Irisin — the future of ischemic stroke therapy?

Irisin is a recently discovered hormone, synthesized mainly by the muscles. Expression of irisin and its precursor named FNDC5 was also found in the heart, kidneys, liver, pancreas, adipose tissue, and brain including cortical neurons, hippocampus, cerebellum, hypothalamus, and spinal cord. The purpose of this study is to review the latest research on the properties of the irisin and its cytoprotective effect against neuronal damage and to draw attention to its possible clinical use in the treatment of stroke. Notch pathway activity increases after ischemic damage, stimulating the repair of the affected brain area. Irisin activates the Notch pathway which inhibits the activity of microglia, secretion of inflammatory factors, and finally leads to reduction of the brain edema. Studies revealed that irisin increases levels of brain-derived neurotrophic factor (BDNF), leading to enhancement of survival and migration of the neurons, and protecting nerve cells from damage during the ischemic stroke. It was also found that irisin maintains mitochondrial integrity, reduces oxidative stress, and exerts a protective effect on the blood-brain barrier. Irisin entails a neuroprotective effect, reducing the extent of the infarcted area and the degree of brain damage. Stimulation of the irisin expression by physical activity or its exogenous administration remains the subject of research that raises hope for development of the new therapeutic options for diseases, especially ischemic stroke

Type 2 endoleak embolization and utilization of non-contrast-enhanced magnetic resonance angiography (NCE-MRA) as a non-invasive imaging follow-up method.

Endovascular aneurysm repair (EVAR) is a minimally invasive technique widely used in abdominal aortic aneurysm treatment. The most common complications after EVAR remain endoleaks, type 2 endoleak (T2EL) being the most prevalent. T2EL detection and surveillance require imaging techniques such as computed tomography angiography (CTA), contrast-enhanced magnetic resonance angiography (CE-MRA), Doppler ultrasound, or digital subtraction angiography (DSA). However, these modalities are associated with numerous limitations, including exposure to ionizing radiation, contrast media administration, or operator dependency, as in the case of ultrasonography. A non-contrast-enhanced MRA could be a substitute non-invasive method for endoleak monitoring. Our case report describes an 83-year-old female patient with type 2 endoleak and enlarging aneurysm sac detected on a CT scan. Despite the enormous aneurysm size, the patient underwent endovascular treatment owing to multiple comorbidities. Due to challenging feeding vessel anatomy, catheterization of the aneurysmal sac was impossible. Attempted polymerization of the aneurysmal sac with Glubran-2 partially sealed the sac and obliterated the feeders' inflow. Unfortunately, a non-targeted embolization resulted in the loss of patency of the right feeder and adjacent communicating branch. The patient underwent follow-up imaging that included non-contrast-enhanced as well as contrast-enhanced MRA. The examination revealed the presence of a small residual endoleak, a freshly formed thrombus, and areas of old thrombi. The NCE-MR appeared to be a valuable tool in endoleak detection and provided a detailed clot morphology