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      The left atrial appendage: from embryology to prevention of thromboembolism

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

          J Blackshear, J. A. Odell (1996)
          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.

            Timothy Watson, Eduard Shantsila, Gregory Lip (2009)
            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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              Percutaneous left atrial appendage closure vs warfarin for atrial fibrillation: a randomized clinical trial.

              Vivek Reddy, Horst Sievert, Jonathan S. Halperin … (2014)
              While effective in preventing stroke in patients with atrial fibrillation (AF), warfarin is limited by a narrow therapeutic profile, a need for lifelong coagulation monitoring, and multiple drug and diet interactions.
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                Author and article information

                Journal
                Title: European Heart Journal
                Abbreviated Title: Eur Heart J
                Publisher: Oxford University Press (OUP)
                ISSN (Print): 0195-668X
                ISSN (Electronic): 1522-9645
                Publication date (Print): April 2016
                Volume:
                Issue:
                Page: ehw159
                Article
                DOI: 10.1093/eurheartj/ehw159
                PubMed ID: 27122600
                SO-VID: 8c074e02-d894-44d6-8200-93c1810e8fff
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