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Multiple randomized clinical trials are currently underway to determine the best timing for administration of anticoagulants following acute ischemic stroke.The pace of understanding cognitive decline and dementia has rapidly accelerated over the past decade, with constantly evolving insights into the vascular contributions to cognitive impairment and dementia (VCID). Notably, more overlap has been discovered in the pathophysiology between what was previously understood to be Alzheimer’s disease and VCID, leading to a heightened emphasis on disease prevention through early and aggressive control of vascular risk factors. One particularly vulnerable population may be those with cardiac disease, as they are at risk for cerebrovascular disease, which itself can lead to dementia, and increasing evidence supports cognitive impairment in disease processes such as heart failure and atrial fibrillation, independent of ischemic stroke, suggesting other potential mechanisms. In this article, we review the evidence supporting the relationship between cardiac disease, cerebrovascular disease, and cognitive decline and discuss the ongoing and future research efforts aimed at defining the important relationship between these entities.Prevention of ischemic stroke relies on the use of antithrombotic medications comprising antiplatelet agents and anticoagulation. Stroke risk is particularly high in patients with cardiovascular disease. This review will focus on the role of antithrombotic therapies in the context of different types of cardiovascular disease. We will discuss oral antiplatelet medications and both IV and parental anticoagulants. Different kinds of cardiovascular disease contribute to stroke via distinct pathophysiological mechanisms, and the optimal treatment for each varies accordingly. We will explore the mechanism of stroke and evidence for antithrombotic therapy in the following conditions atrial fibrillation, prosthetic heart values (mechanical and bioprosthetic), aortic arch atherosclerosis, congestive heart failure (CHF), endocarditis (infective and nonbacterial thrombotic endocarditis), patent foramen ovale (PFO), left ventricular assist devices (LVAD), and extracorporeal membrane oxygenation (ECMO). While robust data exist for antithrombotic use in conditions such as atrial fibrillation, optimal treatment in many situations remains under active investigation.The use of left ventricular assist devices (LVADs) has been increasing in the last decade, along with the number of patients with advanced heart failure refractory to medical therapy. Ischemic stroke and intracranial hemorrhage remain the leading causes of morbidity and mortality in LVAD patients. Despite the common occurrence and the significant outcome impact, underlying mechanisms and management strategies of stroke in LVAD patients are controversial. In this article, we review our current knowledge on pathophysiology and risk factors of LVAD-associated stroke, outline the diagnostic approach, and discuss treatment strategies.Extracorporeal membrane oxygenation (ECMO) represents an established technique to provide temporary cardiac and/or pulmonary support. ECMO, in veno-venous, veno-arterial or in extracorporeal carbon dioxide removal modality, is associated with a high rate of brain injuries. These complications have been reported in 7 to 15% of adults and 20% of neonates, and are associated with poor survival. Thromboembolic events, loss of cerebral autoregulation, alteration of the blood-brain barrier, and hemorrhage related to anticoagulation represent the main causes of severe brain injury during ECMO. The most frequent forms of acute neurological injuries in ECMO patients are intracranial hemorrhage (2-21%), ischemic stroke (2-10%), seizures (2-6%), and hypoxic-ischemic brain injury; brain death may also occur in this population. Other frequent complications are infarction (1-8%) and cerebral edema (2-10%), as well as neuropsychological and psychiatric sequelae, including posttraumatic stress disorder.Delirium is a common occurrence in cardiac and cardiovascular surgical intensive care units. Due to multiple confounding factors, this diagnosis remains challenging for medical professionals. Multiple theories exist regarding the pathophysiology of delirium, which include disruption of neurotransmitters as well as inflammation. Delirium has been associated with prolonged hospitalizations and an increase in mortality. Although there are widely used screening tools for delirium, none have been validated in this particular patient population. SP-13786 inhibitor Limited treatments exist for delirium, so both pharmacologic and nonpharmacologic preventative measures should be employed in this patient population.Acute ischemic stroke (AIS) and acute myocardial infarction (AMI) may co-occur simultaneously or in close temporal succession, with occurrence of one ischemic vascular event increasing a patient’s risk for the other. Both employ time-sensitive treatments, and both benefit from expert consultation. Patients are at increased risk of stroke for up to 3 months following AMI, and aggressive treatment of AMI, including use of reperfusion therapy, decreases the risk of AIS. For patients presenting with AIS in the setting of a recent MI, treatment with alteplase, an intravenous tissue plasminogen activator, can be given, provided anterior wall myocardial involvement has been carefully evaluated. It is important for clinicians to recognize that troponin elevations can occur in the setting of AIS as well as other clinical scenarios and that this may have implications for short- and long-term mortality.A series of cases with rare thromboembolic incidents including cerebral sinus vein thrombosis (some of them fatal) and concomitant thrombocytopenia occurring shortly after vaccination with the coronavirus disease 2019 (COVID-19) vaccine AZD1222 (Vaxzevria) have caused significant concern and led to its temporary suspension in many countries. Immediate laboratory efforts in four of these patients have identified a tentative pathomechanism underlying this syndrome termed initially vaccine-induced prothrombotic immune thrombocytopenia (VIPIT) and renamed recently vaccine-induced immune thrombotic thrombocytopenia (VITT). It encompasses the presence of platelet-activating antibodies to platelet factor-4/heparin complexes, possibly emulated by polyanionic constituents of AZD1222, and thus resembles heparin-induced thrombocytopenia (HIT). Because these immune complexes bind and activate platelets via Fcγ receptor IIA (FcγRIIA), high-dose intravenous immunoglobulin G has been suggested for treatment of VITT in addition to non-heparin anticoagulants.