[Successful multidisciplinary management of tetraplegia with a thoracic operation. Unicentric, mediastinal Castleman disease]. / Tetraplegia sikeres multidiszciplináris kezelése mellkassebészeti mutéttel. Unicentrikus mediastinalis Castleman-betegség esete.

Castleman disease is a rare lymphoproliferative disease the exact cause of which is not known. The diagnosis is based on the adequate histological examination. While in the unifocal form, the disease most commonly affects the chest, and symptoms may resolve as a result of intact excision of the tumour; other treatment methods may be performed in addition to or instead of surgical incision in the case of the multifocal form. We present the case of a patient with Castleman disease who received multidisciplinary treatment. Speech difficulty, dysphagia, and progressive paresis occurred in the upper and lower extremities of the 56-year-old male patient 18 weeks before his check-up examinations. Although the complaints temporarily resolved with plasmapheresis, surgical sampling could not confirm the origin of the mediastinal lymphadenomegaly detected with thoracic CT. The patient was admitted to our department to remove the 5 cm large subcarinal lymph node or to gain a tissue sample from it. On admission, significant atrophy, hypotonia and tetraplegia were seen in the four extremities, and areflexia was detected all over the body. The 5.5 × 3.5 cm large subcarinal lymph node conglomerate was removed from posterolateral thoracotomy. Histology was performed, Castleman disease was confirmed. 3 days after the surgery, the patient was able to move the extremities, and then on the 9th postoperative day, the patient could walk using a walking frame, and he was transferred back to the Department of Neurorehabilitation. At transfer, the muscle strength of the upper extremities was almost intact, and 4/5 muscle strength was detected in the lower extremities. After this, methylprednisolone, vitamin B1, calcium citrate, famotidine therapy was administered, and 2 weeks after his transfer, he was discharged home; at that time, the patient was able to walk safely without a walking frame. The symptoms resolved almost completely 3 months after the surgery. Diagnosis and treatment of Castleman disease are multidisciplinary tasks. If the patient is suitable for surgery, surgical removal has to play a key role in the treatment of unifocal Castleman disease. Orv Hetil. 2020; 161(1): 33-38.

Utilization of acute vascular imaging and neurointervention for acute ischaemic stroke patients in 20 Hungarian stroke centers.

BACKGROUND AND PURPOSE: Acute mortality rate of stroke in Hungary is significantly higher than in Western Europe, which is likely to be partially attributable to suboptimal treatment. METHODS: We examined the use of acute vascular imaging and mechanical thrombectomy for acute ischaemic stroke patients. We collected data on 20 consecutive patients from Hungarian stroke centers before 31st August 2016. RESULTS: Out of the reported 410 patients, 166 (40.4%) underwent CT angiography and 44 (10.7%) had mechanical thrombectomy. CONCLUSION: Only about 1/3 of acute ischaemic stroke patients eligible for thrombectomy actually had it. The underlying reasons include long onset-to-door time, low utilization of acute vessel imaging and a limited neuro-intervention capacity needing improvement.

Mitochondria, Oxidative Stress and the Kynurenine System, with a Focus on Ageing and Neuroprotection.

In this review, the potential causes of ageing are discussed. We seek to gain insight into the main physiological functions of mitochondria and discuss alterations in their function and the genome, which are supposed to be the central mechanisms in senescence. We conclude by presenting the potential modulating role of the kynurenine pathway in the ageing processes. Mitochondrial dynamics are supposed to have important physiological roles in maintaining cell homeostasis. During ageing, a decrease in mitochondrial dynamics was reported, potentially compromising the function of mitochondria. Mitochondrial biogenesis not only encompasses mitochondrial dynamics, but also the regulation of transcription and translation of genes, and mitochondria are supposed to play a prominent role in cell death during senescence. Defects in the mtDNA replication machinery and failure in the repair of mtDNA might result in the accumulation of mutations, leading to mitochondrial dysfunction and bioenergetic failure of the cell. The role of reactive oxygen species (ROS) in the ageing processes is widely acknowledged. Exaggerated oxidative damage to mDNA is supposed to take place during senescence, including single-nucleotide base alterations, nucleotide base pair alterations, chain breaks and cross linkage. A broad repertoire for the repair of DNA faults has evolved, but they do not function efficiently during senescence. Poly (ADP-ribose) polymerase (PARP) is an enzyme that assists in DNA repair, i.e., it participates in the repair of single-stranded DNA nicks, initiating base excision repair (BER). In the case of extensive DNA damage, PARP-1 becomes overactivated and rapidly depletes the intracellular NAD⁺ and ATP pools. This results in a profound energy loss of the cell and leads to cell dysfunction, or even cell death. Alterations in the kynurenine system have been linked with ageing processes and several age-related disorders. The kynurenine pathway degrades tryptophan (TRP) to several metabolites, among others kynurenine (KYN), kynurenic acid (KYNA) and quinolinic acid (QUIN). The end product of the route is NAD⁺. The first metabolic reaction is mediated by TRP-2,3-dioxygenase (TDO) or indolamine-2,3-dioxygenases (IDO), the latter being induced by inflammation, and it is thought to have a significant role in several disorders and in ageing. Research is currently focusing on the KYN pathway, since several intermediates possess neuro- and immunoactive properties, and hence are capable of modulating the activity of certain brain cells and inflammatory responses. During ageing, and in many age-associated disorders like obesity, dyslipidaemia, hypertension, insulin resistance and neurodegenerative diseases, low-grade, sustained inflammation and upregulation of IDO have been reported. However, TRP downstream catabolites create a negative feedback loop by weakening the activated immune system through several actions, including a decline in the Th1 response and an enhancement of Th2-type processes. The broad actions of the KYN-intermediates in brain excitation/inhibition and their role in regulating immune responses may provide the possibility of modifying the pathological processes in an array of age-associated diseases in the future.

Stroke in essential thrombocythemia.

BACKGROUND: Our aim was to assess the incidence and the special characteristics of stroke, as a severe complication of patients diagnosed with essential thrombocythemia (ET). METHODS: A retrospective analysis was carried out on 102 patients with ET enrolled and analyzed from the period between 1999 and 2012. Patients with one or more strokes were selected. The characteristics of stroke events, the medication, and the median platelet counts were revised. RESULTS: One or more stroke events were revealed in 11 cases (4 males and 7 females) with a median age of 67 years [range: 45-82 years]. The median platelet count at hematological diagnosis was 658×10(9)/L [range: 514-1157×10(9)/L], while during the time of stroke it was 450×10(9)/L [range: 320-885×10(9)/L]. The median follow-up of the patients with stroke was 60 months [range: 19-127 months]. At the time of the stroke, almost all the patients (8/11 cases, 73%) were already on anti-platelet therapy, alone or in combination with cytoreductive therapy (e.g. hydroxyurea). Brain imaging modalities in most cases demonstrated periventricular and/or subcortical and/or basal ganglia lacunes or confluent chronic white matter ischemic lesions in all cerebral arterial regions. Most patients (9/11; 82%) presented at least two serious conventional vascular risk factors, which may have influenced both the clinical course and the morphologic alterations. No correlation was found between the platelet count and the occurrence of stroke. CONCLUSION: Our findings lead us to suppose that ET may be regarded as a risk factor for stroke (mainly of ischemic, small-vessel type), and the early diagnosis and the personalized management of the patient's global vascular risk in the treatment of ET may promote the prevention of further cerebrovascular events.

Aspirin and clopidogrel resistance: possible mechanisms and clinical relevance. Part II: Potential causes and laboratory tests.

Recent meta-analyses have indicated that patients with vascular disease demonstrated by laboratory tests to be aspirin or clopidogrel-resistant are at an increased risk of major vascular events. The suggested mechanisms of aspirin resistance include genetic polymorphism, alternative pathways of platelet activation, aspirin-insensitive thromboxane biosynthesis, drug interactions, or a low aspirin dose. Clopidogrel resistance is likely to develop as a result of a decreased bioavailability of the active metabolite, due to genetic variation or concomitant drug treatment. Additional work is required to improve and validate laboratory tests of platelet function, so that they may become useful tools for selection of the most appropriate antiplatelet therapy for an individual patient. Improvements in antiplatelet treatment strategies in the future should lead to a reduction in premature vascular events.

Aspirin and clopidogrel resistance: possible mechanisms and clinical relevance. Part I: Concept of resistance.

Aspirin and clopidogrel are well established as antiplatelet medication in the treatment of atherothrombotic vascular disease. However, despite treatment, a substantial number of patients experience recurrent ischemic episodes, referred to as aspirin or clopidogrel treatment failure. Various laboratory techniques are available with which to evaluate the effectiveness of antiplatelet drugs. Interestingly, the agreement between the results of the different tests may be poor. The term aspirin or clopidogrel resistance denotes those conditions in which an inadequate inhibitory efficacy of the given antiplatelet agent is detected by an in vitro assay of platelet function. It has been estimated that on average some 30% of patients treated with aspirin, and 20% on clopidogrel, do not achieve an appropriate level of efficacy as concerns platelet activity.

Dementia, stroke and migraine--some common pathological mechanisms.

Dementia, stroke and migraine are very common neurological disorders affecting a large percentage of the population, and leading to a high degree of disability. Often, adequate therapy is not available. Although the symptoms, the progression and the outcome differ in these disorders, to some extent they may share some common pathophysiological mechanisms. The genetic background, an energy deficit, and excitotoxicity, vascular and thrombotic properties can influence all three disorders, resulting in a neuronal dysfunction, increased cellular vulnerability, neurodegeneration and ultimately cell death. All these cellular events occur in dementias and stroke, moreover recent studies suggest that, besides a dysfunction, neuronal damage may be an issue in migraine too. One of the most central events in the multiple mechanisms involved in the pathogenesis of these disorders is a metabolic disturbance of certain brain cells. As mitochondria provide the cells with energy, realization of the importance of these organelles in the aetiopathogenesis of several disorders has emerged in recent years. This review surveys the most important features of the pathogenesis of dementia, stroke and migraine from the aspect of mitochondrial malfunction highlighting some of the considerable connections between these neurological disorders.

Kynurenine diminishes the ischemia-induced histological and electrophysiological deficits in the rat hippocampus.

The neuroprotective effect of L-kynurenine sulfate (KYN), a precursor of kynurenic acid (KYNA, a selective N-methyl-D-aspartate receptor antagonist), was studied. KYN (300 mg/kg i.p., applied daily for 5 days) appreciably decreased the number of injured pyramidal cells from 1850+/-100/mm(2) to 1000+/-300/mm(2) (p<0.001) in the CA1 region of the hippocampus in the four-vessel occlusion (4VO)-induced ischemic adult rat brain. A parallel increase in the number of intact, surviving neurons was demonstrated. Post-treatment with KYN (applied immediately right after reperfusion) proved to be much less effective. In parallel with the histology, a protective effect of KYN on the functioning of the CA1 region was observed: long-term potentiation was abolished in the 4VO animals, but its level and duration were restored by pretreatment with KYN. It is concluded that the administration of KYN elevates the KYNA concentration in the brain to neuroprotective levels, suggesting its potential clinical usefulness for the prevention of neuronal loss in neurodegenerative diseases.

The pentylenetetrazole-induced activity in the hippocampus can be inhibited by the conversion of L-kynurenine to kynurenic acid: an in vitro study.

The kynurenine pathway converts tryptophan into various compounds, including L-kynurenine, which in turn can be converted into the excitatory amino acid receptor antagonist kynurenic acid. The ionotropic glutamate receptors have been considered to be attractive targets for new anticonvulsants in neurological disorders such as epileptic seizure. This study was designed to examine the conversion of L-kynurenine to kynurenic acid and to investigate the effects of kynurenic acid on pentylenetetrazole-treated rat brain slices, and in parallel to draw attention to the fact that a well-designed in vitro model has many advantages in pharmacological screening. Schaffer collateral stimulation-evoked field EPSPs were recorded from area CA1 of rat hippocampal slices in vitro; drugs were bath-applied. Pretreatment with the kynurenic acid precursor L-kynurenine led to the elimination of the effect of pentylenetetrazole on hippocampal slices in vitro. N-Omega-nitro-L-arginine, which inhibits kynurenine aminotransferase I and II, abolished this neuroprotective effect. This study has furnished the first in vitro electrophysiological evidence that rat brain slices have the enzymatic capacity to convert exogenously administered L-kynurenine (16 microM) to kynurenic acid in an amount sufficient to protect them against pentylenetetrazole (1 mM)-induced hyperexcitability.

Neuroprotection achieved in the ischaemic rat cortex with L-kynurenine sulphate.

L-kynurenine is a metabolic precursor of kynurenic acid, which is one of the few known endogenous N-methyl-D-aspartate receptor inhibitors. In contrast with kynurenic acid, L-kynurenine is transported across the blood-brain barrier, and it may therefore come into consideration as a therapeutic agent in certain neurobiological disorders, e.g. ischaemia-induced events. The present study evaluated the effect of L-kynurenine administration (300 mg/kg i.p.) on the global ischaemic brain cortex both pre- and post-ischemic intervention. The statistical evaluation revealed that L-kynurenine administration beneficially decreased the number of neurones injured per mm(2) in the cortex, not only in the pre-treated animals, but also in those which received L-kynurenine after the ischaemic insult. It is concluded that even the post-traumatic administration of L-kynurenine may be of substantial therapeutic benefit in the treatment of global brain ischaemia. This is the first histological proof of the neuroprotective effect achieved by the post-traumatic administration of L-kynurenine in the global ischaemic cortex.

Chronic infections and genetic factors in the development of ischemic stroke.

The aim of this study was to examine whether chronic infections and genetic factors of the host play roles in the pathophysiology of acute noncardioembolic ischemic stroke. Blood samples from 59 subjects with ischemic stroke and 52 control patients were investigated by nested PCR for the presence of C. pneumoniae DNA, HCMV DNA and enterovirus RNA, by ELISA for the levels of antibodies to C. pneumoniae, HCMV, HSV, HHV-6, EBV and the inflammatory chemokine IL-8, and by PCR for promoter polymorphism of the IL-8 and CD14 host genes. Associations of stroke with the HCMV IgG and HSV-1 IgA antibody levels were observed. No association of stroke was detected with the presence of C. pneumoniae, HCMV or enterovirus nucleic acids in the peripheral blood, C. pneumoniae IgM, IgG and IgA, the HSV IgG, the EBV IgG, or HHV-6 IgG antibody levels, the pathogen burden, the IL-8 or CD14 promoter polymorphisms, or with the serum levels of IL-8 in the overall study population. These results are consistent with the hypothesis that certain pathogens are involved in the development of ischemic stroke.

[Amnesic syndrome following lesion of the fornix or does reversible Korsakow's syndrome exist?]. / Fornix léziót követo amnesztikus szindróma, avagy létezik-e reverziblis Korsakow szindróma?

The 53-year-old female patient had suffered massive subarachnoid bleeding due to rupture of left-localized aneurysm of the anterior communicant artery. Following the neurosurgical intervention, deterioration of consciousness related to strong vasospasm occurred. Cerebral CT examination was performed, showing a 0.5 cm ischaemic lesion of the left hippocampal fornix. Due to intensive therapy, the patient recovered gradually, however considerable short-time memory deficit and severe anterograde amnesia remained. Admission of the patient in psychiatric care 5 weeks after the operation was necessary since acute deterioration had been added to memory disturbance and anterograde amnesia. Clinical features included severe short-time memory deficit, continuous and severe anterograde amnesia, disorientation, alterations of verbal fluency and abstraction. The amnesic syndrome was probably related to the hippocampal damage, but considering the development of cognitive deficits, cerebral CT was performed again, which verified internal hydrocephalus. A ventriculo-peritoneal shunt has been implanted and the patient was re-admitted in psychiatry care because of her memory deficit, anterograde amnesia and disorientation. Thereafter, low doses of citalopram and donepezil therapy was started together with temporarily used antipsychotic medication (risperidone). Gradual, but continuous improvement of memory and cognitive function could be detected, with total recovery after one year. The deficits in long- and short-term memory, orientation and cognition were totally restored.

Neuroprotective effect of L-kynurenine sulfate administered before focal cerebral ischemia in mice and global cerebral ischemia in gerbils.

Excessive stimulation of N-methyl-D-aspartate (NMDA) receptors during ischemia contributes to apoptotic and excitotoxic nerve cell death. Kynurenic acid is a selective antagonist at the glycine co-agonist site of the NMDA receptor complex at low concentration, and it is a broad-spectrum excitatory amino acid receptor blocker at high concentration. Kynurenic acid provides neuroprotection in animal models of cerebral ischemia only at very high doses as it hardly crosses the blood-brain barrier. The neuroprotective effect of L-kynurenine sulfate, a precursor of kynurenic acid, was therefore studied because L-kynurenine readily crosses the blood-brain barrier. L-kynurenine sulfate was administered 15 min before permanent focal cerebral ischemia produced by electrocoagulation of the distal middle cerebral artery in mice. L-kynurenine sulfate induced a small decrease in the surface area of the brain infarction (10%, P<0.05) at 30 mg/kg i.p., and it caused strong reductions in infarct size (24-25%, P<0.01) at 100 and 300 mg/kg i.p. Treatment of gerbils with L-kynurenine sulfate at 300 mg/kg i.p. 2 h before a 3-min bilateral carotid occlusion decreased (40%, P<0.01) the pyramidal cell loss in the CA1 area of the hippocampus. Furthermore, L-kynurenine sulfate inhibited the ischemia-induced hypermotility (77%, P<0.001), and decreased (50%, P<0.01) the ischemia-induced deterioration of spontaneous alternation, a measure of spatial memory, without altering the rectal temperature. In conclusion, the administration of L-kynurenine can elevate the brain concentration of kynurenic acid to neuroprotective levels, suggesting the potential clinical usefulness of L-kynurenine for the prevention of neuronal loss.

Mitochondria, metabolic disturbances, oxidative stress and the kynurenine system, with focus on neurodegenerative disorders.

The mitochondria have several important functions in the cell. A mitochondrial dysfunction causes an abatement in ATP production, oxidative damage and the induction of apoptosis, all of which are involved in the pathogenesis of numerous disorders. This review focuses on mitochondrial dysfunctions and discusses their consequences and potential roles in the pathomechanism of neurodegenerative disorders. Other pathogenetic factors are also briefly surveyed. The second part of the review deals with the kynurenine metabolic pathway, its alterations and their potential association with cellular energy impairment in certain neurodegenerative diseases. During energy production, most of the O(2) consumed by the mitochondria is reduced fully to water, but 1-2% of the O(2) is reduced incompletely to give the superoxide anion (O(2)(-)). If the function of one or more respiratory chain complexes is impaired for any reason, the enhanced production of free radicals further worsens the mitochondrial function by causing oxidative damage to macromolecules, and by opening the mitochondrial permeability transition pores thereby inducing apoptosis. These high-conductance pores offer a pathway which can open in response to certain stimuli, leading to the induction of the cells' own suicide program. This program plays an essential role in regulating growth and development, in the differentiation of immune cells, and in the elimination of abnormal cells from the organism. Both failure and exaggeration of apoptosis in a human body can lead to disease. The increasing amount of superoxide anions can react with nitric oxide to yield the highly toxic peroxynitrite anion, which can destroy cellular macromolecules. The roles of oxidative, nitrative and nitrosative damage are discussed. Senescence is accompanied by a higher degree of reactive oxygen species production, and by diminished functions of the endoplasmic reticulum and the proteasome system, which are responsible for maintenance of the normal protein homeostasis of the cell. In the event of a dysfunction of the endoplasmic reticulum, unfolded proteins aggregate in it, forming potentially toxic deposits which tend to be resistant to degradation. Cells possess adaptive mechanisms with which to avoid the accumulation of incorrectly folded proteins. These involve molecular chaperones that fold proteins correctly, and the ubiquitin proteasome system which degrades misfolded, unwanted proteins. Both the endoplasmic reticulum and the ubiquitin proteasome system fulfill cellular protein quality control functions. The kynurenine system: Tryptophan is metabolized via several pathways, the main one being the kynurenine pathway. A central compound of the pathway is kynurenine (KYN), which can be metabolized in two separate ways: one branch furnishing kynurenic acid, and the other 3-hydroxykynurenine and quinolinic acid, the precursors of NAD. An important feature of kynurenic acid is the fact that it is one of the few known endogenous excitatory amino acid receptor blockers with a broad spectrum of antagonistic properties in supraphysiological concentrations. One of its recently confirmed sites of action is the alpha7-nicotinic acetylcholine receptor and interestingly, a more recently identified one is a higher affinity positive modulatory binding site at the AMPA receptor. Kynurenic acid has proven to be neuroprotective in several experimental settings. On the other hand, quinolinic acid is a specific agonist at the N-methyl-d-aspartate receptors, and a potent neurotoxin with an additional and marked free radical-producing property. There are a number of neurodegenerative disorders whose pathogenesis has been demonstrated to involve multiple imbalances of the kynurenine pathway metabolism. These changes may disturb normal brain function and can add to the pathomechanisms of the diseases. In certain disorders, there is a quinolinic acid overproduction, while in others the alterations in brain kynurenic acid levels are more pronounced. A more precise knowledge of these alterations yields a basis for getting better therapeutic possibilities. The last part of the review discusses metabolic disturbances and changes in the kynurenine metabolic pathway in Parkinson's, Alzheimer's and Huntington's diseases.

Hippocampal (CA1) activities in Wistar rats from different vendors. Fundamental differences in acute ischemia.

Two-vessel occlusion, a frequently used model of global cerebral ischemia in rats, results in a dysfunction predominantly within the CA1 field of the hippocampus; it induces many processes with different time-scales. However, the great divergence in the results of the studies reported in the literature suggests valuable differences in response to hypoperfusion-induced ischemia among the laboratory rats used in these studies. In the present work, the acute effects of two-carotid occlusion-induced global ischemia (2VO) on the CA3 stimulation-evoked population spike activity in the CA1 region of Wistar rats from different suppliers (Charles-River and Harlan) were compared. In the acute electrophysiological experiments, the hippocampal CA1 responses revealed that the Charles-River rats immediately compensated the 2VO much better than did the Harlan rats. However, 3 days later, no difference could be observed between the CA1 activities of these rats. The presented data show that the Wistar rats from different vendors represent an important source of variability in the results of acute experiments on the hippocampal ischemia. These observations draw attention to the importance of the careful choice of the laboratory rats (both strains and breeds) used in such experiments.

Aspirin resistance in stroke: 2004.

Aspirin is a well-established medication in the treatment of atherothrombotic vascular disease. However, despite aspirin treatment a substantial number of patients experience recurring ischaemic episodes. Aspirin resistance denotes those situations when it is unable to protect individuals from thrombotic complications, or when it fails to produce an anticipated effect in laboratory tests of platelet function. There are various laboratory techniques with which to evaluate the effectiveness of aspirin and other antiplatelet drugs. It has been estimated that in 5-60% of patients, aspirin does not achieve adequate efficacy in various measures of platelet activity. Some studies have revealed that vascular patients shown by laboratory tests to be aspirin-resistant are at an increased risk of major vascular events. The suggested mechanisms of aspirin resistance, among others, include genetic polymorphisms, alternate pathways of platelet activation, aspirin-insensitive thromboxane biosynthesis, drug interactions, or low aspirin dose. An increase in the dosage of aspirin or conversion to clopidogrel or clopidogrel plus aspirin might be beneficial in the management of those patients who are aspirin resistant. Additional work is required to improve and validate laboratory tests of platelet function, so that they may become useful tools for selecting the most appropriate antiplatelet therapy for an individual patient. Improvements in antiplatelet treatment strategies in the future should lead to a reduction in premature vascular events.

Favorable early outcome of carotid artery stenting without protection devices.

BACKGROUND AND PURPOSE: Protection devices are increasingly used in carotid artery stenting. However, no randomized trial has been conducted to evaluate the efficacy of such devices, and arguments have also been formulated against their routine use. We set out to investigate the complication rates associated with carotid artery stenting performed without protection devices. Applicability of covered stents in the carotid system was also evaluated. METHODS: Between January 2001 and July 2003, 245 consecutive patients (260 hemispheres) underwent carotid artery stenting. No protection devices were applied. Covered stents were implanted in 31 (12.1%) cases. The incidence of complications during the intervention and the subsequent 30-day follow-up period was recorded. RESULTS: The technical success rate was 98.8%. One postprocedural nonneurological death (0.4%) occurred. Neurological complications (inclusive of transient ischemic attacks) were observed in 14 cases (5.4%). The rate of major complications (death, major stroke, and myocardial infarction) was 1.6% among the symptomatic and 1.5% among the asymptomatic cases. The rate of minor strokes was 3.2% in the symptomatic and 1.5% in the asymptomatic group. Of the neurological complications, 64.3% occurred postprocedurally. No ipsilateral neurological complications were detected in the subgroup treated with covered stents. CONCLUSIONS: Carotid artery stenting without protection devices appears to be safe. Most of the neurological complications could not have been prevented with protection devices, because they occurred after the intervention. The application of covered stents may reduce the rate of embolization-related complications in the periprocedural period.