Browsing by Subject "Atrial Fibrillation"

Now showing 1 - 4 of 4
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    Importance of Transesophageal Echocardiography for Stroke Prevention in Patients Undergoing Coronary Artery Bypass Graft Surgery - Case Report
    (2022-09-17) Moseman, Anthony; Raniwsky, Alec; Carmony, Megan
    Background: Transesophageal echocardiography (TEE) has become routine during cardiovascular and thoracic anesthesia. It plays a key role in surgical planning and provides vital hemodynamic information intraoperatively. Case Presentation: A 61-year-old female undergoing coronary artery bypass graft surgery, in which an intraoperative TEE was performed. Subsequently, a left atrial appendage thrombus was discovered. The case was postponed allowing for adequate anticoagulation. Successful CABG was performed after outpatient TEE determined the resolution of the left atrial appendage thrombus. Conclusions: The use of TEE intraoperatively stresses the importance of stroke prevention in patients undergoing high-risk surgeries.
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    Neuronally released vasoactive intestinal polypeptide alters atrial electrophysiological properties and may promote atrial fibrillation
    (Elsevier, 2015-06) Xi, Yutao; Chao, Zhi-Yang James; Yan, Wen; Abbasi, Shahrzad; Yin, Xiaomeng; Mathuria, Nilesh; Patel, Mehul; Fan, Christopher; Sun, Junping; Wu, Geru; Wang, Suwei; Elayda, MacArthur; Gao, Lianjun; Wehrens, Xander H. T.; Lin, Shien-Fong; Cheng, Jie; Department of Medicine, IU School of Medicine
    BACKGROUND: Vagal hyperactivity promotes atrial fibrillation (AF), which has been almost exclusively attributed to acetylcholine. Vasoactive intestinal polypeptide (VIP) and acetylcholine are neurotransmitters co-released during vagal stimulation. Exogenous VIP has been shown to promote AF by shortening action potential duration (APD), increasing APD spatial heterogeneity, and causing intra-atrial conduction block. OBJECTIVE: The purpose of this study was to investigate the effects of neuronally released VIP on atrial electrophysiologic properties during vagal stimulation. METHODS: We used a specific VIP antagonist (H9935) to uncover the effects of endogenous VIP released during vagal stimulation in canine hearts. RESULTS: H9935 significantly attenuated (1) the vagally induced shortening of atrial effective refractory period and widening of atrial vulnerability window during stimulation of cervical vagosympathetic trunks (VCNS) and (2) vagal effects on APD during stimulation through fat-pad ganglion plexus (VGPS). Atropine completely abolished these vagal effects during VCNS and VGPS. In contrast, VGPS-induced slowing of local conduction velocity was completely abolished by either VIP antagonist or atropine. In pacing-induced AF during VGPS, maximal dominant frequencies and their spatial gradients were reduced significantly by H9935 and, more pronouncedly, by atropine. Furthermore, VIP release in the atria during vagal stimulation was inhibited by atropine, which may account for the concealment of VIP effects with muscarinic blockade. CONCLUSION: Neuronally released VIP contributes to vagal effects on atrial electrophysiologic properties and affects the pathophysiology of vagally induced AF. Neuronal release of VIP in the atria is inhibited by muscarinic blockade, a novel mechanism by which VIP effects are concealed by atropine during vagal stimulation.
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    Progress toward the prevention and treatment of atrial fibrillation: A summary of the Heart Rhythm Society Research Forum on the Treatment and Prevention of Atrial Fibrillation, Washington, DC, December 9–10, 2013.
    (Elsevier, 2015-01) Van Wagoner, David R.; Piccini, Jonathan P.; Albert, Christine M.; Anderson, Mark E.; Benjamin, Emelia J.; Brundel, Bianca; Califf, Robert M.; Calkins, Hugh; Chen, Peng-Sheng; Chiamvimonvat, Nipavan; Darbar, Dawood; Eckhardt, Lee L.; Ellinor, Patrick T.; Exner, Derek V.; Fogel, Richard I.; Gillis, Anne M.; Healey, Jeff; Hohnloser, Stefan H.; Kamel, Hooman; Lathrop, David A.; Lip, Gregory Y. H.; Mehra, Reena; Narayan, Sanjiv M.; Olgin, Jeffrey; Packer, Douglas; Peters, Nicholas S.; Roden, Dan M.; Ross, Heather M.; Sheldon, Robert; Wehrens, Xander H. T.; Department of Medicine, IU School of Medicine
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    Role of the Autonomic Nervous System in Atrial Fibrillation: Pathophysiology and Therapy
    (Ovid Technologies Wolters Kluwer -American Heart Association, 2014-04-25) Chen, Peng-Sheng; Chen, Lan S.; Fishbein, Michael C.; Lin, Shien-Fong; Nattel, Stanley; Department of Medicine, IU School of Medicine
    Autonomic nervous system activation can induce significant and heterogeneous changes of atrial electrophysiology and induce atrial tachyarrhythmias, including atrial tachycardia (AT) and atrial fibrillation (AF). The importance of the autonomic nervous system in atrial arrhythmogenesis is also supported by circadian variation in the incidence of symptomatic AF in humans. Methods that reduce autonomic innervation or outflow have been shown to reduce the incidence of spontaneous or induced atrial arrhythmias, suggesting that neuromodulation may be helpful in controlling AF. In this review we focus on the relationship between the autonomic nervous system and the pathophysiology of AF, and the potential benefit and limitations of neuromodulation in the management of this arrhythmia. We conclude that autonomic nerve activity plays an important role in the initiation and maintenance of AF, and modulating autonomic nerve function may contribute to AF control. Potential therapeutic applications include ganglionated plexus ablation, renal sympathetic denervation, cervical vagal nerve stimulation, baroreflex stimulation, cutaneous stimulation, novel drug approaches and biological therapies. While the role of the autonomic nervous system has long been recognized, new science and new technologies promise exciting prospects for the future.