Notes

Enzymatic combination regarding fluorinated materials.
Risk stratification models exist, which derive from findings on clinical exam and neuroimaging, but care should be taken to avoid a self-fulfilling prophecy of poor outcome from limiting treatment due to a presumed poor prognosis. Cerebral venous thrombosis is an additional subtype of hemorrhagic stroke that has a unique set of causes, natural history, and treatment and is discussed as well.Endovascular therapy (EVT) has become the standard treatment for large-vessel occlusion (LVO) acute ischemic stroke (AIS). EVT is now indicated in patients up to 24h from their last known well, provided that the patient meets specific clinical and imaging criteria. Improvements in thrombectomy devices, techniques, and operator experience have allowed successful EVT of ICA terminus, M1-MCA occlusions as well as proximal M2-MCA, basilar artery occlusions, and revascularization of tandem lesions. Mechanical thrombectomy failures still occur due to several factors, however, highlighting the need for further device and technical improvements. An ongoing debate exists regarding the need for pre-EVT thrombolytic agents, thrombectomy techniques, distal occlusions, anesthesia methods, the role of advanced neuroimaging, the treatment of patients with larger infarct core, and those presenting with milder stroke symptoms. Many of these questions are the subject of current or upcoming clinical trials. This review aims to provide an outline and discussion about the established recommendations and emerging topics regarding EVT for LVO AIS.Dural arteriovenous fistulae (dAVFs) are diverse, complex lesions that share the common feature of arteriovenous shunting without an intervening nidus. In this chapter, the ensuing discussion is organized by dAVF location, followed by further consideration of less common, distinct types of dAVFs-carotid cavernous fistulae, pial arteriovenous fistulae, and vein of Galen malformations. For each lesion type, epidemiology, clinical presentation, imaging findings, classification considerations, and treatment options are discussed.Brain arteriovenous malformations are an important cause of intracerebral hemorrhage in the young. Ruptured AVM's are often treated, as the risk of rebleeding is high. The treatment of incidentally discovered, unruptured AVMs is controversial as the morbidity and mortality of treatment may exceed that of the AVM's natural history. Management is multimodal and includes observation with follow up, as well as microsurgical resection, endovascular embolization, and stereotactic radiosurgery. Multidisciplinary teams are important in evaluating patients for treatment. The goal of treatment is complete AVM obliteration while preserving neurologic function.The worldwide incidence of spontaneous subarachnoid hemorrhage is about 6.1 per 100,000 cases per year (Etminan et al., 2019). Eighty-five percent of cases are due to intracranial aneurysms. The mean age of those affected is 55 years, and two-thirds of the patients are female. The prognosis is related mainly to the neurologic condition after the subarachnoid hemorrhage and the age of the patient. Overall, 15% of patients die before reaching the hospital, another 20% die within 30 days, and overall 75% are dead or remain disabled. Case fatality has declined by 17% over the last 3 decades. Despite the improvement in outcome probably due to improved diagnosis, early aneurysm repair, administration of nimodipine, and advanced intensive care support, the outcome is not very good. Even among survivors, 75% have permanent cognitive deficits, mood disorders, fatigue, inability to return to work, and executive dysfunction and are often unable to return to their premorbid level of functioning. The key diagnostic test is computed tomography, and the treatments that are most strongly supported by scientific evidence are to undertake aneurysm repair in a timely fashion by endovascular coiling rather than neurosurgical clipping when feasible and to administer enteral nimodipine. The most common complications are aneurysm rebleeding, hydrocephalus, delayed cerebral ischemia, and medical complications (fever, anemia, and hyperglycemia). Management also probably is optimized by neurologic intensive care units and multidisciplinary teams.Unruptured intracranial aneurysms (UIAs) have a prevalence of 3% in the adult population worldwide. The majority of UIAs are incidental findings, but some UIAs cause cranial nerve palsies, brainstem compression, ischemic events, or epileptic seizures. The most frequent clinical presentation of intracranial aneurysms is, however, rupture and thereby subarachnoid hemorrhage (SAH). To avoid SAH with its fatal consequences, patients with UIAs require counseling by dedicated and interdisciplinary neurovascular specialists. For the purpose of assessment and decision-making for the management of patients with UIAs, numerous aspects have to be considered radiological characteristics, clinical symptoms, estimated rupture risk of an individual aneurysm as well as patient- and aneurysm-related risks of preventive repair. Generally, two management options exist observation with follow-up imaging or preventive repair. This chapter discusses current data on pathogenesis, clinical presentation, diagnostics, risk factors for rupture and preventive repair, and guidance tools for the management of patients with UIAs according to current evidence.As a refresher course on current techniques and practice of cerebral angiography, this chapter outlines the steps in effective angiography, incorporating modern quality and safety considerations. The format is step-by-step from preprocedure to intraprocedure to postprocedure for ease of reference. The chapter will serve as a framework for the fledgling angiographer, augmenting the important teaching provided by a seasoned angiographer.An understanding of neurovascular anatomy is essential to endovascular diagnosis and therapy. This chapter provides an overview of the arterial anatomy from the aortic arch to the vertex.The development of technology to treat unmet clinical patient needs in the United States has been an important focus for the U.S. Food and Drug Administration and the 2016 Congressional 21st Century Cures Act. In response, a program of early feasibility studies (EFS) has been developed. One of the important issues has been the outmigration of the development and testing of medical devices from the United States. The EFS committee has developed and implemented processes to address issues to develop strategies for early treatment of these patient groups. Initial implementation of the U.S. Food and Drug Administration EFS program has been successful, but residual significant problems have hindered the opportunity to take full advantage of the program. These include delays in gaining Institutional Review Board approval, timeliness of budget and contractual negotiations, and lack of access to and enrollment of study subjects. This paper reviews improvements that have been made to the U.S. EFS ecosystem and outlines potential approaches to address remaining impediments to program success.Over 1.5 million deaths worldwide are caused by neurocardiogenic syndromes. SGI-1027 inhibitor Furthermore, the consequences of deleterious brain-heart interactions are not limited to fatal complications. Cardiac arrhythmias, heart failure, and nonfatal coronary syndromes are also common. The brain-heart axis is implicated in post-stroke cardiovascular complications known as the stroke-heart syndrome, sudden cardiac death, and Takotsubo syndrome, among other neurocardiogenic syndromes. Multiple pathophysiological mechanisms with the potential to be targeted with novel therapies have been identified in the last decade. In the present state-of-the-art review, we describe recent advances in the understanding of anatomical and functional aspects of the brain-heart axis, cardiovascular complications after stroke, and a comprehensive pathophysiological model of stroke-induced cardiac injury.
Pulmonary vascular disease, pulmonary endothelial dysfunction, liver fibrosis, renal disease, and exercise intolerance are common in adults with Fontan physiology. Although the pathophysiologic mechanisms linking these phenomena have been studied, certain aspects are not well understood.

This study hypothesized that impaired pulmonary vascular reserve (VR) plays a central role linking these abnormalities, and that patients with abnormal pulmonary VR with exercise, compared with patients with normal VR, would display poorer pulmonary endothelial function, greater liver stiffness, more renal dysfunction, and poorer exercise capacity.

Symptomatic adults with the Fontan palliation (n=29) underwent invasive cardiopulmonary exercise testing, echocardiography, and assessment of microvascular function. Abnormal pulmonary VR was defined by the slope of increase in pulmonary pressure relative to cardiac output with exercise >3mmHg/l/min. Pulmonary endothelial function was assessed using reactive hyperemia inder filtration rate (r =-0.52 vs. r =-0.24; Meng test p=0.03), N-terminal pro-B-type natriuretic peptide (r=0.56 vs. r=0.17; Meng test p=0.02), and peak Vo
(r =-0.63 vs. r =-0.26; Meng test p=0.02).

Pulmonary vascular limitations in Fontan physiology are related to pulmonary endothelial and end-organ dysfunction, suggesting a mechanistic link between these commonly observed findings, and these abnormalities are more apparent during exercise testing, with little relationship at rest.
Pulmonary vascular limitations in Fontan physiology are related to pulmonary endothelial and end-organ dysfunction, suggesting a mechanistic link between these commonly observed findings, and these abnormalities are more apparent during exercise testing, with little relationship at rest.
Inhibition of the sodium-glucose cotransporter-2 (SGLT2i) improves outcomes in patients with heart failure (HF) and reduced ejection fraction (HFrEF), but the mechanism by which they improve outcomes remains unclear.

This study aimed to investigate the effects of sodium-glucose cotransporter-2 inhibitor empagliflozin on central hemodynamics in patients with HF and HFrEF.

This investigator-initiated, double-blinded, placebo-controlled, randomized trial enrolled 70 patients with HFrEF from March 6, 2018, to September 10, 2019. Patients were assigned to empagliflozin of 10mg or matching placebo once daily on guideline-driven HF therapy for 12weeks. The primary outcome was ratio of pulmonary capillary wedge pressure (PCWP) to cardiac index (CI) at peak exercise after 12weeks. Patients underwent right-heart catheterization at rest and during exercise at baseline and 12-week follow-up.

Patients with HFrEF, mean age of 57 years, mean left-ventricular ejection fraction, 26%, and 12 (17%) with type 2 diabetes mellitus were randomized. There was no significant treatment effect on peak PCWP/CI (-0.13mmHg/l/min/m
; 95% confidence interval-1.60 to 1.34mmHg/l/min/m
; p=0.86). Considering hemodynamics over the full range of exercise loads, PCWP was significantly reduced (-2.40mmHg; 95% confidence interval-3.96 to-0.84mmHg; p=0.003), but not CI (-0.09 l/min/m
; 95% confidence interval-0.14 to 0.32 l/min/m
; p=0.448) by empagliflozin. This was consistent among patients with and without type 2 diabetes.

Among patients with stable HFrEF, empagliflozin for 12weeks reduced PCWP compared with placebo. There was no significant improvement in neither CI nor PCWP/CI at rest or exercise.
Among patients with stable HFrEF, empagliflozin for 12 weeks reduced PCWP compared with placebo. There was no significant improvement in neither CI nor PCWP/CI at rest or exercise.
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