Feasibility and efficacy of real-time ultrasound-guided venous closure with suture-mediated vascular closure device.

BACKGROUND: Venous vascular access complications are usually nonfatal but are the most common complications after transvenous catheter intervention. Vascular closure devices (VCDs) have recently become available for venous closure. OBJECTIVE: This study aimed to evaluate the feasibility and efficacy of real-time ultrasound-guided venous closure with suture-mediated VCDs in patients who underwent catheter ablation. METHODS: This single-center observational study enrolled 226 consecutive patients who underwent elective catheter ablation with femoral venipuncture. For hemostasis, vessel closure by VCD was performed with real-time ultrasound guidance after 2022 (n = 123) and without ultrasound guidance in 2021 (n = 103). The occurrence of venous access site-related complications (major, minor, or other) was compared. RESULTS: The rate of device failure was significantly lower in patients with ultrasound guidance than in those without (1.6% vs 6.3%; P = .048). The occurrence of all venous access site-related complications was significantly lower in patients with ultrasound guidance than in those without (4.9% vs 18.4%; P = .001). Time to ambulation was shorter in patients with ultrasound guidance than in those without (2.0 ± 0.1 hours vs 2.2 ± 0.6 hours; P < .001). CONCLUSION: Real-time ultrasound guidance can reduce device failure, access site-related complications, and time to ambulation in performing venous closure with a VCD.

Comparison of the oxidative profiles before and after revascularization in peripheral arterial disease: a pilot study.

Reactive and highly reactive oxygen species (ROS and hROS) produced by white blood cells are essential for innate immunity; however, they may cause oxidative stress in the host. We developed systems for simultaneously monitoring ROS and hROS, i.e., superoxide radicals (O2•-) and hypochlorite ions (OCl-) secreted from stimulated white blood cells in a few microliters of whole blood. We previously reported on the evaluation of healthy volunteers' blood using the developed system; however, whether patients' blood can be assessed remains unclear. Here, we report a pilot study of 30 cases (28 patients) with peripheral arterial disease, in whom we measured the ROS and hROS levels before and approximately one month after endovascular treatment (EVT) using the system (CFL-H2200) that we developed. At approximately the same time points, physiological indices of blood vessels, oxidative stress markers, and standard clinical parameters in the blood were also monitored. The ankle-brachial index, a diagnostic tool for peripheral arterial disease, was significantly improved after EVT (p<0.001). The ROS-hROS ratio, low-density lipoprotein cholesterol, and hematocrit levels were decreased after EVT (p<0.05), while triglyceride and lymphocyte levels were increased after EVT (p<0.05). The correlations between the study parameters were also analyzed.

Presence of myocardial hypoenhancement on multidetector computed tomography after primary percutaneous coronary intervention in acute myocardial infarction predicts poor prognosis.

BACKGROUND: Recent research has suggested that patients with greater delayed contrast-enhanced size by multidetector computed tomography (MDCT) are more likely to experience adverse cardiac events and have poor prognoses over the long term. The myocardial hypoenhancement area in the delayed contrast-enhanced effect suggests microvascular obstruction. The outcomes of patients with a hypoenhancement area detected by MDCT have not been clear. We examined the clinical importance of myocardial hypoenhancement detected by delayed contrast-enhanced MDCT after percutaneous coronary intervention (PCI) in patients with acute myocardial infarction. METHODS AND RESULTS: In 80 patients with acute myocardial infarction, MDCT was performed immediately after primary PCI. We investigated the outcomes of the patients with hypoenhancement detected by MDCT. Myocardial hypoenhancement was observed in 14 patients (17.5%). All 14 of these patients with hypoenhancement had a transmural infarction, and their infarct volume was significantly higher than those of the patients without hypoenhancement (n=66). During the median follow-up period of 309 days, the appearance of myocardial hypoenhancement was associated with the presence of slow flow/no-reflow, time from onset to reperfusion ≥6 h, aging, smoking, chronic kidney disease, and hyper-low-density lipoprotein cholesterolemia. The incidence of major adverse cardiovascular events (MACE) was significantly higher in the patients with hypoenhancement compared to those without hypoenhancement, regardless of the myocardial infarct volume. CONCLUSIONS: These results indicate that the presence of myocardial hypoenhancement in delayed contrast-enhanced MDCT after PCI as well as the extent of infarct area is an important predictor of MACE.

Protective role of Gipie, a Girdin family protein, in endoplasmic reticulum stress responses in endothelial cells.

Continued exposure of endothelial cells to mechanical/shear stress elicits the unfolded protein response (UPR), which enhances intracellular homeostasis and protect cells against the accumulation of improperly folded proteins. Cells commit to apoptosis when subjected to continuous and high endoplasmic reticulum (ER) stress unless homeostasis is maintained. It is unknown how endothelial cells differentially regulate the UPR. Here we show that a novel Girdin family protein, Gipie (78 kDa glucose-regulated protein [GRP78]-interacting protein induced by ER stress), is expressed in endothelial cells, where it interacts with GRP78, a master regulator of the UPR. Gipie stabilizes the interaction between GRP78 and the ER stress sensor inositol-requiring protein 1 (IRE1) at the ER, leading to the attenuation of IRE1-induced c-Jun N-terminal kinase (JNK) activation. Gipie expression is induced upon ER stress and suppresses the IRE1-JNK pathway and ER stress-induced apoptosis. Furthermore we found that Gipie expression is up-regulated in the neointima of carotid arteries after balloon injury in a rat model that is known to result in the induction of the UPR. Thus our data indicate that Gipie/GRP78 interaction controls the IRE1-JNK signaling pathway. That interaction appears to protect endothelial cells against ER stress-induced apoptosis in pathological contexts such as atherosclerosis and vascular endothelial dysfunction.