Clinical results of 30 consecutive patients of carotid artery stenosis treated with CASPER stent placement: 1-year follow-up and in-stent findings on intravascular ultrasound examination immediately and 6 months after treatment.

BACKGROUND: The CASPER stent is expected to reduce periprocedural ischemic complications, but there is concern about restenosis in the early period. One-year follow-up results of CASPER stenting and findings on intravascular ultrasound (IVUS) immediately and 6 months after treatment are evaluated. METHODS: Thirty consecutive patients were treated with CASPER stents for carotid artery stenosis. IVUS was performed immediately after stenting, and MRI and carotid ultrasonography were performed the next day, at 1 week, at 2 weeks, and then every 3 months. One-year follow-up results were evaluated. Twenty-five patients underwent follow-up angiography and IVUS after 6 months and their findings were investigated. RESULTS: All patients were treated without complications during the intraoperative and periprocedural periods. After 6 months, all 25 patients with follow-up angiography and IVUS showed various degrees of intimal formation on IVUS and 8 of them had ≥50% stenosis on angiography. Three of the 30 patients required retreatment within 6 months because of severe restenosis. In these patients, the inner layer of the stent was deformed toward the inside due to intimal hyperplasia on follow-up IVUS, and there was dissociation between the inner and outer layers. All but the 3 of 30 patients with 1-year follow-up did not lead to symptomatic cerebrovascular events or retreatment. CONCLUSIONS: The CASPER stent appears to be effective for preventing periprocedural ischemic complications. IVUS showed various degrees of intimal formation within 6 months after treatment, and it is possible that the CASPER stent is structurally prone to intimal formation or hyperplasia.

Factors related to insufficient hemostasis using the EXOSEAL vascular closure device with five-minutes compression for femoral artery punctures after neuro-endovascular therapy: A retrospective, single-center experience.

OBJECTIVES: The aim was to identify the factors related to inadequate hemostasis with five minutes of manual compression using the EXOSEAL vascular closure device (VCD), and to evaluate the optimal time to hemostasis (TTH). METHODS: A total of 119 consecutive patients who underwent neuro-endovascular therapy via common femoral arterial puncture between February 2019 and August 2021 were included. These patients underwent hemostasis using an EXOSEAL with manual compression for five minutes. In this retrospective study, the 119 patients were divided into two groups: (1) achieved hemostasis with five minutes (n = 76); and (2) required more than five minutes to achieve hemostasis (n = 43, Add group). In both groups, patient's characteristics, endovascular procedures, and closure procedures were assessed. RESULTS: On univariable analysis, activated clotting time (ACT), multiple antiplatelets, closure with an under-sized EXOSEAL VCD (U-VCD), endovascular procedure, and use of a 7Fr. VCD were significantly associated with additional compression (p < 0.05). On multivariate logistic regression analysis, the following three factors were found to be associated with additional compression: pre-closure ACT (adjusted OR, 0.136; 95% CI, 1.017-1.056; p < 0.001); multiple antithrombotics (adjusted OR, 12.843; 95% CI, 3.458-47.693; p < 0.001); and closure with a U-VCD (adjusted OR, 5.653; 95% CI, 1.751-18.151; p = 0.004). On the receiver-operating characteristic curve analysis for prediction of the need for additional compression, the cutoff point for pre-closure ACT was calculated to be 268 s. In the Add group, mean TTH was 9.8 ± 1.5 min. CONCLUSION: Multiple antiplatelets and closure with a U-VCD may increase the risk of insufficient hemostasis with five-minutes compression using an EXOSEAL VCD for femoral puncture sites if the pre-closure ACT is greater than 268 s. In these patients, mean TTH was 9.8 ± 1.5 min.

Aphasic status epilepticus of frontal origin treated by resective surgery.

Aphasic status epilepticus (SE) is a clinical entity of SE, but it has not been well recognized. We report a 43-year-old female with a chronic drug-resistant epilepsy with aphasic SE, treated by resective surgery. The patient showed long-lasting weekly episodes of hypokinesia, slow verbal response, and dysphasia, which were diagnosed as symptoms of aphasic SE. Magnetic resonance imaging showed encephalomalacia in the left frontal lobe with a hemosiderin rim. Intracranial electroencephalography revealed continuous spikes, predominantly on the left superior frontal gyrus with hemosiderin deposit. The aphasic symptoms were seen when ictal discharges gradually spread to the wide area of the left anterior frontal lobe, including the language area. The episodes of recurrent aphasic SE had disappeared by one year after the left anterior frontal resection. We should consider aphasic SE when language impairment is episodic, and consider surgical intervention in cases where it repeatedly occurs despite appropriate medical therapy.

Loss of thioredoxin-binding protein-2/vitamin D3 up-regulated protein 1 in human T-cell leukemia virus type I-dependent T-cell transformation: implications for adult T-cell leukemia leukemogenesis.

Human T-cell leukemia virus type I (HTLV-I) is the causative agent of adult T-cell leukemia (ATL). However, the low incidence of ATL among HTLV-I-infected carriers, together with a long latent period, suggests that multiple host-viral events are involved in the progression of HTLV-I-dependent transformation and subsequent development of ATL. Human thioredoxin (TRX) is a redox active protein highly expressed in HTLV-I-transformed cell lines, whereas the TRX-binding protein-2/vitamin D3 up-regulated protein 1 (TBP-2/VDUP1) was recently identified as a negative regulator of TRX. We report here that expression of TBP-2 is lost in HTLV-I-positive, interleukin-2-independent T-cell lines but maintained in HTLV-I-positive, interleukin-2-dependent T-cell lines, as well as HTLV-I-negative T-cell lines. Ectopic overexpression of TBP-2 in HTLV-I-positive T cells resulted in growth suppression. In the TBP-2-overexpressing cells, a G1 arrest was observed in association with an increase of p16 expression and reduction of retinoblastoma phosphorylation. The results suggest that TBP-2 plays a crucial role in the growth regulation of T cells and that the loss of TBP-2 expression in HTLV-I-infected T cells is one of the key events involved in the multistep progression of ATL leukemogenesis.

Anti-oxidant effects of coenzyme Q10 on experimental viral myocarditis in mice.

We studied the effects of coenzyme Q10 (CoQ10) on mice with acute myocarditis inoculated with the encephalomyocarditis (EMC) virus with the analysis of indices of effects of oxidative injury and DNA damage in the myocardium. The mice were treated as follows: CoQ10 group (n = 118); CoQ10 1.0 mg (0.1 mL) x 2/d (0.1 mg/g/d), control group (n = 128); sham-liquid 0.1 mL x 2/d. The mice were injected intraperitoneally 1 day before and daily for 12 days after EMC virus inoculation. The expression of thioredoxin, a marker of oxidative stress overload, as well as 8-hydroxy-2'-deoxyguanosine, an established marker of DNA damage, in the myocardium was investigated. The survival rate was significantly higher (P < 0.01) in the CoQ10 group (46.8%, 29/62) than in the control group (14.3%, 10/70). There were significant increases of CoQ9 and CoQ10 in the heart, which are the biologically active forms of CoQ in mice, and significant decrease of serum creatine kinase (CK)-MB in the CoQ10 group as compared with the control group. Histologic examination showed that the severity of myocarditis was less severe (P < 0.01) in the CoQ10 group than in the control group. In addition, the up-regulation of myocardial thioredoxin with DNA damage, which was induced by the inflammatory stimuli by the virus, was suppressed by the CoQ10 treatment, which may reflect the anti-oxidant effects of CoQ10 treatment. Thus, pretreatment with CoQ10 may reduce the severity of viral myocarditis in mice associated with decreasing oxidative stress in the condition.