Efficacy of intentional undersized thoracic endovascular repair for Stanford type B aortic dissection.

OBJECTIVE: Thoracic endovascular aneurysm repair (TEVAR) is widely used for the treatment of aortic dissection. Endograft oversizing is a risk factor for stent graft-induced new entry tears and retrograde type A aortic dissection. However, there is no clear consensus on the optimal graft size selection for Stanford type B acute or subacute aortic dissection (TBAD). Herein, we examined the safety and efficacy of TEVAR using an intentionally undersized endograft to treat TBAD. METHODS: This retrospective chart review study included 82 patients who underwent TEVAR for acute or subacute Stanford TBAD between 2015 and 2022. We measured the true lumen diameter just distal to the subclavian artery and opted for a stent graft of the same diameter. In instances where deformation resulting from false lumen pressure displacement was pronounced, we measured the diameter at the site just proximal to the subclavian artery. Patients' characteristics, procedural, in-hospital, and follow-up data, and aortic remodeling were analyzed. The aortic diameter was analyzed using one-way analysis of variance followed by Dunnett's test. Survival and freedom from reintervention were estimated using Kaplan-Meier curves. RESULTS: The follow-up rate was 98.4%. The mean age was 58.3 ± 12.3 years, and 76 were men (92.7%). The mean diameters of the stent graft and native proximal landing zone were 30.9 ± 3.2 mm and 30.8 ± 3.0 mm, respectively. The oversize rate of the stent graft in relation to the native proximal aortic diameter was 0.3% ± 4.7%. In-hospital mortality was observed in one patient, retrograde type A aortic dissection in one patient, distal stent graft-induced new entry tear in zero patients, and type 1a endoleak in 22 patients (26.8%). Type 1a endoleaks, characterized by antegrade false lumen blood flow originating from the primary entry, in 12 patients spontaneously disappeared within 1 year of follow-up. According to aortic remodeling, 59 patients (86.8%) achieved complete aortic remodeling at the aortic arch level and 51 (75.0%) at the eighth thoracic vertebral level. The diameters of the aortic arch and descending aorta were significantly reduced compared with the postoperative measurements (P <.001). Survival rates were 97.5% and 93.6% at 1 and 3 years, respectively. Freedom from reintervention was 84.7% and 84.7% at 1 and 3 years, respectively. CONCLUSIONS: Intentionally undersized TEVAR was safe and achieved acceptable aortic remodeling despite a high rate of type 1a endoleaks. A type 1a endoleak was acceptable as it primarily diminished during the mid-term follow-up.

Molecular Mechanisms of IL18 in Disease.

Interleukin 18 (IL18) was originally identified as an inflammation-induced cytokine that is secreted by immune cells. An increasing number of studies have focused on its non-immunological functions, with demonstrated functions for IL18 in energy homeostasis and neural stability. IL18 is reportedly required for lipid metabolism in the liver and brown adipose tissue. Furthermore, IL18 (Il18) deficiency in mice leads to mitochondrial dysfunction in hippocampal cells, resulting in depressive-like symptoms and cognitive impairment. Microarray analyses of Il18-/- mice have revealed a set of genes with differential expression in liver, brown adipose tissue, and brain; however, the impact of IL18 deficiency in these tissues remains uncertain. In this review article, we discuss these genes, with a focus on their relationships with the phenotypic disease traits of Il18-/- mice.

[Transient Left Ventricular Dysfunction after Giant Coronary Aneurysm Resection and Repair of Coronary Arteriovenous Fistula with Coronary Artery Bypass Grafting:Report of a Case].

Coronary artery aneurysm with coronary arteriovenous fistula is a relatively rare clinical setting. We report a surgical case of a 69-year-old male with a giant coronary artery aneurysm, finding coronary arteriovenous fistula on computed tomography (CT). We performed complete aneurysm excision and coronary artery bypass grafting with the left internal thoracic artery to the posterolateral branch. The fistula was located between the giant aneurysm on the circumflex artery and the coronary vein close to the coronary sinus, closed with aneurysm sac. The postoperative CT found no residual aneurysm and fistula. However, the great cardiac vein was thrombosed, and the impeded venous flow by the thrombus seemed to reduce the left ventricular ejection fraction (LVEF). Four months after the operation, the LVEF improved to the preoperative level.

Direct Comparison of Therapeutic Effects on Diabetic Polyneuropathy between Transplantation of Dental Pulp Stem Cells and Administration of Dental Pulp Stem Cell-Secreted Factors.

Stem cell transplantation is a potential novel therapy for diabetic polyneuropathy. Dental pulp stem cells (DPSCs) are attractive stem cell sources because DPSCs can be isolated from extracted teeth and cryopreserved while retaining viability. In this study, we directly compared the efficacy of the transplantation of DPSCs and the administration of the secreted factors from DPSCs (DPSC-SFs) on diabetic polyneuropathy. Eight weeks after streptozotocin injection, DPSCs (1.0 × 106 cells/rat) or DPSC-SFs (1.0 mL/rat) were administered into the unilateral hindlimb skeletal muscles of diabetic Sprague-Dawley rats. DPSC transplantation and DPSC-SF administration did not affect blood glucose levels and body weights in the diabetic rats. Both DPSC transplantation and DPSC-SF administration significantly ameliorated sciatic nerve conduction velocity and sciatic nerve blood flow, accompanied by increases in muscle bundle size, vascular density in the skeletal muscles and intraepidermal nerve fiber density in the diabetic rats, while there was no difference between the results for DPSCs and DPSC-SFs. These results suggest that the efficacy of both DPSC transplantation and DPSC-SF administration for diabetic polyneuropathy four weeks after transplantation/administration was mainly due to the multiple secretomes secreted from transplanted DPSCs or directly injected DPSC-SFs in the early phase of transplantation/administration.

[Cystic Myxoma which Obstructed the Mitral Valve Orifice;Report of a Case].

A 44-year-old male presented to our hospital with exertional dyspnea. Transthoracic echocardiography revealed a large cystic mass in the left atrium obstructing the mitral valve orifice. Transesophageal echocardiography during emergency operation showed a large cystic mass along with a solid part near the stalk. The mass was resected en bloc including the margin of the left atrium around the stalk. His hemodynamics improved immediately after the operation and the patient was discharged shortly with uneventful postoperative course. While intra cardiac cystic mass has some possible pathologies including malignancy, pathological examination of this tumor revealed a myxoma with large hematoma which had probably grown up rapidly. This tumor was successfully eradicated under the guide of both transthoracic and transesophageal echocardiography.

Dysfunction of Arabidopsis MACPF domain protein activates programmed cell death via tryptophan metabolism in MAMP-triggered immunity.

Plant immune responses triggered upon recognition of microbe-associated molecular patterns (MAMPs) typically restrict pathogen growth without a host cell death response. We isolated two Arabidopsis mutants, derived from accession Col-0, that activated cell death upon inoculation with nonadapted fungal pathogens. Notably, the mutants triggered cell death also when treated with bacterial MAMPs such as flg22. Positional cloning identified NSL1 (Necrotic Spotted Lesion 1) as a responsible gene for the phenotype of the two mutants, whereas nsl1 mutations of the accession No-0 resulted in necrotic lesion formation without pathogen inoculation. NSL1 encodes a protein of unknown function containing a putative membrane-attack complex/perforin (MACPF) domain. The application of flg22 increased salicylic acid (SA) accumulation in the nsl1 plants derived from Col-0, while depletion of isochorismate synthase 1 repressed flg22-inducible lesion formation, indicating that elevated SA is needed for the cell death response. nsl1 plants of Col-0 responded to flg22 treatment with an RBOHD-dependent oxidative burst, but this response was dispensable for the nsl1-dependent cell death. Surprisingly, loss-of-function mutations in PEN2, involved in the metabolism of tryptophan (Trp)-derived indole glucosinolates, suppressed the flg22-induced and nsl1-dependent cell death. Moreover, the increased accumulation of SA in the nsl1 plants was abrogated by blocking Trp-derived secondary metabolite biosynthesis, whereas the nsl1-dependent hyperaccumulation of PEN2-dependent compounds was unaffected when the SA biosynthesis pathway was blocked. Collectively, these findings suggest that MAMP-triggered immunity activates a genetically programmed cell death in the absence of the functional MACPF domain protein NSL1 via Trp-derived secondary metabolite-mediated activation of the SA pathway.

Anatomical features of the aortic root in aortic stenosis and a novel approach for transcatheter aortic valve implantation.

A narrow and calcified sinotubular junction (STJ) represents a risk for ascending aortic dissection after balloon-expandable transcatheter aortic valve implantation (TAVI). The aim of this study was to assess computed tomography (CT)-based aortic root morphology in patients with aortic stenosis (AS), and to evaluate the feasibility of a two-step inflation technique that we devised for TAVI using the SAPIEN 3 in patients with a narrow and calcified STJ. We retrospectively analyzed the STJ diameter (STJD) as well the as aortic annulus diameter (AAD) and STJ calcification using CT imaging in 412 patients undergoing TAVI. We defined a "narrow STJ" as a minimum STJD that was smaller than the diameter corresponding to a 10% oversized annulus area, and a "calcified STJ" as an STJ calcification angle > 90°. A "narrow and calcified STJ" was identified in 54 patients (13.1%) of patients. Among them, we performed TAVI using the two-step inflation technique with SAPIEN 3 in 20 patients and compared with 11 patients that underwent the conventional inflation procedure. Two-step inflation was successfully performed without ascending aortic dissection in all 20 patients. The effective orifice area index at discharge in these 20 patients was similar to that in 11 patients who underwent the conventional inflation procedure for a "narrow and calcified STJ" [1.40 (1.20-1.51) vs. 1.33 (1.18-1.41) cm2/m2, p = 0.23]. Although further assessment is required, the two-step inflation technique with the SAPIEN 3 is feasible for a narrow and calcified STJ.

Simultaneous Transcatheter Intervention for Coarctation of the Aorta and Bicuspid Aortic Valve.

Coarctation of the aorta (CoA) is a relatively common congenital heart anomaly, and bicuspid aortic valve (BAV) is a common congenital heart disease that coexists with CoA. In larger children and adults with CoA, transcatheter intervention has gained acceptance, but for surgical high-risk patients with aortic stenosis, the use of transcatheter aortic valve implantation (TAVI) has been established. Recently, although favorable data have been reported for TAVI when treating BAV, simultaneous transcatheter intervention for CoA and BAV will prove to be a challenge because of the unique anatomy involved requires multiple procedural steps and also has problems of site access. Herein is reported a successful case of simultaneous thoracic endovascular repair (TEVAR) for CoA and transfemoral TAVI for congenital BAV dysfunction. A 62-year-old male with CoA and congenital BAV with severe aortic stenosis and aortic regurgitation had NYHA class IV heart failure symptoms. Because of the patient's extremely poor left ventricular function, the authors' heart team decided to perform simultaneous TEVAR for CoA and transfemoral TAVI. After deployment of a 32 mm stent graft, a 29 mm SAPIEN 3 valve (Edwards Lifesciences, Irvine, CA, USA) was successfully deployed through the stent graft. This resulted in no significant pressure gradient within the aorta, and no aortic regurgitation. Video 1: Cineradiography showing delivery of the Edwards Commander delivery system through the stent graft. Video 2: Final aortography showing no residual aortic regurgitation.

[Ascending Aorta Replacement and Extended Myectomy for Acute Aortic Dissection and Coexistent Hypertrophic Obstructive Cardiomyopathy;Report of a Case].

Emergent ascending aortic replacement and extended myectomy were performed in a woman with acute aortic dissection who was aged 63 years. Preoperative transthoracic echocardiography performed in the intensive care unit showed only slight left ventricular outflow tract (LVOT) obstruction, but intraoperative transesophageal echocardiography after induction of anesthesia revealed pericardial effusion, systolic anterior motion(SAM), and associated mitral regurgitation(MR). Perioperative SAM and MR are sometimes facilitated under various hemodynamic conditions, but in this case, the left ventricular wall was thick and LVOT appeared to be obstructive by a hypertrophied septum. Structural hypertrophic obstructive cardiomyopathy (HOCM) was diagnosed, and septal myectomy and aortic replacement were performed. After ascending aortic replacement and simultaneous extended myectomy with resection of abnormal band, weaning from cardiopulmonary bypass was smooth without SAM and MR. The patient was discharged from hospital 24 days postoperatively with no major complications. Extended myectomy should be considered if structural HOCM is diagnosed, even when aortic replacement for the dissected aorta is the primary procedure.

[Surgical Embolectomy for Acute Massive Pulmonary Thromboembolism Requiring Percutaneous Cardiopulmonary Support after Thoracoabdominal Aorta Replacement].

A 48-year-old man was admitted to our hospital and underwent thoracoabdominal aorta replacement. Eight days postoperatively, he developed severe dyspnea and transient drop in blood pressure suddenly following walk rehabilitation. Contrast-enhanced computed tomography showed thrombi in the bilateral main pulmonary artery. Respiratory failure and unstable hemodynamics developed, which required percutaneous cardiopulmonary support (PCPS). Because catheter embolectomy and thrombolytic therapy via pulmonary artery catheter were not effective, surgical thrombectomy was performed. PCPS was successfully removed on the following day. The patient was extubated on postoperative day 10 and discharged without complications on day 46 following rehabilitation. It is important to save a critically ill patient with acute pulmonary embolism requiring PCPS, and surgical treatment should be performed without delay in such patients.

Dysfunction of mitochondria and deformed gap junctions in the heart of IL-18-deficient mice.

Interleukin-18 (IL-18) was discovered as an interferon-γ-inducing factor and has been regarded as a proinflammatory cytokine. However, IL-18 is ubiquitously expressed both in immune/inflammatory cells and in nonimmune cells, and its biological roles have not been sufficiently elucidated. Here, we demonstrate that IL-18-deficient [IL-18 knockout (KO)] mice have heart abnormalities that may be related to impaired autophagy. In endurance running tests, IL-18KO mice ran significantly shorter distances compared with wild-type (WT) mice. Echocardiographs indicated disability in the systolic and diastolic functions of the IL-18KO mouse heart. Immunostaining of connexin 43 showed heterogeneous localization of gap junctions in the lateral membranes of the IL-18KO cardiac myocytes. Western blotting analysis revealed decreased phosphorylated connexin 43 in the IL-18KO heart. Electron microscopy revealed unusual localization of intercalated disks, swollen or damaged mitochondria, and broad, indistinct Z-lines in the IL-18KO heart. In accordance with the morphological observation, mitochondrial respiratory function, including that of complexes I and IV, was impaired, and production of reactive oxygen species was augmented in IL-18KO hearts. Notably, levels of LC3-II were markedly lower in the IL-18KO hearts than in WT hearts. In the culture of cardiac myocytes of IL-18KO neonates, exogenous IL-18 upregulated LC3-II and increased the number of intact mitochondria with high mitochondrial membrane potential. These results indicated that IL-18 has roles apart from those as a proinflammatory cytokine in cardiac myocytes and suggested that IL-18 contributes to the homeostatic maintenance of mitochondrial function and gap-junction turnover in cardiac myocytes, possibly by upregulating autophagy.

Functional analysis of differences in transcriptional activity conferred by genetic variants in the 5' flanking region of the IL12RB2 gene.

Interleukin 12 receptor ß chain (IL12RB2) is a crucial regulatory factor involved in cell-mediated immune responses, and genetic variants of the gene encoding IL12RB2 are associated with susceptibility to various immune-related diseases. We previously demonstrated that haplotypes with single nucleotide polymorphisms (SNPs) in the 5' flanking region of IL12RB2, including -1035A>G (rs3762315) and -1023A>G (rs3762316), affect the expression of IL12RB2, thereby altering susceptibility to leprosy and periodontal diseases. In the present study, we identified transcription factors associated with the haplotype-specific transcriptional activity of IL12RB2 in T cells and NK cells. The -1023G polymorphism was found to create a consensus binding site for the transcription factor activating protein (AP)-1, and enzyme-linked immunosorbent assay (ELISA)-based binding assays showed that these SNPs enhanced AP-1 binding to this region. In reporter assays, suppression of JunB expression using siRNA eliminated differences in the -1035G/-1023G and -1035A/-1023A regions containing IL12RB2 promoter activity in Jurkat T cells and NK3.3 cells. These results suggested that the -1035/-1023 polymorphisms created differential binding affinities for JunB that could lead to differential IL12RB2 expression. Moreover, the -1035G and -1035A alleles formed binding sites for GATA-3 and myocyte enhancer factor-2 (MEF-2), respectively. Our data indicated that in addition to JunB, the SNP at -1035/-1023 influenced GATA-3 and MEF-2 binding affinity, potentially altering IL12RB2 transcriptional activity. These findings confirm the effects of rs3762315 and rs3762316 on IL12RB2 transcription. These genetic variants may alter cellular activation of T cells and NK cells and modify cell-mediated immune responses.

Estrogen decreases the expression of claudin-5 in vascular endothelial cells in the murine uterus.

Vascular endothelial (VE)-cadherin and claudin-5 are major components of the adherens and tight junctions of vascular endothelial cells, respectively, and decreases in their expression are associated with increases in endothelial paracellular permeability. In the uterus, estrogen induces endometrial edema. However, the in vivo effect of estrogen on endothelial paracellular permeability is unknown. Therefore, we studied the expression of VE-cadherin and claudin-5 in vascular endothelial cells in murine uteri stimulated by estrogen or progesterone. Ovariectomized mature mice were injected with estradiol-17ß (1 µg/mouse) or progesterone (1 mg/mouse) at intervals of 24 hours for 6 days. The frozen transverse sections of the uteri of these mice and untreated mice were stained for CD31 (vascular endothelial cell marker) plus VE-cadherin or claudin-5 using a double-immunofluorescence method. Then, the percentages of VE-cadherin- or claudin-5-positive vessels among CD31-positive vessels were examined in the uterine endometria. VE-cadherin and claudin-5 were expressed in most CD31-positive vessels in the endometria of the untreated mice. Progesterone did not affect the expression of both VE-cadherin and claudin-5 and estradiol-17ß also did not affect the VE-cadherin expression, but estradiol-17ß significantly decreased the claudin-5 expression. This decreasing effect of estradiol-17ß was detected from 24 hours later when the water content per a uterus significantly increased. The present study indicates that estrogen, but not progesterone, decreases the expression of claudin-5 in vascular endothelial cells in the murine uterine endometrium from 24 hours later, suggesting that the decrease in the claudin-5 expression contributes to the endometrial edema late after the estrogen stimulation.

Decreased expression of VE-cadherin and claudin-5 and increased phosphorylation of VE-cadherin in vascular endothelium in nasal polyps.

VE-cadherin and claudin-5 are major components of adherens and tight junctions of vascular endothelial cells and a decrease in their expression and an increase in the tyrosine-phosphorylation of VE-cadherin are associated with an increase in endothelial paracellular permeability. To clarify the mechanism underlying the development of edema in nasal polyps, we studied these molecules in polyp microvessels. Normal inferior turbinate mucosal tissues and nasal polyps from patients treated with or without glucocorticoid were stained for VE-cadherin or claudin-5 and CD31 by a double-immunofluorescence method and the immunofluorescence intensities were graded 1-3 with increasing intensity. To correct for differences in fluorescence intensity attributable to a different endothelial area being exposed in a section or to the thickness of a section, the relative immunofluorescence intensity was estimated by dividing the grade of VE-cadherin or claudin-5 by that of CD31 in each microvessel. Tyrosine-phosphorylation of VE-cadherin was examined by Western blot analysis. The relative intensities of VE-cadherin and claudin-5 in the CD31-positive microvessels significantly decreased in the following order; inferior turbinate mucosa, treated polyps and untreated polyps. The ratio of tyrosine-phosphorylated VE-cadherin to VE-cadherin was significantly higher in untreated polyps than in the inferior turbinate mucosa and treated polyps, between which no significant difference in the ratio was seen. Thus, in nasal polyps, the barrier function of endothelial adherens and tight junctions is weakened, although glucocorticoid treatment improves this weakened barrier function.

Three-dimensional quantitative ultrasound for detecting lymph node metastases.

PURPOSE: Detection of metastases in lymph nodes (LNs) is critical for cancer management. Conventional histological methods may miss metastatic foci. To date, no practical means of evaluating the entire LN volume exists. The aim of this study was to develop fast, reliable, operator-independent, high-frequency, quantitative ultrasound (QUS) methods for evaluating LNs over their entire volume to effectively detect LN metastases. METHODS: We scanned freshly excised LNs at 26 MHz and digitally acquired echo-signal data over the entire three-dimensional (3D) volume. A total of 146 LNs of colorectal, 26 LNs of gastric, and 118 LNs of breast cancer patients were enrolled. We step-sectioned LNs at 50-µm intervals and later compared them with 13 QUS estimates associated with tissue microstructure. Linear-discriminant analysis classified LNs as metastatic or nonmetastatic, and we computed areas (Az) under receiver-operator characteristic curves to assess classification performance. The QUS estimates and cancer probability values derived from discriminant analysis were depicted in 3D images for comparison with 3D histology. RESULTS: Of 146 LNs of colorectal cancer patients, 23 were metastatic; Az = 0.952 ± 0.021 (95% confidence interval [CI]: 0.911-0.993); sensitivity = 91.3% (specificity = 87.0%); and sensitivity = 100% (specificity = 67.5%). Of 26 LNs of gastric cancer patients, five were metastatic; Az = 0.962 ± 0.039 (95% CI: 0.807-1.000); sensitivity = 100% (specificity = 95.3%). A total of 17 of 118 LNs of breast cancer patients were metastatic; Az = 0.833 ± 0.047 (95% CI: 0.741-0.926); sensitivity = 88.2% (specificity = 62.5%); sensitivity = 100% (specificity = 50.5%). 3D cancer probability images showed good correlation with 3D histology. CONCLUSIONS: These results suggest that operator- and system-independent QUS methods allow reliable entire-volume LN evaluation for detecting metastases. 3D cancer probability images can help pathologists identify metastatic foci that could be missed using conventional methods.

Claudin-2-deficient mice are defective in the leaky and cation-selective paracellular permeability properties of renal proximal tubules.

Claudin-2 is highly expressed in tight junctions of mouse renal proximal tubules, which possess a leaky epithelium whose unique permeability properties underlie their high rate of NaCl reabsorption. To investigate the role of claudin-2 in paracellular NaCl transport in this nephron segment, we generated knockout mice lacking claudin-2 (Cldn2(-/-)). The Cldn2(-/-) mice displayed normal appearance, activity, growth, and behavior. Light microscopy revealed no gross histological abnormalities in the Cldn2(-/-) kidney. Ultrathin section and freeze-fracture replica electron microscopy revealed that, similar to those of wild types, the proximal tubules of Cldn2(-/-) mice were characterized by poorly developed tight junctions with one or two continuous tight junction strands. In contrast, studies in isolated, perfused S2 segments of proximal tubules showed that net transepithelial reabsorption of Na(+), Cl(-), and water was significantly decreased in Cldn2(-/-) mice and that there was an increase in paracellular shunt resistance without affecting the apical or basolateral membrane resistances. Moreover, deletion of claudin-2 caused a loss of cation (Na(+)) selectivity and therefore relative anion (Cl(-)) selectivity in the proximal tubule paracellular pathway. With free access to water and food, fractional Na(+) and Cl(-) excretions in Cldn2(-/-) mice were similar to those in wild types, but both were greater in Cldn2(-/-) mice after i.v. administration of 2% NaCl. We conclude that claudin-2 constitutes leaky and cation (Na(+))-selective paracellular channels within tight junctions of mouse proximal tubules.

Radixin deficiency causes conjugated hyperbilirubinemia with loss of Mrp2 from bile canalicular membranes.

The ezrin-radixin-moesin (ERM) family of proteins crosslink actin filaments and integral membrane proteins. Radixin (encoded by Rdx) is the dominant ERM protein in the liver of wildtype mice and is concentrated at bile canalicular membranes (BCMs). Here we show that Rdx(-/-) mice are normal at birth, but their serum concentrations of conjugated bilirubin begin to increase gradually around 4 weeks, and they show mild liver injury after 8 weeks. This phenotype is similar to human conjugated hyperbilirubinemia in Dubin-Johnson syndrome, which is caused by mutations in the multidrug resistance protein 2 (MRP2, gene symbol ABCC2), although this syndrome is not associated with overt liver injury. In wildtype mice, Mrp2 concentrates at BCMs to secrete conjugated bilirubin into bile. In the BCMs of Rdx(-/-) mice, Mrp2 is decreased compared with other BCM proteins such as dipeptidyl peptidase IV (CD26) and P-glycoproteins. In vitro binding studies show that radixin associates directly with the carboxy-terminal cytoplasmic domain of human MRP2. These findings indicate that radixin is required for secretion of conjugated bilirubin through its support of Mrp2 localization at BCMs.

[Thoraco-abdominal aortic replacement in chronic phase in a patient with temporary paraplegia after Stanford B acute dissection].

A 42-year-old man underwent was performed with thoraco-abdominal aneurysm replacement accompaniedy with reconstruction of abdominal branches and intercostal arteries. Eighteen months before, he had suffered from Stanford already been cured with paraplegia on being type B acute aortic dissection combined with paraplegia. When paraplegia had been occurred, cerebrospinal fluid drainage was had been performed promptly, and 4 days later, neurologic deficit was disappeared in 1 day. During the thoraco-abdominal aortic operation, cerebrospinal fluid drainage was performed done again. After the operation, paraplegia did was not occurred and he did not feel somewhat wrong with his legs. He was discharged from hospital on foot by himself. This case showed the efficacy of cerebral spinal fluid drainage for not only both with the prevention but also and treatment of paraplegia.

[Endovascular repair for coarctation of the aorta in an adult].

A 27-year-old woman with Turner's syndrome who underwent successful endovascular treatment for coarctation of the aorta is presented. She was admitted to our hospital complaining of upper extremity hypertension. Computed tomography revealed discrete stenosis of the proximal descending aorta and developed collateral circulation. After endovascular repair with a balloon expandable stent, her transcoarctation gradient fell from 44 mmHg preoperatively to less than 10 mmHg. She was discharged with no complications on the 7th postoperative day. Coarctation of the aorta in an adult patient could be safely and effectively managed by endovascular treatment.

Detection of left coronary ostial obstruction during transcatheter aortic valve replacement by coronary flow velocity measurement in the left main trunk by intraoperative transesophageal echocardiography.

BACKGROUND: Coronary obstruction is a rare but catastrophic complication of transcatheter aortic valve replacement (TAVR) and occurs mostly at the left coronary artery (LCA) ostium. However, some patients do not show any clinical findings, and thus, its detection is sometimes difficult. The peak diastolic flow velocity in left main coronary artery (LM) was reportedly increased in significant stenosis lesions. We evaluated the effectiveness of measuring blood flow velocities in LM by transesophageal echocardiography (TEE) for the detection of LCA ostial obstruction during a TAVR procedure. METHODS: A total of 1105 consecutive patients who underwent TAVR in Sendai Kousei Hospital between September 2014 and December 2020 were enrolled. The LM blood flow velocity was measured at pre- and post-valve implantation. RESULTS: Among the 1105 patients, 9 had LCA ostial obstruction. The peak LM blood flow velocity at post-TAVR [0.90 (0.39-1.15) vs. 0.37 (0.28-0.50) m/s; p = 0.0046) was significantly higher in 9 patients who had LCA ostial obstruction, compared with the remaining 1096 patients who had not (controls), although no significant difference was observed before the TAVR procedures between the two groups. The post- to pre-TAVR LM flow velocity ratio [2.26 (1.31-3.42) vs. 1.06 (0.82-1.36); p = 0.0030] was also significantly higher in patients with LCA obstruction, compared to the controls. Furthermore, the post- to pre-TAVR LM blood flow velocity ratio was >2.0 in all six hemodynamically stable patients with LCA obstruction, whereas <2.0 in all three patients with LCA obstruction who showed hemodynamic collapse at post-TAVR procedure. CONCLUSION: Coronary blood flow velocity in LM significantly increased in hemodynamically stable LCA obstruction patients. The intraprocedural TEE measurement of the LM flow velocities would be potentially useful to detect asymptomatic and hemodynamically stable LCA ostial obstruction.