Ulceration location is associated with clinical course in carotid stenosis.

OBJECTIVE: Plaque ulceration in carotid artery stenosis is a risk factor for cerebral ischemic events; however, the characteristics that determine plaque vulnerability are not fully understood. We thus assessed the association between plaque ulceration sites and cerebrovascular ischemic attack. METHODS: We retrospectively collected the clinical data of 72 consecutive patients diagnosed with carotid artery stenosis with plaque ulcers. After excluding patients with pseudo-occlusion, a history of previous carotid endarterectomy or carotid artery stenting before the ulcer was first discovered, follow-up data of less than 1 month, or carotid endarterectomy or carotid artery stenting performed within 1 month after the ulcer was first discovered, 60 patients were ultimately included. Patients were divided into proximal and distal groups based on the ulcer location relative to the most stenotic point. The primary endpoints were ipsilateral cerebrovascular ischemic events ("ischemic events"), such as amaurosis fugax, transient ischemic attack, or ischemic stroke due to carotid artery stenosis with plaque ulceration. The association between ulcer location and ischemic events was also assessed. RESULTS: In the patients with plaque ulcer, more patients had proximal than distal plaque ulcers (39 vs 21; P = .028). The median follow-up duration was 3.8 years (interquartile range, 1.5-6.2 years). Nineteen patients (32%) experienced ischemic event. Ischemic events occurred more frequently in the distal than in the proximal group (18% vs 59%; P = .005). Kaplan-Meier curves demonstrated a significantly shorter event-free time in the distal group (log-rank P = .021). In univariate analysis, distal ulcer location was associated with ischemic events (odds ratio [OR], 2.94; 95% confidence interval [CI], 1.13-7.65; P = .03). Multivariate analysis using two different models also showed that distal ulcer location was independently associated with ischemic events (Model 1: OR, 3.85; 95% CI, 1.26-11.78; P = .03; Model 2: OR, 4.31; 95% CI, 1.49-12.49; P = .009). CONCLUSIONS: Patients with carotid artery stenosis and plaque ulcers located distal to the most stenotic point are more likely to experience cerebrovascular ischemic attacks. Therefore, carotid plaques with ulcers located distal to the most stenotic point may be a potential indication for surgical treatment.

Irreversible postoperative cognitive impairment after unruptured intracranial aneurysm treatment in the elderly.

PURPOSE: Postoperative cognitive dysfunction and recovery remain unclear in older patients undergoing interventional therapies for unruptured intracranial aneurysms (UIAs). This study aimed to compare changes in postoperative cognitive function between younger and older patients and to detect factors associated with non-recovery from postoperative cognitive dysfunction. METHODS: This study reviewed 59 consecutive patients with UIAs who underwent interventional therapies, including microsurgical clipping or endovascular treatment, from 2021 to 2022. All patients were divided into the older (aged ≥ 70 years) and younger (aged < 70 years) groups. Mini-Mental State Examination (MMSE) and Frontal Assessment Battery (FAB) were performed within 2 months before interventions, at 1 week postoperatively (POW1), and 3-6 months postoperatively (POM3-6). RESULTS: MMSE and FAB scores decreased more frequently in the older group than in the younger group at POW1 (older vs. younger: MMSE: 48% vs. 21%, p < 0.05; FAB: 56% vs. 18%, p < 0.01). In the older group, the FAB Z-score decreased in POW1 and recovered by POM3-6 (p < 0.01), while the MMSE Z-score continued to decrease (p = 0.04). Age and the preoperative MSME Z-score were significantly associated with non-recovery from decreased MMSE score at POM3-6 (recovery vs. non-recovery, age: 62 years old vs. 72 years old, p = 0.03, preoperative MMSE Z-score: 0.16 vs. - 0.90, p < 0.01). CONCLUSIONS: This retrospective study found that older patients were more likely to have a postoperative cognitive decline after UIA treatment and implicated that global cognitive function tended to decline more than executive function in the long term. In addition, this study demonstrated that lower preoperative cognitive function was associated with inadequate postoperative cognitive recovery. The findings potentially contribute to the establishment of indications for treating UIAs in older patients.

Pathological changes in the lenticulostriate artery indicate the mechanisms leading to intracranial hemorrhage in Moyamoya disease: a case report.

This case report details the pathological findings of a vessel wall identified as the bleeding point for intracranial hemorrhage associated with Moyamoya disease. A 29-year-old woman experienced intracranial hemorrhage unrelated to hyperperfusion following superficial temporal artery-middle cerebral artery bypass surgery. A pseudoaneurysm on the lenticulostriate artery (LSA) was identified as the causative vessel and subsequently excised. Examination of the excised pseudoaneurysm revealed a fragment of the LSA, with a disrupted internal elastic lamina and media degeneration. These pathological findings in a perforating artery, akin to the circle of Willis, provide insights into the underlying mechanisms of hemorrhage in Moyamoya disease.

Impact of tailored multimodal treatment for unruptured brain arteriovenous malformation: comparison with a randomized trial of unruptured brain arteriovenous malformations.

PURPOSE: The first randomized controlled study on unruptured brain arteriovenous malformations (bAVM), the ARUBA trial, demonstrate the superiority of medical management; however, it failed to completely rule out the efficacy of therapeutic interventions due to several limitations. This study aimed to examine the outcomes of multimodal interventional treatment for bAVM in terms of safety and efficacy. METHODS: We reviewed 226 consecutive patients with unruptured bAVM admitted to our institute between 2002 and 2022. Treatment methods were divided into medical management and therapeutic intervention, including microsurgery, stereotactic surgery, and endovascular intervention. First, the choice of therapeutic modalities was assessed in the pre-ARUBA (before February 2014) and post-ARUBA (after March 2014) eras. Second, the incidence of symptomatic stroke or death and functional prognosis with a modified Rankin scale (mRS) score of ≥2 at 5 years was compared between the medical management and therapeutic intervention. RESULTS: In the pre- and post-ARUBA groups, 73% and 84% of patients underwent therapeutic interventions, respectively (p = 0.053). The rate of symptomatic stroke or death was lower in patients who underwent interventional therapies than in those who underwent medical management (9.7% vs. 22%, p = 0.022); however, the opposite was observed in the ARUBA trial (31% vs. 10%). The annual incidence of stroke or death was also lower in the interventional therapy group (4.3%/y vs. 1.8%/year, hazard ratio = 0.45, 95% confidence interval: 0.18-1.08, p = 0.032). The rate of mRS score of ≥2 after a 5-year follow-up was 18% and 6% in the medical treatment and intervention groups (p = 0.14). CONCLUSIONS: The therapeutic intervention rate did not decrease, even after the publication of the ARUBA trial. The rate of stroke or death was lower in the intervention group, indicating that a tailored choice of multimodality is safe and effective for managing unruptured bAVM.

[Changes in Gamma Knife Radiosurgery(GKRS)in Patients with Metastatic Brain Tumors before and after COVID-19].

The spread of coronavirus disease 2019(COVID-19)is a concern as it may delay the detection of malignant tumors due to delayed medical checkups. We examined changes in the treatment of metastatic brain tumors before and after COVID- 19. A retrospective review of 211 patients with metastatic brain tumors who underwent initial gamma knife radiosurgery between July 2019 and December 2021 was conducted. Data collected include patient age, gender, the Karnofsky performance status(KPS), primary tumor control, number, total volume, and outcome during the COVID-19 emergency declaration period and outside of it. The patient number was 164 outside of the emergency period and 47 during the period. Symptomatic cases(KPS<90)and poor control of the primary site increased during the COVID-19 period. The treatment number and volume of brain metastasis did not change. Metastatic control after 4 months of treatment also showed no difference. The number of symptomatic patients increased during the emergency declaration period, suggesting that COVID- 19 may have reduced the rate of asymptomatic patients being seen. However, these were not enough to affect the prognosis at 4 months. Overall, the COVID-19 pandemic had a small impact on the provision of stereotactic radiotherapy for metastatic brain tumors.

EP4 receptor-associated protein regulates gluconeogenesis in the liver and is associated with hyperglycemia in diabetic mice.

Prostaglandin E2 receptor 4-associated protein (EPRAP) is a key molecule in suppressing inflammatory responses in macrophages. EPRAP is expressed not only in macrophages but also in hepatocytes; however, the role of EPRAP in hepatocytes has not yet been defined. To examine the physiological role of hepatic EPRAP in mice, we performed the glucose tolerance test and the hyperinsulinemic-euglycemic clamp in high-fat sucrose diet (HFSD)-fed wild-type (WT) and Eprap null mice. We evaluated the contribution of EPRAP to gluconeogenesis by pyruvate tolerance test and primary hepatocyte experiments. Furthermore, lentivirus-expressing Eprap-specific small-hairpin RNA was injected in db/ db mice. HFSD-fed Eprap null mice had significantly lower blood glucose levels than HFSD-fed WT mice. Eprap null mice also had low glucose levels after fasting or pyruvic acid injection. Moreover, primary hepatocytes from Eprap-deficient mice showed decreased glucose production and lower expression of the Phosphoenol pyruvate carboxykinase and Glucose 6-phosphatase genes. Lentivirus-mediated hepatic Eprap suppression decreased glucose levels and the expression of gluconeogenic genes in db/ db mice. We conclude that EPRAP regulates gluconeogenesis in hepatocytes and is associated with hyperglycemia in diabetic mice. Our data suggest that suppression of EPRAP could be a novel strategy for the treatment of diabetes.

Imaging mass spectroscopy delineates the thinned and thickened walls of intracranial aneurysms.

OBJECT: The wall thickness of intracranial aneurysms (IAs) is heterogeneous. Although thinning of the IA wall is thought to contribute to IA rupture, the underlying mechanism remains poorly understood. Recently, imaging mass spectroscopy (IMS) has been used to reveal the distribution of phospholipids in vascular diseases. To investigate the feature of phospholipid composition of IA walls, we conducted IMS in a rat model of experimentally induced IA. MATERIAL AND METHODS: IAs were surgically induced in 7-week-old male rats and analyzed by IMS in negative-ion mode. RESULTS: A molecule at m/z 885.5 was more abundant in the thickened wall than in the thinned wall (P = 0.03). Multiple-stage mass spectroscopy revealed the molecule to be phosphatidylinositol containing stearic acid and arachidonic acid (PI 18:0/20:4). Immunohistochemistry indicated that vascular smooth muscle cells (SMCs) in the thickened wall had dedifferentiated phenotypes. To investigate the relationship between accumulation of PI (18:0/20:4) and phenotypic changes in SMCs, we subjected primary mouse aortic SMCs to liquid chromatography-tandem mass spectrometry. Notably, dedifferentiated SMCs had 1.3-fold more PI (18:0/20:4) than partly differentiated SMCs. CONCLUSIONS: Our study demonstrated the heterogeneity in phospholipid composition of the aneurysmal walls using experimentally induced IAs. PI (18:0/20:4) accumulated at high levels in the thickened aneurysmal wall where synthetic dedifferentiated SMCs exist, suggesting that this phospholipid may be involved in the phenotypic switching of medial SMCs in the IA wall.

Deficiency in EP4 Receptor-Associated Protein Ameliorates Abnormal Anxiety-Like Behavior and Brain Inflammation in a Mouse Model of Alzheimer Disease.

Microglia are thought to play key roles in the progression of Alzheimer disease (AD). Overactivated microglia produce proinflammatory cytokines, such as tumor necrosis factor-α, which appear to contribute to disease progression. Previously, we reported that prostaglandin E2 type 4 receptor-associated protein (EPRAP) promotes microglial activation. We crossed human amyloid precursor protein transgenic mice from strain J20+/- onto an EPRAP-deficient background to determine the role of EPRAP in AD. Behavioral tests were performed in 5-month-old male J20+/-EPRAP+/+ and J20+/-EPRAP-/- mice. EPRAP deficiency reversed the reduced anxiety of J20+/- mice but did not affect hyperactivity. No differences in spatial memory were observed between J20+/-EPRAP+/+ and J20+/-EPRAP-/- mice. In comparison with J20+/-EPRAP+/+, J20+/-EPRAP-/- mice exhibited less microglial accumulation and reductions in the Cd68 and tumor necrosis factor-α mRNAs in the prefrontal cortex and hippocampus. No significant differences were found between the two types of mice in the amount of amyloid-ß 40 or 42 in the cortex and hippocampus. J20+/-EPRAP-/- mice reversed the reduced anxiety-like behavior and had reduced microglial activation compared with J20+/-EPRAP+/+ mice. Further research is required to identify the role of EPRAP in AD, but our results indicate that EPRAP may be related to behavioral and psychological symptoms of dementia and inflammation in patients with AD.

EP4 Receptor-Associated Protein in Macrophages Protects against Bleomycin-Induced Pulmonary Inflammation in Mice.

Excessive activation of inflammatory macrophages drives the pathogenesis of many chronic diseases. EP4 receptor-associated protein (EPRAP) has been identified as a novel, anti-inflammatory molecule in macrophages. In this study, we investigated the role of EPRAP using a murine model of bleomycin (BLM)-induced pulmonary inflammation. When compared with wild-type mice, EPRAP-deficient mice exhibited significantly higher mortality, and increased accumulation of macrophages and proinflammatory molecules in the lung 7 d post-BLM administration. Accordingly, the levels of phosphorylated p105, MEK1/2, and ERK1/2 were elevated in EPRAP-deficient alveolar macrophages following BLM administration. In contrast, macrophage-specific EPRAP overexpression decreased the production of proinflammatory cytokines and chemokines, suggesting that EPRAP in macrophages plays a key role in attenuating BLM-induced pulmonary inflammation. As EPRAP is phosphorylated after translation, we examined the role of posttranslational modifications in cellular inflammatory activation using mouse embryo fibroblasts (MEFs) expressing mutant EPRAP proteins. Expression of mutant EPRAP, in which serine-108 and serine-608 were replaced with alanine (EPRAP S108A/S608A), markedly suppressed TNF-α production in LPS-treated MEFs. Conversely, the serine phosphatase 2A (PP2A) inhibitor, cantharidic acid, increased LPS-induced TNF-α production in MEFs expressing wild-type EPRAP, but not in MEFs expressing EPRAP S108A/S608A. Immunoprecipitation analyses demonstrated that EPRAP associated with PP2A in both MEFs and alveolar macrophages from BLM-treated mice. Our data suggest that PP2A dephosphorylates EPRAP, which may be a crucial step in exertion of its anti-inflammatory properties. For these reasons, we believe the EPRAP-PP2A axis in macrophages holds the key to treating chronic inflammatory disorders.

Behavioral abnormalities and reduced norepinephrine in EP4 receptor-associated protein (EPRAP)-deficient mice.

EP4 receptor-associated protein (EPRAP) is a newly identified molecule that regulates macrophage activation. We recently demonstrated the presence of EPRAP in the mice brain; however, little is known about the function of EPRAP in this tissue. Therefore, we investigated the role of EPRAP in behavior and emotion using behavioral analysis in mice. In this study, we subjected EPRAP-deficient (KO) mice and wild-type C57BL/6 (WT) mice to a battery of behavioral tests. EPRAP-KO mice tended to have shorter latencies to fall in the wire hang test, but had normal neuromuscular strength. EPRAP-KO mice exhibited elevated startle responses and reduced pre-pulse inhibition. Compared with WT mice, EPRAP-KO mice increased depression-like behavior in the forced swim test. These abnormal behaviors partially mimic symptoms of depression, attention deficit hyperactivity disorder (ADHD) and schizophrenia. Methylphenidate administration increased locomotor activity less in EPRAP-KO mice than in WT mice. Finally, levels of norepinephrine were reduced in the EPRAP-KO mouse brain. These behavioral abnormalities in EPRAP-KO mice may result from the dysfunction of monoamines, in particular, norepinephrine. Our results suggest that EPRAP participates in the pathogenesis of various behavioral disorders.

EP4 Receptor-Associated Protein in Microglia Promotes Inflammation in the Brain.

Microglial cells play a key role in neuronal damage in neurodegenerative disorders. Overactivated microglia induce detrimental neurotoxic effects through the excess production of proinflammatory cytokines. However, the mechanisms of microglial activation are poorly understood. We focused on prostaglandin E2 type 4 receptor-associated protein (EPRAP), which suppresses macrophage activation. We demonstrated that EPRAP exists in microglia in the brain. Furthermore, EPRAP-deficient mice displayed less microglial accumulation, and intraperitoneal administration of lipopolysaccharide (LPS) led to reduced expression of tumor necrosis factor-α and monocyte chemoattractant protein-1 mRNA in the brains of EPRAP-deficient mice. Consistently, EPRAP-deficient microglia showed a marked decrease in the production of tumor necrosis factor-α and monocyte chemoattractant protein-1 induced by LPS treatment compared with wild-type controls. In addition, EPRAP deficiency decreased microglial activation and neuronal cell death induced by intraventricular injection of kainic acid. EPRAP deficiency impaired the LPS-induced phosphorylation of c-jun N-terminal kinase and p38 mitogen-activated protein kinase in microglia. The phosphorylation levels of mitogen-activated protein kinase kinase 4-which phosphorylates c-jun N-terminal kinase and p38 mitogen-activated protein kinase-were also decreased in EPRAP-deficient microglia after LPS stimulation. Although EPRAP in macrophages plays a role in the attenuation of inflammation, EPRAP promotes proinflammatory activation of microglia through mitogen-activated protein kinase kinase 4-mediated signaling and may be key to the deteriorating neuronal damage brought on by brain inflammation.

Plaque Ulcerations are Associated with Recurrence in Symptomatic Low-Grade Carotid Stenosis.

OBJECTIVE: Surgical indications for low-grade carotid stenosis have not yet been established. This study aimed to clarify the characteristics of low-grade carotid stenosis refractory to medical treatment. METHODS: We retrospectively analyzed 48 patients with symptomatic low-grade carotid stenosis (<50%). Recurrence was defined as an ipsilateral ischemic event in the symptomatic lesions during the follow-up period. Patient demographics and imaging findings were compared between the recurrence and nonrecurrence groups to investigate risk factors associated with medical treatment. RESULTS: The mean age was 74.1 (58-90 years), and the mean follow-up period was 35.4 months (2.0-97 months). Recurrence occurred in 15 of the symptomatic patients. Ulceration was significantly associated with recurrence under medical treatment (P = 0.001). The median time to recurrence was 26.1 months in patients with ulcers and 54.3 months in those without ulcers (P = 0.04). Pathological study with recurrence showed plaque rupture with multilayered lesions, indicating lesions refractory to medical treatment. CONCLUSIONS: In cases of low-grade carotid stenosis, lesions with ulcerations are likely refractory to medical therapy. Consideration of the indications for surgical treatment may be warranted for lesions with ulceration, even if the degree of stenosis is low.

A Review of Current Flow Diverters.

Flow diverter (FD) devices are new-generation stents placed in the parent artery at the aneurysmal neck to obstruct intra-aneurysmal blood flow, thus favoring intra-aneurysmal thrombosis. In Japan, about eight years have passed since health insurance approval was granted for FD devices, and FD placement to treat aneurysms has become widespread. Treatment indications have also been expanded with the introduction of novel devices. At present, three types of FD (Pipeline, FRED, and Surpass Streamline) are available in Japan. This report represents a compilation of available FD technologies and describes the current consensus on this treatment.

One-Stage Combined Open and Endovascular Treatment Using a Hybrid Operating Room is Safe and Effective for Distal Middle Cerebral Artery Aneurysms.

BACKGROUND: Aneurysms located in the distal middle cerebral artery (DMCA) are relatively rare and lack an established treatment strategy. For DMCA aneurysms, we performed a one-stage combined procedure of endovascular parent artery occlusion (PAO) with coils and superficial temporal artery to middle cerebral artery (STA-MCA) bypass in a hybrid operating room (HOR). The aim of this study was to evaluate the safety and efficacy of this procedure. METHODS: Cases of unruptured DMCA aneurysms treated with the one-stage combined PAO and STA-MCA bypass in HOR were retrospectively examined, and patients' and aneurysmal backgrounds, surgical procedures, and treatment outcomes were analyzed. RESULTS: Six patients were included in the study. The average maximum diameter of the aneurysms was 14.4 mm. One aneurysm was located at M2 and five at M3. All aneurysms had a fusiform shape. No cases were associated with infection, trauma, or malignant tumors. In all 6 cases, the combined PAO and STA-MCA bypass was successfully completed. No postoperative hemorrhagic complications occurred. A symptomatic ischemic complication occurred in 1 case whose symptom disappeared in a week. Three months after surgery, complete obliteration of the aneurysm and patency of the bypass was confirmed in all cases. CONCLUSIONS: The one-stage combined PAO and STA-MCA bypass in the HOR is safe and effective for DMCA aneurysms, potentially serving as a treatment option for this complex aneurysm.

Vitamin D deficiency promotes intracranial aneurysm rupture.

Intracranial aneurysm rupture causes severe disability and high mortality. Epidemiological studies show a strong association between decreased vitamin D levels and an increase in aneurysm rupture. However, the causality and mechanism remain largely unknown. In this study, we tested whether vitamin D deficiency promotes aneurysm rupture and examined the underlying mechanism for the protective role of vitamin D against the development of aneurysm rupture utilizing a mouse model of intracranial aneurysm. Mice consuming a vitamin D-deficient diet had a higher rupture rate than mice with a regular diet. Vitamin D deficiency increased proinflammatory cytokines in the cerebral arteries. Concurrently, vitamin D receptor knockout mice had a higher rupture rate than the corresponding wild-type littermates. The vitamin D receptors on endothelial and vascular smooth muscle cells, but not on hematopoietic cells, mediated the effect of aneurysm rupture. Our results establish that vitamin D protects against the development of aneurysmal rupture through the vitamin D receptors on vascular endothelial and smooth muscle cells. Vitamin D supplementation may be a viable pharmacologic therapy for preventing aneurysm rupture.

Hemodynamic differences determining rupture and non-rupture in middle cerebral aneurysms after growth.

BACKGROUND AND PURPOSE: Intracranial aneurysm growth is a significant risk factor for rupture; however, a few aneurysms remain unruptured for long periods, even after growth. Here, we identified hemodynamic features associated with aneurysmal rupture after growth. MATERIALS AND METHODS: We analyzed nine middle cerebral artery aneurysms that grew during the follow-up period using computational fluid dynamics analysis. Growth patterns of the middle cerebral artery aneurysms were divided into homothetic growth (Type 1), de novo bleb formation (Type 2), and bleb enlargement (Type 3). Hemodynamic parameters of the four ruptured aneurysms after growth were compared with those of the five unruptured aneurysms. RESULTS: Among nine aneurysms (78%), seven were Type 1, one was Type 2, and one was Type 3. Three (43%) Type 1 aneurysms ruptured after growth. Maximum oscillatory shear index after aneurysmal growth was significantly higher in ruptured Type 1 cases than in unruptured Type 1 cases (ruptured vs. unruptured: 0.455 ± 0.007 vs. 0.319 ± 0.042, p = 0.003). In Type 1 cases, a newly emerged high-oscillatory shear index area was frequently associated with rupture, indicating a rupture point. Aneurysm growth was observed in the direction of the high-pressure difference area before enlargement. In Types 2 and 3 aneurysms, the maximum oscillatory shear index decreased slightly, however, the pressure difference values remain unchanged. In Type 3 aneruysm, the maximum OSI and PD values remained unchanged. CONCLUSIONS: This study suggests that hemodynamic variations and growth pattern changes are crucial in rupture risk determination using computational fluid dynamics analysis. High-pressure difference areas may predict aneurysm enlargement direction. Additionally, high maximum oscillatory shear index values after enlargement in cases with homothetic growth patterns were potential rupture risk factors.

Impact of Morphological Factors on the Future Growth of Unruptured Posterior Communicating Artery Aneurysms.

BACKGROUND: No previous study has established the factors associated with intracranial aneurysm growth using imaging data obtained before the appearance of morphological changes. Therefore, we investigated the factors related to future aneurysm growth in posterior communicating artery (Pcom) aneurysms. METHODS: Using a longitudinal database of intracranial aneurysm cases, we reviewed the findings for consecutive patients with unruptured Pcom aneurysms admitted to our institute from 2012 to 2021. Magnetic resonance images obtained over time were used to evaluate aneurysm growth. Aneurysms showing growth over time (group G) and unchanged aneurysms (group U) were compared in terms of background data and morphological factors. RESULTS: 93 Pcom aneurysms (group G: 25 aneurysms, 25%; group U: 68 aneurysms, 75%) were eligible for the present study. Six aneurysm rupture events occurred in group G (24%). Among morphological factors, Pcom diameter (1.2 ± 0.3 mm vs. 0.8 ± 0.7 mm, P < 0.01), bleb formation (group G: 39% vs. group U: 10%; odds ratio, 5.6; P = 0.01), and the lateral projection of the dome (group G: 52% vs. group U: 13%; odds ratio, 3.2; P = 0.023) were significantly different between the 2 groups. The sensitivity and specificity of a cutoff Pcom diameter of 0.73 mm for predicting enlargement were 96% and 53%, respectively. CONCLUSIONS: Pcom diameter, bleb formation, and lateral dome projection were associated with growth of Pcom aneurysms. Aneurysms with these risk factors require careful follow-up imaging, which may facilitate early detection of aneurysm growth and prevention of rupture through therapeutic interventions.

Aspect Ratio Is Associated with Recanalization after Coiling of Unruptured Intracranial Aneurysms.

The rate of recanalization after coil embolization for unruptured intracranial aneurysms (UIAs) is reported to occur around 11.3%-49%. This study aims to investigate the factors that influence the recanalization after coil embolization for UIAs in our institution. We retrospectively investigated 307 UIAs in 296 patients treated at our institution between April 2004 and December 2016. The stent-used cases were excluded. Cerebral angiography and 3D time-of-flight magnetic resonance angiography (TOF MRA) were used for evaluation of the postoperative occlusion status. Volume embolization ratio (VER), aneurysmal size, neck width, and aspect ratio (AR) were compared between the recanalized and non-recanalized groups. The mean follow-up period ranged from 6 to 172 months (mean: 79.0 ± 39.8 months). Recanalization was noted in 78 (25.4%) aneurysms, and 19 (6.2%) aneurysms required retreatment. There was no aneurysmal rupture during the follow-up period. Univariate analysis showed that the aneurysm size (p < 0.001), neck width (p < 0.001), AR (p = 0.003), and VER (p = 0.012) were associated with recanalization. Multivariate logistic regression analysis showed that the AR (p =0.004) and VER (p =0.015) were significant predictors of recanalization. To summarize, a higher AR and a lower VER could lead to recanalization after coil embolization of UIAs. Careful follow-up is required for coiled aneurysms with these features.

Coronary artery aneurysms of unknown origin in a 14-year-old girl.

The case of a 14-year-old girl with acute myocardial infarction due to coronary artery aneurysms (CAAs) of unknown origin, which resembled coronary artery lesions caused by Kawasaki disease, is reported. She was transferred to our hospital due to chest pain with ST-T elevation. She had no history of Kawasaki disease. On the first admission, she was misdiagnosed with acute myocarditis. Then, 54 days later, she experienced chest pain with exertional dyspnea. Her electrocardiogram showed negative T waves in the chest leads. A CAA of the left coronary artery was suspected on two-dimensional echocardiography. Coronary angiograms showed 90% stenosis and multiple CAAs of the left anterior descending artery and the bifurcation of the left coronary artery. Both the right coronary artery and left circumflex artery were occluded. A left ventriculogram showed dyskinesis and an aneurysm at the apex. She underwent triple-vessel coronary artery bypass grafting, and her symptoms improved. In addition, an intracranial aneurysm was also found on cerebral angiography. There were no specific laboratory findings other than SS-A antibodies. It was suspected that the weakness of the vessels was related to the disease. It may have been a different disease that was never previously detected, but her CAAs were Kawasaki-like CAAs.