Active clinical trials for "Ischemia"

Antiphospholipid syndrome (APS) has a close association with ischemic stroke; however, the optimal treatment strategy for APS-related stroke has yet to be established. The clinical guidelines suggest using warfarin for APS-related stroke, but these suggestions are largely based on retrospective studies from the 1990s and expert opinion, rather than high-quality clinical trials. Moreover, the evidence on the role of antiplatelet drugs other than aspirin (e.g., clopidogrel) in APS-related stroke is particularly limited. Considering the relatively young age of patients with APS and the high clinical burden of using warfarin, it is necessary to verify whether warfarin is essential. Thus, the investigators aim to compare clopidogrel-based antiplatelet therapy and warfarin as a secondary preventive medication for patients with APS-related stroke. APS-STROKE is an exploratory, multicenter, prospective, randomized, open, blinded-endpoint clinical trial. Adult patients with definite APS who have a history of ischemic stroke will be included. Patients with high-risk APS (triple positivity or persistently high titers of anti-cardiolipin or anti-β2-glycoprotein I antibodies), systemic lupus erythematous, or indications for continued antiplatelet or anticoagulant therapy will be excluded. Eligible patients will be 1:1 randomized to receive clopidogrel-based antiplatelet therapy or warfarin. Patients assigned to the clopidogrel-based antiplatelet therapy group will be permitted to use additional antiplatelet drugs other than clopidogrel at the investigator's discretion. The primary outcome is a composite of any death, major adverse cardiovascular events, systemic thromboembolic events, and major bleeding during a follow-up period of at least 2 years. This study would provide valuable information for determining the optimal secondary prevention strategy for APS-related stroke.

Acute compartment syndrome (ACS) is a surgical emergency that can develop in patients on extracorporeal membrane oxygenation (ECMO). ACS is a type of limb ischemia, which means that the limb, such as the arm or leg, loses blood flow. Patients on ECMO can develop this condition for many reasons, but most commonly from the ECMO procedure itself. This most commonly involves the leg. Key symptoms of ACS include severe pain, loss of pulses, loss of feeling, and inability to move the limb. However, because patients on ECMO are often sedated, ACS is difficult to diagnose as patients can not report symptoms. As a result, the only available tool for diagnosing ACS may be measurement of pressures in the limb. This is normally done with a needle-device, which is inserted into the leg for a single measurement. However, a recently developed device, called the MY01 Continuous Compartment Pressure Monitor, allows for continuous pressure readings instead of a single measurement. Multiple measurements may allow for much greater accuracy in diagnosing ACS, which may result in faster time to surgery and potentially save more limbs than single measurements. This device may also be less invasive than an older method of continuous pressure measuring, which uses a needle and tubing that is 14-gauge in size. Therefore, this study aims to compare 3 different types of methods for diagnosing ACS in patients on ECMO, which are 1) Standard of Care, 2) Standard of Care and MY01, and 3)Standard of Care and 14-gauge slit catheter.

Single-institution, prospective nonrandomized pilot study of critical limb ischemia patients with planned lower extremity revascularization will undergo Flowmet-D measurements in a wound care center setting to determine threshold values associated with wound healing and amputation. A subset of patients will undergo hyperbaric oxygen therapy and will have Flowmet-D measurements to determine those who respond best to therapy.

To compare the outcome of bypass surgery and plaque excision for treatment of critical limb ischemia in the lower limbs

Ischemic preconditioning is defined as the development of tolerance to ischemia-reperfusion injury by a previous short bout of ischemia resulting in a marked reduction in infarct size. This mechanism can be mimicked by several pharmacological substances such as acetylcholine and adenosine. To detect ischemia-reperfusion injury in humans in vivo Kharbanda et al. developed a method in which endothelial dysfunction represents the effects of ischemic preconditioning. This method, however, uses acetylcholine to measure endothelial function before and after forearm ischemia. We, the investigators at Radboud University, hypothesize that the use of acetylcholine in this model reduces ischemia-reperfusion injury. Therefore, we will compare this protocol with a protocol in which endothelial function is only measured after ischemia. We expect an increase in ischemia-reperfusion injury when endothelial function is only measured after the forearm ischemia. After determining the optimal method to measure ischemia-reperfusion injury of the vascular endothelium we will determine the effect of acute and chronic caffeine, an adenosine receptor antagonist, on ischemic preconditioning. With this study we expect to find that adenosine mimics ischemic preconditioning of the vascular endothelium. Moreover, we expect to find that acute caffeine intake reduces ischemia-reperfusion injury whereas chronic caffeine intake does not. This study will increase our knowledge about the mechanism of ischemic preconditioning and may also provide leads to exploit this endogenous protective mechanism in a clinical setting.

This is an open, observational, prospective, descriptive, single-centre study including 60 patients. The study is designed to investigate if IscAlert sensor system can be used for reliable and continuous tissue carbon dioxide (pCO2)- and temperature monitoring in muscular tissue in lower extremity in patients at risk of developing acute compartment syndrome.

The purpose of this registry is to evaluate the safety and efficacy of RIC for patients with symptomatic intracranial atherosclerotic stenosis (sICAS) undergoing endovascular therapy.

Any platelet function tests have not been widely used in the clinical practice of acute cerebrovascular disease because of the concerns in repeatability, economic performance, and simplicity. Soluble C-type lectin-like receptor 2 (sCLEC-2) is a new marker for platelet activation, which can be easily measured by usual blood collection in routine clinical practice. We planned the sCLEC-2 in Stroke (CLECSTRO), which is a prospective cohort study in patients with acute ischemic stroke (AIS) and transient ischemic attack (TIA). We planned the sCLEC-2 in Stroke (CLECSTRO), which is a prospective cohort study in patients with acute ischemic stroke (AIS) and transient ischemic attack (TIA). The purpose of this study is to evaluate the clinical utility of sCLEC-2 as a biomarker for pathophysiology, differential diagnosis, prediction of prognosis, and monitoring of antiplatelet therapy in patients with AIS and TIA. Subjects are patients with AIS or TIA and control patients required for differentiation from AIS or TIA. The target population is 600 including the patients and the controls. The outcomes include difference in plasma sCLEC-2 level between patients with AIS or TIA and patient controls, correlation between sCLEC-2 after antithrombotic therapy and recurrence or worsening of stroke, difference in sCLEC-2/D-dimer ratio between non-cardioembolic and cardioembolic AIS or TIA, and correlation between baseline sCLEC-2 and outcome (modified Rankin scale score) after 3 months. sCLEC-2 could be a widely useful biomarker to contribute to the progress of precision medicine in clinical practice of AIS and TIA.

Autonomic modulation by transcutaneous vagal nerve stimulation in acute ischaemic stroke requiring mechanical thrombectomy: a phase IIa, sham controlled randomised trial.

Recent years have witnessed a change in the therapeutic paradigm of stroke with the advent of mechanical thrombectomy as the reference treatment. However, despite the achievement of effective proximal recanalization in nearly 80% of patients, nearly half of these patients have an unfavorable functional outcome. Several causes can be mentioned, such as the extent of the initial ischemic damage, the occurrence of complications related to reperfusion treatments or the occurrence of thrombosis of the downstream microvascularization. The latter is a phenomenon that has been known and studied increasingly over the last twenty years. It is the result of multiple cellular remodeling following ischemia and at the origin of an endoluminal filling by platelets, inflammatory cells and fibrin. This phenomenon introduces the fundamental difference between recanalization, i.e. the removal of the obstruction by the thrombus, and reperfusion, which translates into a satisfactory supply of oxygen to the ischemic tissues and therefore the expected result of these treatments. However, not all recanalization is necessarily accompanied by reperfusion, which is the phenomenon of no-reflow. This last situation could be explained by downstream microvascular thrombosis. Studies have shown the interest of intravenous thrombolysis associated with mechanical thrombectomy to preserve this vascular bed and improve cerebral reperfusion. More recently, a study has also shown the value of adding intra-arterial thrombolysis after mechanical thrombectomy. Nevertheless, there is currently no clinical evidence of the reality and prognostic importance of downstream microvascular thrombosis. Advances in imaging have allowed the development of susceptibility weighted imaging (SWI) sequences with millimeter resolution, allowing a precise study of vascular damage and the appearance of previously unseen remodeling. Among them, the existence of cortical or juxta-cortical microinfarcts whose remnographic characteristics differed by the presence of a SWI hyposignal. The hypothesis evoked is that of a hemorrhagic remodeling consecutive to the barrier rupture. However, in view of the pathophysiology explained so far and the hypointense character of the thrombi on the SWI sequences, these remodeling could in fact be not microbleeding but rather markers of thrombosis in the downstream microcirculation. MRI would allow to identify the presence and the importance of microvascular thrombosis and thus to bring arguments to specifically target this microvascular component, consequence of cerebral ischemia, by antithrombotic or thrombolytic treatments. The objective of our project is therefore to carry out a study focused on a better description and understanding of cortical and basal ganglia SWI hyposignals with a histopathological correlation and with the clinical prognosis.