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Atypical atrial flutters are complex supraventricular arrhythmias that share different pathophysiological aspects in common. In most cases, the arrhythmogenic substrate is essentially embodied by slow-conducting areas eliciting re-entrant circuits. Although atrial scarring seems to promote slow conduction, these arrhythmias may occur even in the absence of structural heart disease. To set out the ablation strategy in this setting, three-dimensional mapping systems have proved invaluable over the last decades, helping the cardiac electrophysiologist understand the electrophysiological complexity of these circuits and easily identify critical areas amenable to effective catheter ablation.Nowadays, the pathophysiology mechanism of initiation and maintenance of reentrant arrhythmias, including atrial flutter, is well characterized. However, the anatomic and functional elements of the macro reentrant arrhythmias are not always well defined. In this article, we illustrate the anatomic structures that delineate the typical atrial flutter circuit, both clockwise and counterclockwise, paying attention to the inferior vena cava-tricuspid isthmus (CTI) and crista terminalis crucial role. Finally, we describe the left atrial role during typical atrial flutter, electrophysiologically a by-stander but essential in the phenotypic electrocardiogram (ECG).Atrial flutter (AFL) is a macro-reentrant arrhythmia characterized, in a 12 lead ECG, by the continuous oscillation of the isoelectric line in at least one lead. In the typical form of AFL, the oscillation is most obvious in the inferior leads, due to a macro-reentrant circuit localized in the right atrium, with the cavo-tricuspid isthmus as a critical zone. This circuit can be activated in a counterclockwise or clockwise direction generating in II, III, and aVF leads, respectively, a slow descending/fast ascending F wave pattern (common form of typical AFL) or a balanced ascending/descending waveform (uncommon form of typical AFL). SAR405838 MDMX antagonist Atypical AFLs (scar-related) do not include the CTI in the circuit and show an extremely variable circuit location and ECG morphology.This article reviews the structure of the atrial chambers to consider the anatomic bases for obstacles and barriers in atrial flutter. In particular, the complex myocardial arrangement and composition of the cavotricuspid isthmus could account for a slow zone of conduction. Prominent muscle bundles within the atria and interatrial, and myoarchitecture of the walls, could contribute to preferential conduction pathways. Alterations from tissue damage as part of aging, or from surgical interventions could lead to re-entry.Atrial flutter (AFL) is a regular supraventricular reentrant tachycardia generating a continuous fluttering of the baseline electrocardiography (ECG) at a rate of 250 to 300 beats per minute. AFL is classified based on the involvement of the cavo-tricuspid isthmus in the circuit. The "isthmic" (or type 1) AFL develops entirely in the right atrium; this circuit is commonly activated in a counter-clockwise direction, generating the common sawtooth ECG morphology in the inferior leads (slow descendent-fast ascendent). AFL can be nonisthmus dependent (type 2), often presenting with faster atrial rate and most commonly a left atrial location.Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating disease that presents with fatigue, sleep disturbances, malaise, and cognitive problems. The pathogenesis of ME/CFS is presently unknown, and serum levels of potential biomarkers have been inconsistent. Here, we show that mitochondrial DNA (mtDNA) associated with serum exosomes, is increased in ME/CFS patients only after exercise. Moreover, exosomes isolated from patients with ME/CFS stimulate significant release of IL-1β from cultured human microglia. These results provide evidence that activation of microglia by serum-derived exosomes may serve as a potential novel pathogenetic factor and target for treatment of ME/CFS.The human microbiome has been recognized as increasingly important to health and disease. This is especially prescient in the development of various cancers, their progression, and the microbiome's modulation of various anticancer therapeutics. Mechanisms behind these interactions have been increasingly well described through modulation of the host immune system as well as induction of genetic changes and local inactivation of cancer therapeutics. Here, we review these associations for a variety of gastrointestinal malignancies as well as contemporary strategies proposed to leverage these associations to improve cancer treatment outcomes.Inflammatory bowel diseases (IBD), including Crohn disease and ulcerative colitis, are chronic inflammatory conditions of the gastrointestinal tract. Individuals with IBD are at increased risk for several malignancies originating in the intestine, such as colorectal cancer, small bowel adenocarcinoma, intestinal lymphoma, and anal cancer. There are also several extraintestinal malignancies associated with IBD and IBD therapies, including cholangiocarcinoma, skin cancer, hematologic malignancies, genitourinary cancer, cervical cancer, and prostate cancer. The authors summarize the risk of cancer in patients with IBD, diagnosis and management of colorectal neoplasia in IBD, and management of patients with IBD and active or recent cancer.Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) are the most common type of neuroendocrine tumors and are being increasingly identified in clinical practice. The diagnosis, staging, management, and surveillance of GEP-NETs rely heavily on endoscopy, and consequently, it is important for gastroenterologists to have a solid understanding of these tumors. This article reviews the presentation, diagnosis, and management of both localized and advanced GEP-NETs, with increased emphasis on the role of endoscopy, to enable gastroenterologists and other practitioners to have the necessary tools for the care of patients with these tumors.Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the gastrointestinal (GI) tract. These tumors have been shown to harbor oncogenic mutations of the c-kit tyrosine kinase receptor or platelet-derived growth factor receptor alpha (PDGFRA). Immunohistochemical analysis of GISTs allows for the differentiation of these tumors from other mesenchymal tumors of the GI tract such as leiomyomas and leiomyosarcomas. All GISTs have the potential to behave in a malignant fashion. Tumor location, size, and mitotic index are factors used to predict the risk of malignant behavior. Endoscopy and endoscopic ultrasound play a critical role in the diagnosis of GISTs and can yield important information to further risk-stratify tumors and determine management. This article provides a gastroenterologist's perspective on the diagnosis and management of GISTs.The traditional approach of one-size-fits-all for colorectal cancer has been replaced by personalized interventions to an individual's unique genetic, molecular, and environmental profile, seeking to identify high-risk individuals who would benefit from individualized screening and surveillance. This change in approach is due, in part, to emerging technologies, such as next-generation DNA sequencing.Early detection of colorectal neoplasia significantly reduces mortality from colorectal cancer (CRC), and numerous screening options exist. Guidelines for CRC screening from US and international professional societies provide menus of options based on strength of evidence. Despite availability of screening and its proven impact, 40% of guideline-eligible patients are not screened as recommended in the United States. Adherence to or uptake of CRC screening is especially poor among underserved populations, including those with low income and African American and Hispanic populations. Consideration of screening options must not only take into account test performance, but issues of resources and individual versus population benefits.Individuals at increased risk of developing pancreatic cancer, including those with a significant family history of the disease and those with pancreatic cancer susceptibility gene variants, can benefit from pancreas surveillance. Most pancreatic cancers diagnosed during surveillance are early-stage and such patients can achieve long-term survival. Determining who should undergo pancreas surveillance is still a work-in-progress, but the main tools clinicians use to estimate an individual's risk of pancreatic cancer are patient's age, the extent of their family history of pancreatic cancer, and whether or not they have a pancreatic cancer susceptibility gene mutation.Early detection of high-risk pancreatic cystic lesions enables potentially curative surgical resection, and early detection of lesions without worrisome features may lead to appropriate surveillance. Regrettably, differentiating premalignant and malignant cysts from nonmalignant ones remains challenging. However, emerging additional diagnostic tools, including the needle biopsy with microforceps and needle-based confocal laser endomicroscopy, are of exciting potential along with cyst fluid analysis".Cholangiocarcinoma is a rare malignancy of the biliary tract with a relatively poor prognosis. As a gastroenterologist, our main role is to differentiate between benign and malignant biliary disease, help achieve a diagnosis, and palliate jaundice related to biliary obstruction. This article focuses on summarizing the various tools currently available for endoscopic evaluation and management of cholangiocarcinoma.Gastric adenocarcinoma (GC) is the fourth leading cause of global cancer mortality, and the leading infection-associated cancer. Helicobacter pylori is the dominant risk factor for GC and classified as an IARC class I carcinogen. Surveillance of gastric premalignant conditions is now indicated in high-risk patients. Upper endoscopy is the gold standard for GC diagnosis, and image-enhanced endoscopy increases the detection of gastric premalignant conditions and early gastric cancer (EGC). Clinical staging is crucial for treatment approach, defining early gastric cancer, operable locoregional disease, and advanced GC. Endoscopic submucosal dissection is the treatment of choice for most EGC. Targeted therapies are rapidly evolving, based on biomarkers including MSI/dMMR, HER2, and PD-L1. These advancements in surveillance, diagnostic and therapeutic strategies are expected to improve GC survival rates in the near term.While patients with Barrett's esophagus without dysplasia may benefit from endoscopic surveillance, those with low-grade dysplasia may be managed with either endoscopic surveillance or endoscopic eradication. Patients with Barrett's esophagus with high-grade dysplasia and/or intramucosal adenocarcinoma will generally require endoscopic eradication therapy. The management of Barrett's esophagus with dysplasia and early esophageal adenocarcinoma is predominantly endoscopic, with multiple effective methods available for the resection of raised neoplasia and ablation of flat neoplasia. High-dose proton-pump inhibitor therapy is advised during the treatment of Barrett's esophagus with dysplasia and early esophageal adenocarcinoma. After the endoscopic eradication of Barrett's esophagus and associated neoplasia, surveillance is required for the diagnosis and retreatment of recurrence or progression.