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Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physician Evidence-Based Clinical Practice Guidelines Online Only ArticlesAntithrombotic and Thrombolytic Therapy for Valvular Disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines
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Summary of Recommendations
Note on Shaded Text: Throughout this guideline, shading is used within the summary of recommendations sections to indicate recommendations that are newly added or have been changed since the publication 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
Methods
The development of the current recommendations followed the general approach of Methodology for the Development 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.3 In brief, literature searches to update the existing database from the AT8 guidelines were performed (January 1, 2005 to October 2009). The literature was rated according to
Rheumatic Mitral Valve Disease
Rheumatic mitral valve disease carries the greatest risk of systemic thromboembolism of any common form of acquired valvular disease. Wood5 cited a prevalence of systemic emboli of 9% to 14% in several large early series of patients with mitral stenosis. In 1961, Ellis and Harken6 reported that 27% of 1,500 patients undergoing surgical mitral valvotomy had a history of clinically detectable systemic emboli. Among 754 patients followed up for 5,833 patient-years, Szekely7 observed an incidence
Mitral Valve Prolapse and Mitral Valve Strands
Mitral valve prolapse (MVP) is a common congenital form of valve disease. Although early evidence from case series and control studies suggested an association with stroke,34, 35, 36, 37, 38, 39, 40 Gilon et al41 and the Framingham Heart Study42 failed to replicate the results. More recently, Avierinos et al43 found that people 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
Mitral Annular Calcification
Mitral annular calcification (MAC), like MVP, may be a source of cardioembolic stroke. The best estimate of the embolic potential of MAC comes from the Framingham Heart Study.46 Among 1,159 individuals with no history of stroke at the index echocardiographic examination, the risk of stroke in those with MAC was 2.1 times greater than those without MAC (5.1% without MAC vs 13.8% with MAC, P = .006), independent of traditional risk factors for stroke. There was a continuous relationship between
Calcified Aortic Valve
Clinically significant systemic emboli in isolated aortic valve disease are uncommon. A lack of association between aortic valve calcification and clinical emboli has been supported by several studies.49, 50, 51 Thus, in the absence of other indications, antithrombotic therapy does not have a role in calcified aortic valve disease.
Atherosclerotic Plaque of the Proximal Aorta
The presence of aortic plaque is associated with stroke risk.52, 53 In a TEE substudy of the Stroke Prevention in Atrial Fibrillation (SPAF) trial, the risk of stroke at 1 year in patients with AF with complex aortic plaque was 12% to 20% vs 1.2% if no plaque was observed.54 Cohen et al55 demonstrated that aortic plaques > 4 mm in thickness increased the risk of vascular events, and this risk was further increased by lack of plaque calcification (RR = 10.3; 95% CI, 4.2-25.2). There are no
Native Valve Endocarditis: Role of Anticoagulants and Antiplatelet Agents
Native valve infective endocarditis (IE) is a serious infectious entity, the morbidity of which is primarily related to the consequences of systemic embolism from valve vegetations. The risk of embolization is proportional to the size of the vegetation and the type of organism (eg, Staphylococcus aureus increases risk).67, 68 The majority of clinically apparent emboli from left-sided lesions involve the CNS resulting in catastrophic stroke. The incidence of pulmonary emboli in right-sided
Early Postoperative Bridging to Intermediate/Long-term Therapy (Postoperative Day 0 to 5)
There are no studies examining early bridging therapy such as UFH or LMWH prior to antiplatelet therapy or VKA initiation in the bioprosthetic valve population. Therefore, we are currently unable to make recommendations on this topic.
Antithrombotic Therapy in the First 3 Months After Surgery
The first 3 months after valve implantation are a high-risk period for thromboembolic events, particularly in the mitral valve population.93, 94 Because the risk of a thromboembolic event varies by valve location, we have generated separate evidence profiles by
Early Postoperative Bridging to Intermediate/Long-term Therapy (Postoperative Day 0 to 5)
The options for antithrombotic therapy immediately after mechanical heart valve replacement include oral VKA therapy with or without initial bridging using UFH or LMWH. We identified no randomized trials comparing these strategies.
Antithrombotic Therapy After Mitral Valve Repair
Mitral valve repair commonly involves the removal of redundant or pathologic leaflet tissue, the placement of a synthetic ring or band to decrease annular size, and perhaps the resuspension of leaflets with new or transposed chordate. We have identified no randomized trial evaluating the use of antithrombotic therapy after mitral valve repair. Aramendi et al106 published a prospective cohort study examining the outcomes of 235 mitral repair or replacement patients. The data suggest superiority
Prosthetic Valve Thrombosis
Prosthetic valve obstruction may be the result of thrombosis, pannus ingrowth, or both.130 Clinical history and echocardiographic study are used to determine the cause. This is important, since thrombolysis will not be effective in pannus ingrowth.
Prosthetic valve thrombosis has an incidence ranging from 0.1% to 5.7% per patient-year. Although rare, this complication is potentially lethal. Treatment of this pathology consists of surgery, thrombolytic therapy, or anticoagulation. The choice of
Acknowledgments
Author Contributions: As Topic Editor, Dr Whitlock oversaw the development of this article, including the data analysis and subsequent development of the recommendations contained herein.
Dr Whitlock: contributed as the Topic Editor.
Dr Sun: contributed as a panelist.
Dr Fremes: contributed as a panelist.
Dr Rubens: contributed as a panelist.
Dr Teoh: contributed as a panelist.
Financial/nonfinancial disclosures: The authors of this guideline provided detailed conflict of interest information related
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Funding/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; Pfizer, Inc; Canyon Pharmaceuticals; and sanofi-aventis US.
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