Post procedural heparin use should be reserved

Post-procedural heparin use should be reserved for patients with the highest thromboembolic risk (e.g., patients with mitral or multiple mechanical amphetamine sulfate valves or prior stroke) (Schulman et al., 2015). Given the rapid onset and offset of action of NOACs, no bridging therapy is required for the majority of interventions, although this is dependent upon balancing the risks of stroke/thromboembolism vs. bleeding in individual cases and the HAS-BLED score can to assist the decision. Following surgery, NOACs can be restarted as soon as effective haemostasis has been achieved, and the anticoagulant effect will be evident within a few hours after the first dose (Camm et al., 2012b).
Left Atrial Appendage Occlusion The left atrial appendage (LAA) is considered the main (but not the only) site of thrombi formation in the heart in AF. Minimally invasive epicardial and interventional trans-septal techniques have been developed for occlusion of the LAA orifice to reduce the stroke risk (Camm et al., 2012b). The two trials assessed the LAA occlusion devices (PROTECT-AF, PREVAIL) and showed that the devices were non-inferior to warfarin for ischemic stroke prevention or systemic embolism during 7days post-procedure, although non-inferiority was not achieved for overall efficacy (Table 6) (Holmes et al., 2009; Holmes et al., 2014). Current consensus is that LAA occlusion may be considered in patients with a high stroke risk and contraindications for long-term OAC (Atrial fibrillation: management Guidance and guidelines NICE, 2015).
Thrombolysis in AF Patients Receiving Oral Anticoagulation Patients with AF who experience acute ischaemic stroke should be considered for urgent thrombolytic therapy to restore perfusion and function of the ischemic brain. However, effective anticoagulation present at the time of reperfusion is a contraindication for thrombolysis because of the possibility of increased risk of symptomatic haemorrhage (De Keyser et al., 2007). Therefore, current guidelines recommend against using the intravenous recombinant tissue-type plasminogen activator alteplase in patients with acute ischemic stroke who have an international normalised ratio (INR)>1.7 (Xian et al., 2012). The possible risk of thrombolysis in patients given NOACs remains unclear. Point-of-care coagulation tests are urgently warranted for management of acute stroke, especially in patients pre-treated with NOAC and who are eligible for intravenous thrombolysis. A patient taking one of the NOACs who experiences an acute ischemic stroke should not be considered a candidate for thrombolysis unless his/her clinical history and the results of laboratory tests reliably indicate the absence of an anticoagulant effect, or until at least two half-lives have elapsed since the most recent dose in patients with normal renal function and coagulation tests are normal (Diener et al., 2013). In a patient taking dabigatran, a quick and simple test could be an activated partial thromboplastin test (aPTT), and for rivaroxaban, a calibrated dilute prothrombin time (Heidbuchel et al., 2015).
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Introduction The human gastrointestinal (GI) tract has coevolved with billions of commensal microorganisms that are considered by many immunologists to be an “extended self” (Reynolds et al., 2015). This symbiotic relationship between microorganisms and the host requires efficient barrier and tolerance mechanisms that preserve intestinal immune balance and tissue integrity. HIV infection leads to disruption of both immune balance and epithelial barrier integrity, contributing to residual immune activation (Younas et al., 2015). Such immune activation persists despite ART and is associated with an increased risk of non-AIDS morbidities, such as cardiovascular diseases and neurocognitive disorders. This persistent immune activation is thought to originate from latently infected cells contributing to residual HIV expression, and gut barrier damage. Cumulative evidence indicates that multiple events occur within the GI tract of pathogenically Simian Immunodeficiency Virus (SIV)-infected Asian macaques and HIV-infected individuals (Estes et al., 2010; Brenchley, 2013). These events cause increased intestinal permeability, resulting in the translocation of bacterial products of the GI microflora through the epithelial barrier and into the systemic circulation. This microbial translocation is considered to be a major driver of chronic immune activation and disease progression, even in patients receiving ART (Brenchley et al., 2006; Vyboh et al., 2015).