic Guide-lines, this would have resulted in a document with . 850 pages of paper text, an unacceptable length. Given this and with the advice of the journal, we decided to adopt a highly focused print version that includes only this executive summary and the following articles:• An introduction describing the major innovations in AT9 • A methods article explaining how we devel-oped the guidelines (a potential model for other guideline groups interested in optimal rigor) • Recommendations and grading from each arti-cle embedded in the table of contents of each article T hose seeking the rationale for the recommenda-tions, including the supporting evidence, should access the online version of the guideline ( h ttp:///content/141/2_suppl )that includes a narrative summaries and support-ing summary of ﬁ ndings tables. The numbering indi-cated beside the recommendations in this summary is aligned with the sections and tables found in the full articles. Those interested in a deeper under-standing of the evidence can turn to online data supplements for each of the articles that include rec-ommendations. There, they will ﬁ nd evidence pro-ﬁ les (expanded versions of the summary of ﬁ ndingsR evision accepted August 31, 2011. A fﬁ liations: From the Department of Clinical Epidemiology and Biostatistics (Drs Guyatt, Akl, and Schü n emann) and Depart-ment of Medicine (Drs Guyatt, Crowther, and Schü n emann), McMaster University Faculty of H ealth Sciences, H amilton, ON, Canada; Departments of Medicine and Family Medicine (Dr Akl), State University of New York, Buffalo, NY; Cardiovascular Research Center (Dr Gutterman), Medical College of Wisconsin, Milwaukee, WI.*For complete panel list, see: /content/141/2_suppl/2S 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 educa-tional grants were 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/1SC orrespondence to: Gordon H . Guyatt, MD, FCCP , Department of Clinical Epidemiology and Biostatistics, McMaster University, Hamilton, ON, L8N 3Z5, Canada; e-mail: guyatt@mcmaster.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.1412S3CHEST / 141 / 2 / FEBRUARY , 2012 SUPPLEMENT 9S3.8 VKA Drug Interactions to Avoid3.8. For patients taking VKAs, we suggest avoid-ing concomitant treatment with nonsteroidal antiinﬂ ammatory drugs, including cyclooxyge-nase-2-selective nonsteroidal antiinﬂ ammatory drugs, and certain antibiotics (see Table 8 in mainarticle1 ) (Grade 2C) .F or patients taking VKAs, we suggest avoiding concomitant treatment with antiplatelet agents except in situations where beneﬁ t is known or is highly likely to be greater than harm from bleeding, such as patients with mechanical valves, patients with acute coronary syndrome, or patients with recent coronary stents or bypass surgery (Grade 2C) .4.1 Optimal Therapeutic INR Range4.1. For patients treated with VKAs, we recom-mend a therapeutic INR range of 2.0 to 3.0 (tar-get INR of 2.5) rather than a lower (INR , 2) or higher (INR 3.0-5.0) range (Grade 1B) . 4.2 Therapeutic Range for High-Risk Groups 4.2. For patients with antiphospholipid syn d rome with previous arterial or venous thromboembolism, we suggest VKA therapy titrated to a moderate-intensity INR range (INR 2.0-3.0) rather than higher intensity (INR 3.0-4.5) (Grade 2B). 5.0 Discontinuation of Therapy5.0. For patients eligible to discontinue treat-ment with VKA, we suggest abrupt discontinua-tion rather than gradual tapering of the dose to discontinuation (Grade 2C) .6.1 Unfractionated Heparin (UFH) Dose Adjustment by Weight6.1. For patients starting IV UFH, we suggest that the initial bolus and the initial rate of the continuous infusion be weight adjusted (bolus 80 units/kg followed by 18 units/kg per h for VTE; bolus 70 units/kg followed by 15 units/kg per h for cardiac or stroke patients) or use of a ﬁ xed dose (bolus 5,000 units followed by 1,000 units/h) rather than alternative regimens (Grade 2C) . 6.2 Dose Management of Subcutaneous (SC) UFH6.2. For outpatients with VTE treated with SC UFH, we suggest weight-adjusted dosing (ﬁ rst dose 333 units/kg, then 250 units/kg) with-out monitoring rather than ﬁ xed or weight-adjusted dosing with monitoring (Grade 2C) .3.1 Monitoring Frequency for VKAs3.1. For patients taking VKA therapy with con-sistently stable INRs, we suggest an INR testing frequency of up to 12 weeks rather than every 4 weeks (Grade 2B) .3.2 Management of the Single Out-of-Range INR3.2. For patients taking VKAs with previously stable therapeutic INRs who present with a single out-of-range INR of Յ 0.5 below or above therapeutic, we suggest continuing the current dose and testing the INR within 1 to 2 weeks (Grade 2C) .3.3 Bridging for Low INRs3.3. For patients with stable therapeutic INRs presenting with a single subtherapeutic INR value, we suggest against routinely adminis-tering bridging with heparin (Grade 2C) . 3.4 Vitamin K Supplementation3.4. For patients taking VKAs, we suggest against routine use of vitamin K supplementa-tion (Grade 2C) .3.5 Anticoagulation Management Services for VKAs 3.5. (Best Practices Statement) We suggest that health-care providers who manage oral antico-agulation therapy should do so in a systematic and coordinated fashion, incorporating patient education, systematic INR testing, tracking, follow-up, and good patient communication of results and dosing decisions.3.6 Patient Self-Testing and Self-Management3.6. For patients treated with VKAs who are motivated and can demonstrate competency in self-management strategies, including the self-testing equipment, we suggest patient self-management rather than usual outpatient INR monitoring (Grade 2B) . For all other patients, we suggest monitoring that includes the safe-guards in our best practice statement 3.5. 3.7 Dosing Decision Support3.7. For dosing decisions during maintenance VKA therapy, we suggest using validated deci-sion support tools (paper nomograms or com-puterized dosing programs) rather than no decision support (Grade 2C) .Remarks: Inexperienced prescribers may be more likely to improve prescribing with use of decision sup-port tools than experienced prescribers.10SExecutive Summaryunfractionated heparin (L DUH) bid, LDUHtid, or fondaparinux (Grade 1B) .R emarks: In choosing the speciﬁ c anticoagulant drug to be used for pharmacoprophylaxis, choices should be based on patient preference, compliance, and ease of administration (eg, daily vs bid vs tid dosing), as well as on local factors affecting acquisition costs (eg, prices of various pharmacologic agents in individual hospital formularies).2.4. For acutely ill hospitalized medical patients at low risk of thrombosis, we recommend against the use of pharmacologic prophylaxis or mechan-ical prophylaxis (Grade 1B) .2.7.1. For acutely ill hospitalized medical patients who are bleeding or at high risk for bleeding, we recommend against anticoagulant thromboprophylaxis (Grade 1B) .2.7.2. For acutely ill hospitalized medical patients at increased risk of thrombosis who are bleeding or at high risk for major bleeding, we suggest the optimal use of mechanical thromboprophylaxis with graduated compression stockings (GCS) (Grade 2C) or intermittent pneumatic compres-sion (IPC) (Grade 2C) , rather than no mechan-ical thromboprophylaxis. When bleeding risk decreases, and if VTE risk persists, we sug-gest that pharmacologic thromboprophylaxis be substituted for mechanical thromboprophy-laxis (Grade 2B) .R emarks: Patients who are particularly averse to the potential for skin complications, cost, and need for clinical monitoring of GCS and IPC use are likely to decline mechanical prophylaxis.2.8. In acutely ill hospitalized medical patients who receive an initial course of thrombopro-phylaxis, we suggest against extending the dura-tion of thromboprophylaxis beyond the period of patient immobilization or acute hospital stay (Grade 2B) .3.0 Critically Ill Patients3.2. In critically ill patients, we suggest against routine ultrasound screening for DVT (Grade 2C) .3.4.3. For critically ill patients, we suggest using LMWH or LDUH thromboprophylaxis over no prophylaxis (Grade 2C) .3.4.4. For critically ill patients who are bleeding, or are at high risk for major bleeding, we suggest mechanical thromboprophylaxis with GCS (Grade 2C) o r IPC (Grade 2C) u ntil the7.1 Therapeutic Dose of LM WH in Patients With Decreased Renal Function7.1. For patients receiving therapeutic LMWH who have severe renal insufﬁ ciency (calculated creatinine clearance , 30 mL/min), we suggest a reduction of the dose rather than using stan-dard doses (Grade 2C) .8.1 Fondaparinux Dose Management by Weight8.1. For patients with VTE and body weight over 100 kg, we suggest that the treatment dose of fondaparinux be increased from the usual 7.5 mg to 10 mg daily SC (Grade 2C) .9.1 Vitamin K for Patients Taking VKAs With High INRs Without Bleeding9.1.(a) For patients taking VKAs with INRs between 4.5 and 10 and with no evidence of bleeding, we suggest against the routine use of vitamin K (Grade 2B) .(b) For patients taking VKAs with INRs . 10.0 and with no evidence of bleeding, we suggest that oral vitamin K be administered (Grade 2C) . 9.2 Clinical Prediction Rules for Bleeding While Taking VKA9.2. For patients initiating VKA therapy, we suggest against the routine use of clinical pre-diction rules for bleeding as the sole criterion to withhold VKA therapy (Grade 2C) .9.3 Treatment of Anticoagulant-Related Bleeding9.3. For patients with VKA-associated major bleeding, we suggest rapid reversal of antico-agulation with four-factor prothrombin complex concentrate rather than with plasma. (Grade 2C) .W e suggest the additional use of vitamin K 5 to 10 mg administered by slow IV injection rather than reversal with coagulation factors alone (Grade 2C) .P revention of VTE in Nonsurgical PatientsF or further details, see Kahn et al. 2 2.0 Hospitalized Acutely Ill Medical Patients2.3. For acutely ill hospitalized medical patients at increased risk of thrombosis, we recom m end anticoagulant thromboprophylaxis with low-molecular-weight heparin [LMWH], low-doseCHEST / 141 / 2 / FEBRUARY , 2012 SUPPLEMENT 11Sknee GCS providing 15 to 30 mm Hg of pressureat the ankle during travel (Grade 2C) . F or all other long-distance travelers, we suggest against the use of GCS (Grade 2C) .6.1.3. For long-distance travelers, we suggest against the use of aspirin or anticoagulants to prevent VTE (Grade 2C) .7.0 Persons With Asymptomatic Thrombophilia7.1. In persons with asymptomatic thrombo-philia (ie, without a previous history of VTE), we recommend against the long-term daily use of mechanical or pharmacologic thrombopro-phylaxis to prevent VTE (Grade 1C) .P revention of VTE in Nonorthopedic Surgical PatientsF or further details, see Gould et al. 3 3.6 Patients Undergoing General, GI, Urological,Gynecologic, Bariatric, Vascular, Plastic, or Recon-structive Surgery3.6.1. For general and abdominal-pelvic sur-gery patients at very low risk for VTE ( , 0.5%; Rogers score, , 7; Caprini score, 0), we recom-mend that no speciﬁ c pharmacologic (Grade 1B) o r mechanical (Grade 2C) p rophylaxis be used other than early ambulation.3.6.2. For general and abdominal-pelvic sur-gery patients at low risk for VTE ( ف 1.5%; Rog-ers score, 7-10; Caprini score, 1-2), we suggest mechanical prophylaxis, preferably with inter-mittent pneumatic compression (IPC), over no prophylaxis (Grade 2C) .3.6.3. For general and abdominal-pelvic sur-gery patients at moderate risk for VTE ( ف 3.0%; Rogers score, . 10; Caprini score, 3-4) who are not at high risk for major bleeding complica-tions, we suggest L MWH (Grade 2B ), L DUH (Grade 2B) , o r mechanical prophylaxis, prefer-ably with IPC (Grade 2C) ,o ver no prophylaxis. R emarks: T hree of the seven authors favored a strong (Grade 1B) recommendation in favor of LMWH or LDUH over no prophylaxis in this group.3.6.4. For general and abdominal-pelvic sur-gery patients at moderate risk for VTE (3.0%; Rogers score, . 10; Caprini score, 3-4) who are at high risk for major bleeding complications or those in whom the consequences of bleed-ing are thought to be particularly severe, webleeding risk decreases, rather than no mechan-ical thromboprophylaxis. When bleeding risk decreases, we suggest that pharmacologic throm-boprophylaxis be substituted for mechanical thromboprophylaxis (Grade 2C) . 4.0 Patients With Cancer in the Outpatient Setting4.2.1. In outpatients with cancer who have no additional risk factors for VTE, we suggest against routine prophylaxis with L MWH or LDUH (Grade 2B) and recommend against the prophylactic use of VKAs (Grade 1B) .R emarks: Additional risk factors for venous throm-bosis in cancer outpatients include previous venous thrombosis, immobilization, hormonal therapy, angio-genesis inhibitors, thalidomide, and lenalidomide.4.2.2. In outpatients with solid tumors who have additional risk factors for VTE and who are at low risk of bleeding, we suggest prophylactic-dose L MWH or L DUH over no prophylaxis (Grade 2B) .R emarks: Additional risk factors for venous thrombo-sis in cancer outpatients include previous venous thrombosis, immobilization, hormonal therapy, angio-genesis inhibitors, thalidomide, and lenali d omide.4.4. In outpatients with cancer and indwelling central venous catheters, we suggest againstroutine prophylaxis with L MWH or L DUH (Grade 2B) and suggest against the prophylactic use of VKAs (Grade 2C) .5.0 Chronically Immobilized Patients5.1. In chronically immobilized persons residing at home or at a nursing home, we suggest against the routine use of thromboprophylaxis (Grade 2C) .6.0 Persons Traveling Long-Distance6.1.1. For long-distance travelers at increased risk of VTE (including previous VTE, recent surgery or trauma, active malignancy, preg-nancy, estrogen use, advanced age, limited mobility, severe obesity, or known thrombo-philic disorder), we suggest frequent ambula-tion, calf muscle exercise, or sitting in an aisle seat if feasible (Grade 2C) .6.1.2. For long-distance travelers at increased risk of VTE (including previous VTE, recent surgery or trauma, active malignancy, pregnancy, estrogen use, advanced age, limited mobility, severe obesity, or known thrombophilic disor-der), we suggest use of properly ﬁ tted, below-12SExecutive Summarygest use of mechanical prophylaxis, preferably with optimally applied IPC, over either no pro-phylaxis (Grade 2C) o r pharmacologic prophy-laxis (Grade 2C) .4.4.2. For cardiac surgery patients whose hos-pital course is prolonged by one or more non-hemorrhagic surgical complications, we suggest adding pharmacologic prophylaxis with LDUH or LMWH to mechanical prophylaxis (Grade 2C) .5.0 Patients Undergoing Thoracic Surgery5.4.1. For thoracic surgery patients at mod-erate risk for VTE who are not at high risk for perioperative bleeding, we suggest L DUH (Grade 2B) , L MWH (Grade 2B) , o r mechanical prophylaxis with optimally applied IPC (Grade 2C)o ver no prophylaxis. R emarks: T hree of the seven authors favored a strong (Grade 1B) recommendation in favor of LMWH or LDUH over no prophylaxis in this group.5.4.2. For thoracic surgery patients at high risk for VTE who are not at high risk for periopera-tive bleeding, we suggest LDUH (Grade 1B) o r LMWH (Grade 1B) o ver no prophylaxis. In addi-tion, we suggest that mechanical prophylaxis with elastic stockings or IPC should be added to pharmacologic prophylaxis (Grade 2C) .5.4.3. For thoracic surgery patients who are at high risk for major bleeding, we suggest use of mechanical prophylaxis, preferably with opti-mally applied IPC, over no prophylaxis until the risk of bleeding diminishes and pharmacologic prophylaxis may be initiated (Grade 2C) .6.0 Patients Undergoing Craniotomy6.4.1. For craniotomy patients, we suggest that mechanical prophylaxis, preferably with IPC, be used over no prophylaxis (Grade 2C) o r phar-macologic prophylaxis (Grade 2C) .6.4.2. For craniotomy patients at very high risk for VTE (eg, those undergoing craniotomy for malignant disease), we suggest adding pharma-cologic prophylaxis to mechanical prophylaxis once adequate hemostasis is established and the risk of bleeding decreases (Grade 2C) .7.0 Patients Undergoing Spinal Surgery7.4.1. For patients undergoing spinal surgery, we suggest mechanical prophylaxis, prefer-ably with IPC, over no prophylaxis (Grade 2C) , u nfractionated heparin (Grade 2C) , o r LMWH (Grade 2C) .suggest mechanical prophylaxis, preferably with IPC, over no prophylaxis (Grade 2C) .3.6.5. For general and abdominal-pelvic sur-gery patients at high risk for VTE ( ف 6.0%; Caprini score, Ն 5) who are not at high risk for major bleeding complications, we recommend pharmacologic prophylaxis with LMWH (Grade 1B) o r L DUH (Grade 1B) o ver no prophylaxis. We suggest that mechanical prophylaxis with elastic stockings or IPC should be added to phar-macologic prophylaxis (Grade 2C) .3.6.6. For high-VTE-risk patients undergoing abdominal or pelvic surgery for cancer who are not otherwise at high risk for major bleeding complications, we recommend extended-duration pharmacologic prophylaxis (4 weeks) with LMWH over limited-duration prophylaxis (Grade 1B) .R emarks: Patients who place a high value on mini-mizing out-of-pocket health-care costs might prefer limited-duration over extended-duration prophylaxis in settings where the cost of extended-duration pro-phylaxis is borne by the patient.3.6.7. For high-VTE-risk general and abdominal-pelvic surgery patients who are at high risk for major bleeding complications or those in whom the consequences of bleeding are thought to be particularly severe, we suggest use of mechan-ical prophylaxis, preferably with IPC, over no prophylaxis until the risk of bleeding diminishes and pharmacologic prophylaxis may be initiated (Grade 2C) .3.6.8. For general and abdominal-pelvic sur-gery patients at high risk for VTE (6%; Caprini score, Ն 5) in whom both L MWH and unfrac-tionated heparin are contraindicated or unavail-able and who are not at high risk for major bleeding complications, we suggest low-dose aspirin (Grade 2C) , f ondaparinux (Grade 2C) , o r mechanical prophylaxis, preferably with IPC (Grade 2C) ,o ver no prophylaxis.3.6.9. For general and abdominal-pelvic sur-gery patients, we suggest that an inferior vena cava (IVC) ﬁ lter should not be used for primary VTE prevention (Grade 2C) .3.6.10. For general and abdominal-pelvic surgery patients, we suggest that periodic surveillance with venous compression ultrasound should not be performed (Grade 2C) .4.0 Patients Undergoing Cardiac Surgery4.4.1. For cardiac surgery patients with an uncomplicated postoperative course, we sug-CHEST / 141 / 2 / FEBRUARY , 2012 SUPPLEMENT 13Sigatran, rivaroxaban, low-dose unfractionatedheparin (LDUH), adjusted-dose VKA, aspirin (all Grade 1B) , or an intermittent pneumatic com-pression device (IPCD) (Grade 1C) .R emarks: We recommend the use of only portable, battery-powered IPCDs capable of recording and reporting proper wear time on a daily basis for inpa-tients and outpatients. Efforts should be made to achieve 18 h of daily compliance. One panel member believed strongly that aspirin alone should not be included as an option.2.1.2. In patients undergoing HFS, we recom-mend use of one of the following rather than no antithrombotic prophylaxis for a minimum of 10 to 14 days: L MWH, fondaparinux, L DUH, adjusted-dose VKA, aspirin (all Grade 1B) , or an IPCD (Grade 1C) .R emarks: We recommend the use of only portable, battery-powered IPCDs capable of recording and reporting proper wear time on a daily basis for inpa-tients and outpatients. Efforts should be made to achieve 18 h of daily compliance. One panel member believed strongly that aspirin alone should not be included as an option.2.2. For patients undergoing major orthopedic surgery (THA, TKA, HFS) and receiving LMWH as thromboprophylaxis, we recommend starting either 12 h or more preoperatively or 12 h or more postoperatively rather than within 4 h or less pre-operatively or 4 h or less postoperatively (Grade 1B) .2.3.1. In patients undergoing THA or TKA, irrespective of the concomitant use of an IPCD or length of treatment, we suggest the use of L MWH in preference to the other agents we have recommended as alternatives: fonda-parinux, apixaban, dabigatran, rivaroxaban, LDUH (all Grade 2B) , adjusted-dose VKA, or aspirin (all Grade 2C) .R emarks: If started preoperatively, we suggest admin-istering LMWH Ն 12 h before surgery. Patients who place a high value on avoiding the inconvenience of daily injections with LMWH and a low value on the limitations of alternative agents are likely to choose an alternative agent. Limitations of alter-native agents include the possibility of increased bleeding (which may occur with fondaparinux, rivar-oxaban, and VKA), possible decreased efﬁ cacy (LDUH, VKA, aspirin, and IPCD alone), and lack of long-term safety data (apixaban, dabigatran, and rivaroxaban). Furthermore, patients who place a high value on avoiding bleeding complications and a low value on7.4.2. For patients undergoing spinal surgery at high risk for VTE (including those with malig-nant disease or those undergoing surgery with a combined anterior-posterior approach), we suggest adding pharmacologic prophylaxis to mechanical prophylaxis once adequate hemo-stasis is established and the risk of bleeding decreases (Grade 2C) . 8.0 Patients With Major Trauma: Traumatic Brain Injury, Acute Spinal Injury, and Traumatic Spine Injury8.4.1. For major trauma patients, we suggest use of LDUH (Grade 2C) , L MWH (Grade 2C) , o r mechanical prophylaxis, preferably with IPC (Grade 2C) ,o ver no prophylaxis.8.4.2. For major trauma patients at high risk for VTE (including those with acute spinal cord injury, traumatic brain injury, and spinal sur-gery for trauma), we suggest adding mechan-ical prophylaxis to pharmacologic prophylaxis (Grade 2C) w hen not contraindicated by lower-extremity injury.8.4.3. For major trauma patients in whom LMWH and LDUH are contraindicated, we sug-gest mechanical prophylaxis, preferably with IPC, over no prophylaxis (Grade 2C) w hen not contraindicated by lower-extremity injury. We suggest adding pharmacologic prophylaxis with either L MWH or L DUH when the risk of bleeding diminishes or the contraindication to heparin resolves (Grade 2C) .8.4.4. For major trauma patients, we suggest that an IVC ﬁ lter should not be used for pri-mary VTE prevention (Grade 2C) .8.4.5. For major trauma patients, we suggest that periodic surveillance with venous compression ultrasound should not be performed (Grade 2C) .P revention of VTE in Orthopedic Surgery PatientsF or further details, see Falck-Ytter et al. 4 2.0 Patients Undergoing Major Orthopedic Surgery: Total Hip Arthroplasty (THA), Total Knee Arthroplasty (TKA), Hip Fracture Surgery (HFS)2.1.1. In patients undergoing THA or TKA, we recommend use of one of the following for a minimum of 10 to 14 days rather than no anti-thrombotic prophylaxis: low-molecular-weight heparin (LMWH), fondaparinux, apixaban, dab-。

美国胸科医师学会：循证临床实践指南——第9版中文执行纲要

21．对主动脉机械瓣膜置换患者，推荐用VKA治疗目标INR, 2.5; （范围, 2.0～3.0)优于更高的IN R目标（1B）。

22．对二尖瓣机械瓣膜置换患者，建议用VKA治疗目标INR, 3.0; （范围, 2.5～3.5)优于较低的IN R目标（2C）。

23．对主动脉瓣和二尖瓣双机械瓣膜置换的患者，建议VKA治疗目标INR 3.0 (范围2.5～3.5)优于目标INR2.5 (范围 2.0～3.0)（2C）。

对主动脉瓣或二尖瓣机械瓣膜置换患者，VKA治疗加抗血小板药。

24．对二尖瓣或主动脉瓣机械瓣置换、出血低危的患者，建议VKA加小剂量抗血小板药如阿司匹林( 50～100 mg/d)治疗（1B）。

25．对主动脉瓣或二尖瓣机械瓣膜置换患者，推荐VKA治疗优于抗血小板药（1B）。

26．对进行了二尖瓣修复、正常窦性心律的患者，建议头3个月用抗血小板药治疗优于VKA治疗（2C ）。

27．对拟行主动脉瓣修复的患者，建议用阿司匹林50 ～100 mg/d（2C）。

28．对右侧人工瓣血栓形成患者，如无禁忌症，建议溶纤治疗（2C）。

29．对左侧人工瓣血栓形成患者，血栓面积≥0.8 cm2，建议早期手术优于溶纤治疗（2C），如果存在手术禁忌症，建议溶纤治疗（2C）。

30．对左侧人工瓣血栓形成患者，血栓面积小（<0.8 cm2），建议溶纤治疗优于手术。

对于极小的、非梗阻性血栓，建议静脉内用普通肝素，并用多谱勒超声心动图监测，证实血栓溶解或改善（2C ）。

缺血性卒中的抗栓或溶栓治疗1．对于急性缺血性卒中、在症状发作3小时内能启动治疗的患者，推荐静脉内（IV）用重组组织型纤溶酶原激活物(r～tPA)治疗（1A）。

2. 对于急性缺血性卒中、在症状发作4.5小时而非3小时内能启动治疗的患者，建议IV用r～tPA（2 C）。

3. 对于急性缺血性卒中、在症状发作4.5小时内不能启动治疗的患者，建议不用IV r～tPA（1B）。

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

美国胸科医师协会抗栓与血栓预防指南培训课件

4.2.2 对于有VTE风险但是出血风险较低的门诊肿瘤患者，我们建议使用预防剂量的低分子量肝素（ LMWH）或低剂量普通肝素（LDUH），优于不预防。（推荐级别：2B 级）
文档仅供参考，不能作为科学依据，请勿模仿；如有不当之处，请联系网站或本人删除。
ACCP9-非手术患者的VET预防
4.4 对于留置中心静脉导管的门诊肿瘤患者，我们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： 2C 级）。
ACCP9-非手术患者的VET预防
文档仅供参考，不能作为科学依据，请勿模仿；如有不当之处，请联系网站或本人删除。
ACCP9-非手术患者的VET预防
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）。
第九版美国胸科医师协会抗栓与血栓预防实践指南汇总
首先针对非手术患者的VET预防，与大家分享ACCP 9 在ACCP 8 基础上新增和改动部分的摘要，供大家学习和参考。
文档仅供参考，不能作为科学依据，请勿模仿；如有不当之处，请联系网站或本人删除。
ACCP9-非手术患者的VET预防
2.3 对于血栓形成风险(Table2)较高的急性住院患者，推荐使用低分子量肝素（LMWH）、低剂量普通肝素（LDUH）（每日2 次或3 次）或璜达肝癸钠这些抗凝药（推荐级别：1B级）进行血栓预防。
6.1.3 对于长途旅行者，我们不建议使用阿司匹林或抗凝剂预防VTE（推荐级别：2C 级）。
文档仅供参考，不能作为科学依据，请勿模仿；如有不当之处，请联系网站或本人删除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）。

ACCP9孕妇应用抗栓药章节翻译

CHEST 附录—抗血栓治疗和血栓预防：ACCP9指南VTE、血栓形成倾向,抗血栓治疗和妊娠美国胸内科医师学会循证临床实践指南(第9版)：抗栓治疗与血栓预防Shannon M . Bates , MDCM ; Ian A. Greer, MD, FCCP ; Saskia Middeldorp , MD , PhD ; David L. Veenstra , PharmD , PhD ; Anne-Marie Prabulos, MD ; and Per Olav Vandvik , MD , PhD背景:妊娠期抗凝治疗的使用是很困难的,因为胎儿和孕妇都存在着潜在的并发症风险。

该指南集中关注于妊娠期VTE、血栓形成倾向和抗血栓药物的管理。

方法：该指南遵循抗血栓治疗和血栓预防发展指南的方法学：抗栓治疗与血栓预防--美国胸内科医师学会循证临床实践指南(第9版)附录。

结果:推荐使用低分子肝素预防和治疗孕妇VTE优于普通肝素(证据级别1B)。

对于急性VTE孕妇，建议产后持续进行抗凝治疗最少6周(至少3个月的治疗时间),优于更短期的治疗(证据级别2C)。

对于满足抗磷脂抗体（APLA）实验室标准和满足临床APLA标准的有三次及三次以上流产史的妇女，建议产前使用中等剂量普通肝素或低分子肝素联合低剂量阿司匹林(75-100 mg/d)进行预防优于无任何治疗（证据级别1B）。

对于有遗传性血栓形成倾向和妊娠期并发症史的妇女，建议不进行抗血栓预防（证据级别2C）。

对于有两次及两次以上流产史但无APLA或血栓形成倾向的妇女，不推荐进行抗血栓预防（证据级别1B）。

结论:指南中大多数推荐都是基于观察性研究和从其他患者群中外推所得出，迫切需要在这个患者群中进行合理设计的研究。

CHEST 2012; 141(2)(Suppl):e691S–e736S缩略语：APLA=抗磷脂抗体；aPPT=活化部分凝血活酶时间；HIT=肝素诱导性血小板减少症；INR=国际标准化比率；LMWH=低分子肝素；NNT=需要治疗的病例数；PE=肺栓塞；RR=危险比；UFH=普通肝素推荐概要文中阴影部分：在整篇指南中，阴影用于指出推荐概要章节中新添加的或从已出版的抗血栓疗法和溶栓治疗--美国胸内科医师学会循证临床实践指南(第8版)中修改的指南推荐。

第9版《抗栓治疗及预防血栓形成指南》（ACCP

第9版《抗栓治疗及预防血栓形成指南》（ACCP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。

聊城市第二人民医院骨病外科刘士明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。

美国胸科医师学会抗栓和溶栓治疗的循证指南——心房颤动的抗栓治

美国胸科医师学会抗栓和溶栓治疗的循证指南——心房颤动的抗栓治心房颤动（ａｔｒｉａｌｆｉｂｒｉｌｌａｔｉｏｎ房颤）是最常见的一种心律失常，它也是脑卒中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。

在所有年龄段中，男性房颤的发病率均明显高于女性。

随着美国人口的老龄化，在未来数十年中房颤病例数可能会显著增多。

一级预防临床试验中和无抗血栓治疗的房颤患者缺血性脑卒中的发病率平均每年４．５％。

与Ｆｒａｍｉｎｇｈａｍ研究中所估计的脑卒中发病率相似。

房颤可使各年龄段脑卒中的危险增加４～５倍。

由于患病率增加，房颤已成为老年人发生脑卒中的一个重要原因。

Ｆｒａｍｉｎｇｈａｍ研究中，房颤导致脑卒中的危险由５０～５９岁时的１．５％增加到８０～８９岁时的２３．５％。

在美国，大约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。

本章的重点是预防非瓣膜性房颤患者发生脑卒中，这些患者的心律失常与风湿性二尖瓣瓣膜病或人工心脏瓣膜无关。

推荐意见要点１．０慢性房颤或心房扑动长期抗栓治疗抗凝和抗血小板药物１．１房颤１．１．１对持续性心房颤动（也称为“持久性”，包括某些分类中的“永久性”的患者）或阵发性（间歇性）心房颤动患者具有脑卒中的高危因素（如具有下列任何一项特征：缺血性脑卒中病史，短暂性脑缺血或系统栓塞的病史，年龄＞７５岁，中度或重度左室收缩期功能受损和／或充血性心力衰竭，高血压病史或糖尿病），建议口服维生素Ｋ拮抗剂（ＶＫＡ）抗凝，如华法林（目标ＩＮＲ为２．５，范围２．０～３．０）。

（１Ａ级）１．１．２持续性房颤或阵发性房颤患者，年龄６５～７５岁没有其他危险因素时，建议抗栓治疗（１Ａ级）。

静脉血栓栓塞性疾病的抗血栓治疗—解读美国胸科医师学会循证医学临床实践指南(+第9+版)

·综述与讲座·静脉血栓栓塞性疾病的抗血栓治疗———解读美国胸科医师学会循证医学临床实践指南（第9版）李圣青(解放军第四军医大学西京医院呼吸与危重症医学科，陕西西安710032)摘要：美国胸科医师学会（ACCP）抗栓治疗和血栓预防临床实践指南第9版的抗血栓治疗篇重点讲述了静脉血栓栓塞性疾病（VTE）的治疗。

与第8版指南相比，第9版指南有很大程度的修改并增添了部分新的内容。

除了抗血栓药物、使用装置或外科手术技术在深静脉血栓形成（DVT）和肺栓塞（PE）（统称为VTE）的使用建议外，还提供了关于血栓后综合征（PTS），慢性血栓栓塞性肺动脉高压（CTPH），偶然诊断的（无症状）DVT或PE，急性上肢深静脉血栓形成（UEDVT），浅静脉血栓形成（SVT），内脏静脉血栓形成和肝静脉血栓形成的治疗建议。

本文对相关部分内容进行了解读。

关键词：静脉血栓栓塞症；急性下肢深静脉血栓；急性肺血栓栓塞；抗凝；溶栓中图分类号：Ｒ543．6文献标志码：A doi：10．3969/j．issn．1671-3826．2013．06．41文章编号：1671-3826（2013）06-0647-04美国胸科医师学会（ACCP）于2012年发布了第9版抗栓治疗和血栓预防临床实践指南［1］，与第8版指南相比有较大程度的修改并增添了部分新的内容，且更为简洁明了。

对待不同的治疗既表现出谨慎而稳妥，又表现出积极和开放。

指南规定高质量的临床证据为A级，中等质量的临床证据为B级，低质量的临床证据为C级。

根据临床证据等级的不同，将推荐等级分为强烈推荐（1级）和建议（2级）。

强烈推荐适用于大多数病人，建议则根据患者的具体情况而定，包括患者的个人选择。

绝大多数推荐和建议都是基于静脉血栓栓塞性疾病（VTE）的复发风险与抗凝或溶栓出血风险二者之间的权衡而得出的结论。

1急性深静脉血栓形成（DVT）的治疗1．1急性DVT抗凝治疗的时机对于高度怀疑VTE患者抗凝时机的把握，第9版指南给出了更加积极的抗凝建议。

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更新血栓预防和治疗指南

ACCP更新血栓预防和治疗指南转载请注明来自丁香园发布日期：2008-11-11 11:01 文章来源：ACCP关键词：ACCP血栓预防和治疗指南点击次数：1044虽然抗凝和溶栓治疗在动脉、静脉以及心脏介入干预后血栓的预防和治疗中得到了长期广泛应用，但是在孕期妇女、儿童及围手术期患者中仍面临着很大的挑战。

2008年7月1日美国胸科医师学会（ACCP）基于大量循证医学证据更新并颁布了血栓预防和治疗指南。

新指南在保留先前指南提出的关于血栓常规预防性治疗建议的同时强调了在儿童、孕期妇女及其他特殊组群患者中的治疗。

其要点如下：●新指南由90位专家组成的国际专家组共同制定。

●该指南包含了700多项综合性建议，其中包括对孕期妇女、儿童及手术期和术后患者血栓的预防、治疗和长期管理。

●该指南保留了先前指南提出的常规应用阿司匹林和其他药物进行血栓预防性治疗的建议。

●华法林和其他维生素K抑制剂(VKA)可使胎儿致畸和流产的发生风险增加，故对妊娠前6个月的患者应禁用。

机械性瓣膜置换术后的孕期妇女因其他抗凝治疗预防卒中和瓣膜血栓疗效欠佳，故可继续应用VKAs。

其他孕期妇女可用低分子肝素（LMWH）或普通肝素钠（UFH）替代VKAs。

●准备受孕的妇女的抗凝治疗有两种选择：一是继续应用VKAs并频繁进行妊娠试验检测，一旦证实怀孕则用LMWH或UFH替代VKAs。

另一种方案是在怀孕前直接用LMWH或UFH替代VKAs。

后一种治疗方案可避免VKAs对胎儿造成不良影响，其不足之处包括LMWH和UFH比VKAs费用高；投药方式为每天一次或两次注射给药；长期应用LMWH或UFH容易导致骨质疏松症。

●儿童卒中在儿童死因中占前10位。

血栓栓塞或血栓形成可引起动脉缺血性卒中(AIS)。

●儿童AIS的鉴别诊断较困难，主要是因为儿童患者同成年人卒中临床表现显著不同，且约15%的儿童AIS患者没有明确的致病危险因素。

●儿童AIS患者一经确诊即应接受抗栓治疗，随后应坚持治疗以预防远期复发。

ACCP美国胸科协会抗栓治疗指南治疗指南

Scottish National Guideline (1995, 2002)
International Consensus Statement (1997) American College of Chest Physicians Consensus (1986, 1989, 1992, 1995, 1998, 2001, 2004)

Pay more attention !
静脉血栓栓塞性疾病
预防和治疗建议
第七届ACCP血栓栓塞预防指南 ——静脉血栓预防
与2001版指南的不同：
74项建议, 18 个表格, 794 篇参考文献
放弃了汇总表格
新增部分: 血管外科通过腹腔镜进行的手术膝关节成形术长途旅行
最新修改的部分: 脑卒中、心肌梗死
VTE: 第3位最常见的血管疾病
“实际上等于卒中的发生率"3 年发生率
单纯DVT 高达 145/100,0001,2
PE 伴有或不伴 DVT
高达 69/100,0003
1. Gillum RF. Am Heart. 1987;114:1262-1264. 2. Anderson et al. Arch Intern Med. 1991;151:933-938. 3. Silverstein et al. Arch Intern Med. 1998;158:585-593.
N=15
血栓预防……
使患者获得最大限度的安全保障
让健康保障更安全: A Critical Analysis of Patient Safety Practices Shojania (2001) /clinic/ptsafety/
使患者获得更显著的临床获益，并降低费用

ACCP9美国胸科医师协会抗栓与血栓预防指南课件

活化凝血酶原时间凝血酶原时间纤维蛋白原测定凝血酶时间 D-D二聚体 FDP
活化部份凝血活酶时间APTT
是反映内源性凝血途径中 VIII、IX、XI、XII因子水平的实验，APTT只反映因子水平，并不反映凝血因子是否活化。
反映内源凝血的筛选实验
白陶土（接触因子激活剂）
部分凝血活酶（脑磷脂）
对于年龄≥50岁且伴有无症状性周围动脉疾病或无症状性颈动脉狭窄的患者，建议使用阿司匹林（75-100mg/ d）治疗用于心血管事件的初级预防，优于不予治疗（2B级）。
对于伴有症状的周围动脉疾病患者（包括已行或将行周围动脉搭桥手术或经皮腔内血管成形术的患者），推荐长期服用阿司匹林（75-100mg/ d）或氯吡格雷（75mg/ d）（ 1A级）
阿司匹林一级预防再受推荐
2023/12/29
Conclusion
对于心血管疾病的初级预防，若患者年龄大于50岁，建议低剂量阿司匹林治疗（75-100mg/d）优于不用阿司匹林（证据 2B）。
2023/12/29
第九版美国胸科医师协会抗栓与血栓预防实践指南汇总
针对房颤抗栓治疗，与大家分ACCP 9 在ACCP 8 基础上新增和改动部分的摘要。
正常血管壁抗血栓形成能力
血管内皮细胞合成
前列环素(PGI2) 扩张血管、抑制plt功能纤溶酶原激活物(PA)
激活纤溶酶、清除小凝块
血栓调节蛋白(TM)
参与蛋白C系统的抗凝作用
肝素或类肝素物质具有多种抗凝活性
二、血小板的作用
血管受损
vWF 血小板黏附
PLT聚集 (Ⅰ)
Fg
PLT释放(5-HT ADP)
2023/12/29
ACCP9-房颤的抗栓治疗

栓与血栓预防实践指南中文解读汇总

第九版美国胸科医师协会抗栓与血栓预防实践指南汇总二十余篇ACCP-9抗栓溶栓指南原文完整版下载地址： /bbs/topic/22270927翻译来自丁香园李慕白的强力之作：/topic/special/20120309/accp2012.htm抗栓热点CHEST ：第9版《美国胸科医师协会抗栓与血栓预防临床实践指南》之房颤的抗栓治疗不同的心房颤动（AF ）患者卒中风险差别很大。

而抗血栓治疗来预防卒中会相应地增加出血的风险。

因此，美国胸科医师协会根据第9版临床实践指南的方法论（Methodologyfor the Development of Antithrombotic Therapy and Prevention of ThrombosisGuidelines ），并基于临床净获益和大量的临床实例为不同卒中风险的房颤患者提供了抗血栓治疗的推荐。

对非风湿性房颤（包括间歇性房颤）的患者：1）低度卒中危险（CHADS2评分=0）（CHADS2评分是指充血性心力衰竭、高血压病、年龄>75岁、糖尿病、卒中或短暂性缺血发作病史，前面4项危险因素各为1分，最后一项为2分），建议无需抗栓治疗；对于选择抗栓治疗的患者，建议单用阿司匹林而不是口服抗凝药或阿司匹林和氯吡格雷联合治疗。

2）中度卒中危险（CHADS2评分=1），推荐口服抗凝药而不是不用药，并建议单用口服抗凝药而不是阿司匹林或阿司匹林和氯吡格雷联合治疗。

3）高度卒中危险（CHADS2评分≥2），推荐口服抗凝药，而不是不用药、单用阿司匹林或阿司匹林和氯吡格雷联合治疗。

上述推荐或建议的口服抗凝药，其建议达比加群150毫克每日2次，而不是剂量调整维生素K 拮抗剂。

因此，对于具有高危卒中风险（CHADS2得分≥2）的房颤患者，口服抗凝药是抗栓治疗的最佳选择。

而对于卒中风险较低的房颤患者，抗栓治疗需要更为个体化。

CHEST ：第9版《ACCP 临床实践指南》之缺血性卒中的抗栓和溶栓治疗指南为卒中和短暂性脑缺血发作（TIA ）患者提供了抗栓治疗推荐，有助于临床医生对卒中患者做出循证治疗决策。

骨科和非骨科手术后抗栓预防-第9版ACCP指南更新简介

中/高危患者
注: LMWH：低分子肝素；IPC：间歇气压疗法
ACCP 9指南的更新进一步提高
LMWH在骨科和非骨科手术后抗栓预防中的地位！！
LMWH优于其他药物：同时满足患者对疗效和安全性需求 LMWH
疗效好，出血风险小，同时满足患者对疗效和安全性的两方面需求
疗效
出血风险
指南推荐LMWH为首选用药已得到大量循证证据的支持！
其他预防药物的限制
其他预防药物的限制
1. 可能增加出血风险
磺达肝癸钠、利伐沙班、VKA
2. 可能疗效降低
ACCP 9指南推荐LMWH为首选预防药物，优于其他预防药物
对行THA或TKA术的患者， ACCP 9同样建议以LMWH为首选血栓预防药物
2B级建议：
LMWH优于以下药物：
磺达肝癸钠达比加群阿哌沙班; 利伐沙班低剂量普通肝素
2C级建议：
LMWH优于以下药物：
调整剂量的维生素K拮抗剂阿司匹林
间歇气压疗法vte危险分新指南推荐的血栓预防药物证据分级非常低05推荐不必进行药物血栓预防1b级或除了离床活动之外的机械性2c级血栓预防低危15建议用机械预防疗法首选ipc优于不进行预防2c级中危3且未合并大出血并发症高危因素的患者建议用lmwh2b级低剂量普通肝素2b级或ipc机械预防疗法2c级优于不进行预防高危6且未合并大出血并发症高危因素的患者推荐用lmwh1b级低剂量普通肝素1b级优于不进行预防对这些患者除了药物预防之外还建议增加机械预防疗法弹力袜或ipc中高危患者且合并大出血并发症高危因素或出血后果被认为特别严重的患者建议应用机械预防疗法首选ipc优于不进行预防直到出血风险消失才可能可以开始药物预防2c级accp9指南的更新进一步提高lmwh在骨科和非骨科手术后抗栓预防中的地位

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2016/10/17
若伴有血栓栓塞低危因素，建议不予桥接抗凝治疗优于桥接抗凝治疗。
对于正在接受阿司匹林治疗且伴有血栓栓塞中危或高危因素的患者，若拟行非心脏手术，建议手术期间继续服用阿司匹林，而不是术前7-10天停用（推荐级别：2C级）。抗凝治疗的桥接
2016/10/17
周围动脉疾病患者抗栓药物的使用
ACCP9-房颤的抗栓治疗
2.1.10 AF患者，包括阵发性AF患者，如果卒中风险高危（CHADS2 ≥ 2分）的话，推荐口服抗凝药（OAC）治疗(1A）。建议OAC治疗，而不是阿司匹林（75-325mg，1/d）或阿司匹林+氯吡格雷。（1B）不耐受或不愿意选择OAC治疗的患者（而不仅仅是考虑出血），建议阿司匹林+氯吡格雷联合治疗，而不是只服用阿司匹林（2B）
APTT的临床意义

APTT延长： Ⅷ、Ⅸ、Ⅺ和Ⅻ因子中某一项或几项因子水Байду номын сангаас缺乏；血友病甲、血友病乙。当凝血酶原、纤维蛋白原及因子V、X缺乏时，但敏感性略差；如肝脏疾病、肝硬化 DIC后期继发纤溶亢进时; 血中抗凝物如凝血因子抑制物或肝素水平增高. 肝素治疗的监护：一般在肝素治疗期间，APTT维持在正常对照的1.5-2.5倍适宜。均需测血小板计数，使其维持在正常范围内，若低于50×109/L需暂时停药。溶栓治疗时，ATPP与PT、TT应将值控制在正常值的2倍。 APTT缩短：见于血液呈高凝状态，DIC早期、血栓前状态、血栓性疾病。
IXa IIa Ca2+ VIII VIIIa Plt------------------ PF3 V
VIIa IIa、IXa VII
XIIa、K
X IIa
Xa Xa Va Ca2+
III Ca2+
PF3（磷脂）凝血酶原(II) 纤维蛋白原(I) 可溶性纤维蛋白
XIII 凝血酶(IIa) XIIIa 稳固性纤维蛋白
参加因子：
VIII、IX、XI、XII
V、X、 II、I
Ca2+、PF3
III、VII

二一九八小板三
加钙聚集形成团
首先激活十因子钙五板三成内源外源莫忘三七钙两步激活凝酶源纤维必当成单体多聚加固靠十三

2016/10/17
临床应用--主要凝血试验
活化凝血酶原时间
凝血酶原时间
纤维蛋白原测定凝血酶时间 D-D二聚体 FDP
ACCP9-房颤的抗栓治疗
2.1.9 AF患者，包括阵发性AF患者，如果卒中风险中度（CHADS2=1分）的话，推荐口服抗凝药（OAC)治疗(1B）。建议OAC治疗，而不是阿司匹林（75325mg，1/d）或阿司匹林+氯吡格雷联合治疗。（2B）不耐受或不愿意选择OAC治疗的患者（而不仅仅是考虑出血），建议阿司匹林+氯吡格雷联合治疗，而不是只服用阿司匹林（2B）。

INR

采用INR监测和调整口服抗凝药物的剂量，使不同来源的临床资料具有可比性 WHO规定不同情况下抗凝治疗时合适的INR范围 1．术前2周或口服抗凝药INR1.5－3(2.25) 2．原发、继发性静脉血栓的预防 INR2.3－3.0(2,5) 3．活动性静脉血栓、反复静脉血栓、肺栓塞预防INR2.0－4.0(3.0) 4．动脉血栓预防INR３－４.5(3.5) 5．INR缩短：表示高凝状态。
西洛他唑，双嘧达莫（2）
CAMP 5’AMP
腺苷酸环化酶（+）
抗凝血酶
GPⅡb/Ⅲa 激活噻氯匹啶、 lloprost GPⅡb/Ⅲa 抑制剂（Abcixmab)(阿昔单抗）血小板聚集血栓形成
低分子肝素（ LMWH)

（Low molecular weight haparins)
抗凝血因子Xa活性，抑制凝血酶的生成抗Xa活性作用强，生物利用度高，半衰期长，出血少不必检测APTT

不适用INR的三种情况包括
INR不适用于测定口服抗凝药初期的病人血浆 INR不适用于肝病凝血因子缺陷病人的血浆 INR不适用于非抗凝治疗而PT延长的病人血浆。

抗血小板药物分类及作用
损伤血小板黏附激活抗凝血酶（PDE）阿司匹林 (1) 磷酸二酯酶
花生四烯酸
噻氯匹啶（3） ATP TXA2 凝血酶胶原肾上腺素 ADP
解读第九版美国胸科医师协会抗栓与血栓预防实践指南
2016/10/17
第九版美国胸科医师协会抗栓与血栓预防实践指南汇总
凝血与抗凝机制的病理生理基础房颤的抗栓治疗 VTE预防(Venous
Thromboembolism- VTE) 周围动脉疾病患者抗栓药物的使用
静脉血栓栓塞性疾病的抗栓治疗

目前公认的凝血因子共14个，按罗马字命名的有12个，以及高分子量激肽原(HMWK) ，激肽释放酶原(PK) 大多数由肝脏产生，其中II 、VII、IX、X合成依赖于 Vitk，称Vitk依赖因子除TF外，都存在于血浆；除FIV（Ca2+）外，均为蛋白质。正常情况下，所有因子都处于无活性状态
常用筛选试验如下：
① 毛细血管抵抗力试验（CRP） ② 出血时间（BT） ③ 血小板计数（PLT） ④ 血块收缩试验(CRT)
三、凝血因子与凝血过程
血液由流动状态变为凝胶状态称血液凝固。是由一系列凝血因子参加的、复杂的酶促反应和分子聚合过程。
凝血因子
Ⅰ 纤维蛋白原
Ⅱ 凝血酶原 Ⅲ 组织因子 Ⅳ 钙离子 Ⅴ 易变因子 Ⅵ 不存在 Ⅶ 稳定因子 Ⅷ 抗血友病因子 Ⅸ Christmas因子 Ⅹ Stuart-Power因子 Ⅺ 血浆凝血活酶前加速素 Ⅻ Hegeman因子 XIII 纤维蛋白稳定因子 PK 激肽释放酶原 HMWK 高分子量激肽原
肝素或类肝素物质
具有多种抗凝活性
二、血小板的作用
血管受损 vWF 血小板黏附 Fg PLT释放(5-HT ADP) PLT聚集 (Ⅰ)
血管收缩
加速 (Ⅱ）聚集
加速Ⅱa 形成
使纤维蛋白网收缩
白色血栓形成
维护血管内皮的完整性

血小板参与血管内皮的再生和修复过程，增强血管壁的抵抗力，减低血管壁的通透性和脆性。
血小板止血功能
①粘附、聚集在血管破损处，形成白色血栓 ②释放活性物质，促进血小板聚集，增强血管收缩
③促进凝血过程
④血块收缩，形成稳固血栓
⑤维持血管壁的完整性，毛细血管的通透性
一期止血缺陷特征
一期止血缺陷指血管壁和血小板的缺陷。 ① 皮肤、粘膜出血为主，内脏出血少见。 ② 创伤后即刻出血，持续时间较长。 ③ 压迫止血有效，止血后不易复发。 ④ 输血或输血制品效果差
阿司匹林一级预防再受推荐
2016/10/17
Conclusion
对于心血管疾病的初级预防，若患者年龄大于50岁，建议低剂量阿司匹林治疗（75-100mg/d）优于不用阿司匹林（证据 2B）。
2016/10/17
第九版美国胸科医师协会抗栓与血栓预防实践指南汇总
针对房颤抗栓治疗，与大家分ACCP 9 在ACCP 8 基础上新增和改动部分的摘要。
凝血酶原时间PT
反映外源性凝血途径中II
、V、VII、X因子水平的实验。
反映外源凝血的筛选实验
组织凝血活酶（含TF） Ca2+ 血浆凝固时间
参考范围
平均值为（12±1）s，超过正常对照值3s 为异常
PT的临床意义
PT延长：先天凝血因子异常 , 如 I 、 II、V、VII、X 因子中某一项或几项因子水平缺乏。可用于外源凝血因子缺陷的筛查。后天凝血因子缺乏，如肝脏疾病、肝硬化（大多数凝血因子由肝脏合成）、维生素K缺乏（可见于阻塞性黄疸）。可用作肝脏蛋白质合成功能的检测手段。 DIC 后期 ( 由于大量消耗和产生的 FDP 拮抗凝血酶的作用使PT延长，因此可用作DIC的检测）、口服抗凝药（可密定、华法林，PT最敏感）、肝素等。 PT缩短：高凝状态：DIC早期，心梗、脑血栓形成，深静脉血栓形成，口服避孕药，PT时间缩短，但并不常见．

维生素K拮抗剂

凝血因子II、VII、IX、X转变为活性型需要 VitK催化,华法林阻碍VitK代谢，使VitK缺乏，显著减少上述四种凝血因子的合成。
2016/10/17
第九版美国胸科医师协会抗栓与血栓预防实践指南汇总
grade分级，1代表强烈推荐，2代表弱推荐，A代表高质量证据，B代表中等质量证据，C代表低质量或极低质量证据
ACCP9-房颤的抗栓治疗
3.1 AF+稳定冠心病CAD患者 3.1 AF+稳定CAD患者（例如，先前没患过急性冠脉综合征ACS），患者选择口服抗凝药OAC，我们推荐剂量调整的VKA单独治疗（目标INR范围 2.0-3.0），而不是联合应用剂量调整的VKA+ASA（2C）
围手术期血栓栓塞的危险因素分层
对于年龄≥50岁且伴有无症状性周围动脉疾病或无症状性颈动脉狭窄的患者，建议使用阿司匹林（75-100mg/ d）治疗用于心血管事件的初级预防，优于不予治疗（2B级）。对于伴有症状的周围动脉疾病患者（包括已行或将行周围动脉搭桥手术或经皮腔内血管成形术的患者），推荐长期服用阿司匹林（75-100mg/ d）或氯吡格雷（75mg/ d）（ 1A级）
肝素诱导的血小板减少症的治疗
凝血与抗凝机制的病理生理基础
正常止血机能
两个方面四个因素
凝血机制抗凝机制血管壁血小板凝血系统抗凝及纤溶系统
一、血管壁的作用
血管受损
神经反射内皮素血管紧张素
血管收缩血液粘稠 PLT黏附聚集