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      Left Atrial Appendage: Physiology, Pathology, and Role as a Therapeutic Target

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          Abstract

          Atrial fibrillation (AF) is the most common clinically relevant cardiac arrhythmia. AF poses patients at increased risk of thromboembolism, in particular ischemic stroke. The CHADS2 and CHA2DS2-VASc scores are useful in the assessment of thromboembolic risk in nonvalvular AF and are utilized in decision-making about treatment with oral anticoagulation (OAC). However, OAC is underutilized due to poor patient compliance and contraindications, especially major bleedings. The Virchow triad synthesizes the pathogenesis of thrombogenesis in AF: endocardial dysfunction, abnormal blood stasis, and altered hemostasis. This is especially prominent in the left atrial appendage (LAA), where the low flow reaches its minimum. The LAA is the remnant of the embryonic left atrium, with a complex and variable morphology predisposing to stasis, especially during AF. In patients with nonvalvular AF, 90% of thrombi are located in the LAA. So, left atrial appendage occlusion could be an interesting and effective procedure in thromboembolism prevention in AF. After exclusion of LAA as an embolic source, the remaining risk of thromboembolism does not longer justify the use of oral anticoagulants. Various surgical and catheter-based methods have been developed to exclude the LAA. This paper reviews the physiological and pathophysiological role of the LAA and catheter-based methods of LAA exclusion.

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          Most cited references66

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          Appendage obliteration to reduce stroke in cardiac surgical patients with atrial fibrillation.

          Left atrial appendage obliteration was historically ineffective for the prevention of postoperative stroke in patients with rheumatic atrial fibrillation who underwent operative mitral valvotomy. It is, however, a routine part of modern "curative" operations for nonrheumatic atrial fibrillation, such as the maze and corridor procedures. To assess the potential of left atrial appendage obliteration to prevent stroke in nonrheumatic atrial fibrillation patients, we reviewed previous reports that identified the etiology of atrial fibrillation and evaluated the presence and location of left atrial thrombus by transesophageal echocardiography, autopsy, or operation. Twenty-three separate studies were reviewed, and 446 of 3,504 (13%) rheumatic atrial fibrillation patients, and 222 of 1,288 (17%) nonrheumatic atrial fibrillation patients had a documented left atrial thrombus. Anticoagulation status was variable and not controlled for. Thrombi were localized to, or were present in the left atrial appendage and extended into the left atrial cavity in 254 of 446 (57%) of patients with rheumatic atrial fibrillation. In contrast, 201 of 222 (91%) of nonrheumatic atrial fibrillation-related left atrial thrombi were isolated to, or originated in the left atrial appendage (p < 0.0001). These data suggest that left atrial appendage obliteration is a strategy of potential value for stroke prophylaxis in nonrheumatic atrial fibrillation.
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            Mechanisms of thrombogenesis in atrial fibrillation: Virchow's triad revisited.

            Atrial fibrillation is the most common sustained cardiac arrhythmia, which is associated with a high risk of stroke and thromboembolism. Increasing evidence suggests that the thrombogenic tendency in atrial fibrillation is related to several underlying pathophysiological mechanisms. Abnormal changes in flow are evident by stasis in the left atrium, and seen as spontaneous echocontrast. Abnormal changes in vessel walls-essentially, anatomical and structural defects-include progressive atrial dilatation, endocardial denudation, and oedematous or fibroelastic infiltration of the extracellular matrix. Additionally, abnormal changes in blood constituents are well described, and include haemostatic and platelet activation, as well as inflammation and growth factor changes. These changes result in the fulfilment of Virchow's triad for thrombogenesis, and accord with a prothrombotic or hypercoagulable state in this arrhythmia. In this Review, we present an overview of the established and purported mechanisms for thrombogenesis in atrial fibrillation.
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              Antithrombotic therapy to prevent stroke in patients with atrial fibrillation: a meta-analysis.

              To characterize the efficacy and safety of anticoagulants and antiplatelet agents for prevention of stroke in patients with atrial fibrillation. Randomized trials identified by using the search strategy developed by the Cochrane Collaboration Stroke Review Group. All published randomized trials testing antithrombotic agents to prevent stroke in patients with atrial fibrillation. Data on interventions, number of participants, duration of exposure and occurrence of all stroke (ischemic and hemorrhagic), major extracranial bleeding, and death were extracted independently by two investigators. Sixteen trials included a total of 9874 participants (mean follow-up, 1.7 years). Adjusted-dose warfarin (six trials, 2900 participants) reduced stroke by 62% (95% CI, 48% to 72%); absolute risk reductions were 2.7% per year for primary prevention and 8.4% per year for secondary prevention. Major extracranial bleeding was increased by warfarin therapy (absolute risk increase, 0.3% per year). Aspirin (six trials, 3119 participants) reduced stroke by 22% (CI, 2% to 38%); absolute risk reductions were 1.5% per year for primary prevention and 2.5% per year for secondary prevention. Adjusted-dose warfarin (five trials, 2837 participants) was more efficacious than aspirin (relative risk reduction, 36% [CI, 14% to 52%]). Other randomized comparisons yielded inconclusive results. Adjusted-dose warfarin and aspirin reduce stroke in patients with atrial fibrillation, and warfarin is substantially more efficacious than aspirin. The benefit of antithrombotic therapy was not offset by the occurrence of major hemorrhage among participants in randomized trials. Judicious use of antithrombotic therapy, tailored according to the inherent risk for stroke, importantly reduces stroke in patients with atrial fibrillation.
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                Author and article information

                Journal
                Biomed Res Int
                Biomed Res Int
                BMRI
                BioMed Research International
                Hindawi Publishing Corporation
                2314-6133
                2314-6141
                2015
                7 July 2015
                : 2015
                : 205013
                Affiliations
                1Non-Invasive Cardiology, Cardio-Thoracic-Vascular Department, San Raffaele Scientific Institute, Via Olgettina 60, 20132 Milano, Italy
                2Arrhythmology and Electrophysiology Unit, Cardio-Thoracic-Vascular Department, San Raffaele Scientific Institute, Via Olgettina 60, 20132 Milano, Italy
                Author notes

                Academic Editor: Kimimasa Tobita

                Article
                10.1155/2015/205013
                4508372
                26236716
                d7dcf028-e50f-47ff-8267-75f20faf417e
                Copyright © 2015 Damiano Regazzoli et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 28 November 2014
                : 22 January 2015
                : 25 January 2015
                Categories
                Review Article

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