View clinical trials related to Ischemia.
Filter by:Patients with primary hyperaldosteronism experience more cardiovascular events compared to patients with primary hypertension, independent of the blood pressure level. In this research we hypothesize that patients with primary hyperaldosteronism are more susceptible to ischemia-reperfusion injury.
Determine whether dalfampridine (Ampyra) can improve visual function in patients who have had nonarteritic ischemic optic neuropathy (NAION) with stable visual impairment.
SPECT is currently the dominant clinical test for diagnostic and prognostic purposes as well as therapeutic decision-making. Given the shortage of nuclear reactor-produced Tc, advancing the use of non-isotope based imaging modalities has the potential to change the standard of care for patients with CAD as each one of these technics (CMR, CT, Stress echocardiography) has its own distinct potential advantages over SPECT.
This study is a non-randomized, Phase 2 clinical trial designed to assess optical cerebral blood flow (CBF) response to bolus normal saline. Subjects will have had an ischemic stroke within 96 hours of enrollment. The study intervention will be a one hour monitoring session. There will be a 15 minute baseline measurement period, followed by intravenous administration of 500cc of 0.9% NaCl over 30 minutes, and finally 15 minutes of monitoring post-bolus. All study measurements will cease after 1 hour. Subjects will be followed during their hospitalization for 7 days or until discharge, whichever is sooner, to monitor for adverse events and to collect clinical information.
The aim of this study is to evaluate the safety of Ginkgolides Meglumine Injection in the treatment of ischemic stroke with Syndrome of Intermingled Phlegm and Blood Stasis.
We aim to investigate the relationship between skin microvascular function and the first hospitalization for ischemic foot ulcer in patients with type 1 diabetes former randomized during 7.5 years to intensified conventional insulin treatment (ICT) compared to standard insulin treatment (ST).
The primary objective of the study is to determine whether one 300 mg dose of intravenous (IV) natalizumab reduces change in infarct volume from Baseline to Day 5 on magnetic resonance imaging (MRI) in participants with acute ischemic stroke when given at ≤6 hours or at >6 to ≤9 hours from when they were last known normal (LKN). The secondary objectives of this study in this study population are as follows: To assess the efficacy of natalizumab on change in infarct volume from Baseline to Day 30; To assess efficacy of natalizumab on change in infarct volume from 24 hours to Day 5 and Day 30; To assess the efficacy of natalizumab on clinical measures of stroke outcome; To assess the safety of natalizumab in participants with acute ischemic stroke.
Ischemic stroke (AIC) is the leading cause of non-traumatic disability in adults, the second leading cause of dementia and the third leading cause of death in France. Clopidogrel is one of the recommended first line in the secondary prevention of AIC non cardioembolic origin. However recurrences occur in approximately 9% of patients receiving clopidogrel. Some studies in patients with coronary artery disease have made the connection between these treatment failures and non-biological response to clopidogrel. This non-biological response is found for approximately 30% to 50% of patients. Several mechanisms may explain this non-response. The most accepted mechanism is pharmacokinetic. Indeed, clopidogrel is a prodrug that requires intestinal absorption by P-glycoprotein (PGP) and a transformation by hepatic cytochrome into active metabolites. The genetic polymorphism of proteins involved in these two steps explain the low plasma concentration of active metabolites and thus the low efficacy of clopidogrel in some patients. A new pharmacodynamic hypothesis suggests the involvement of platelet alpha 2-adrenergic receptors. The activation of these receptors potentiates signaling pathway P2Y12 receptor (channel inhibited by clopidogrel) and helps reduce platelet aggregation inhibiting response to clopidogrel.
BACKGROUND: Alteplase dissolves blood vessel clots in acute ischemic stroke and is the only approved acute drug treatment <4½ hours of stroke onset. The overall benefit from alteplase is substantial, but up to 2/3 of patients with large artery clots may not achieve reopening of the vessel and up to 40% of the patients may remain severely disabled or die, leaving substantial room for improvement. Tenecteplase, widely used in coronary heart disease, may be more effective and may have less bleeding complications than alteplase, and may be the drug of choice also in stroke. HYPOTHESIS: Tenecteplase may be given safely to patients with acute ischemic stroke at a dose that is associated with improved clinical outcome compared with existing treatment options. AIMS: To compare efficacy and safety of tenecteplase vs. alteplase given <4½ hours after symptom onset. STUDY ENDPOINTS: The primary study endpoint is excellent clinical outcome at 3 months (effect). Secondary study endpoints are major early clinical improvement (effect) and bleeding complications (safety).
Out-of-hospital cardiac arrest (CA) is a leading public health problem causing nearly one third of a million deaths annually in the US, accounting for half of all cardiovascular deaths and surpassing deaths from stroke, heart failure, and breast and lung cancer combined. Twenty to fifty percent of CA patients (pts) can be resuscitated initially but many die before hospital discharge or suffer permanent neurologic damage. Therapeutic hypothermia (TH) improves survival and neurological outcomes. Despite aggressive, targeted post arrest management, including TH, approximately 50% of pts die before leaving the hospital due to global ischemia-reperfusion injury (IRI) known as the "post arrest syndrome", 1 which is a sepsis-like state characterized by elevated markers of cellular inflammation and injury. It is believed that TH works by decreasing the body's basal metabolic rate (BMR) and attenuating the systemic inflammatory response (SIR). However, specific triggers of the intense pro-inflammatory response are unclear. This "gap" in knowledge must be closed to identify targeted therapy to decrease IRI and improve outcomes. Blood flow to the gut is decreased markedly and intestinal tissue becomes ischemic during CA and CPR, particularly when vasoconstrictor drugs such as epinephrine, are given. IRI of the intestine increases intestinal permeability leading to intestinal microbial translocation and endotoxin release that can stimulate and perpetuate systemic inflammation and cause subsequent multi-organ dysfunction. Endotoxin also increases body temperature and energy expenditure and may attenuate TH induced reductions in BMR and hence, decrease efficacy. The purpose of this novel pilot study is to detect systemic endotoxin release following CA in humans and determine association with cytokine activation, and BMR alterations during TH.