[A Successful Surgical Treatment of Hemolytic Anemia Caused by Aortic Valve Perivalvular Leakage and Severely Kinked Elephant Trunk:Report of a Case].

Both perivalvular leakage and kinked prosthetic graft may cause hemolysis. A 72-year-old man was refereed to our hospital because of hemolytic anemia. He has past histories of total aortic arch replacement and repeat aortic valve replacement for aortic aneurysm and prosthetic valve endocarditis. Pre-operative examinations demonstrated aortic valve perivalvular leakage and severe graft kinking of the elephant trunk. Repeat aortic valve replacement and axillo-femoral bypass were performed successfully. Hemolysis got better after the operation and the patient discharged home in stable condition.

Delayed bowel necrosis due to inferior mesenteric artery occlusion in Stanford type A acute aortic dissection.

Although inferior mesenteric artery occlusion due to acute aortic dissection sometimes occurs, it is usually not considered an important finding. Herein, we present an extremely rare case of delayed bowel ischaemia due to inferior mesenteric artery occlusion in Stanford type A acute aortic dissection that highlights the need for cardiac surgeons to be mindful of inferior mesenteric artery occlusion in patients with superior mesenteric artery dissection or vascular anomalies in the mesenteric arteries.

Neuroprotective roles of HAX-1 in ischemic neuronal injury.

Hematopoietic cell-specific protein 1 associated protein X-1 (HAX-1) is a novel mitochondrial protein that regulates oxidative stress-induced apoptosis. However, the roles of HAX-1 in ischemic neuronal injury have not been thoroughly elucidated. In this study, the expression and roles of HAX-1 after ischemic stress were investigated using in vivo and in vitro models. The effect of oxidative stress on the regulation of HAX-1 was examined using knockout mice lacking nicotinamide-adenine dinucleotide phosphate oxidase 2 (NOX2), which is a major source of reactive oxygen species (ROS) after cerebral ischemia. Male C57BL/6 J mice were subjected to transient forebrain ischemia induced by 22-min occlusion of the bilateral common carotid arteries, and striatum samples were analyzed. For in vitro ischemic experiments, oxygen and glucose deprivation (OGD) in a rat pheochromocytoma cell line was utilized. Western blotting and immunofluorescence analysis revealed HAX-1 expression in neuronal mitochondria, which was significantly decreased after ischemia in vivo and in vitro. In NOX2 knockout mice, ischemia-induced decrease in HAX-1 expression and ischemic neuronal injury was significantly alleviated compared to those in wild-type mice. Inhibition of HAX-1 using small interfering RNA significantly increased injury in cultured cells after OGD. These findings suggest that HAX-1 has a neuroprotective effect against ischemic neuronal injury, and downregulation of HAX-1 by NOX2-produced ROS induces apoptosis after cerebral ischemia.

Mild Systemic Hypothermic Circulatory Arrest Using a Frozen Elephant Trunk Graft with Endo-Balloon Occlusion for Total Arch Replacement.

BACKGROUND: Stroke and paraplegia are serious complications of total aortic arch replacement (TAR). Hypothermic circulatory arrest and cerebral perfusion reduce the risk of neurologic complications, but longer circulatory arrest time remains a risk factor for such complications. We utilized a frozen elephant trunk (FET) with endo-balloon occlusion under mild systemic hypothermia, which allowed us to shorten circulatory arrest time. METHODS: Between April 2007 and May 2020, 72 patients underwent elective TAR using antegrade cerebral perfusion (ACP). They were divided into 2 groups. 64 patients received conventional TAR with moderate systemic hypothermic (bladder temperature, 25-28°C) circulatory arrest (group C). We used a FET with endo-balloon occlusion and retrograde perfusion through the femoral artery for the newest 8 patients who had mild hypothermic (bladder temperature of 30°C) circulatory arrest (group B). RESULTS: The mean operation time (257.5 ± 42.1 versus 327.8 ± 84.9 min, P = .023), CPB time (144.4 ± 28.1 versus 178.2 ± 26.4 min, P = .003), cardiac arrest time (75.5 ± 21.2 versus 95.7 ± 56.4 min, P < .001), SCP time (100.8 ± 25.5 versus 124 ± 23.2 min, P < .001), lower body circulation arrest time (17.2 ± 4.2 versus 62.5 ± 19.3 min, P < .001) were significantly shorter in the endo-balloon occlusion group. There were no perioperative neurological and renal complications or mortality in FET group. The new technique enabled a decrease in mechanical ventilation time (8.6 ± 1.4 versus 13.9 ± 5.7 min, P = .015) and hospital length of stay (9.7 ± 1.8 versus 18.3 ± 4.6 min, P = .005). CONCLUSION: FET using an endo-balloon occlusion with mild hypothermia is a safe and an effective approach in TAR.

Hypo-attenuated leaflet thickening in surgically-implanted mitral bioprosthesis.

BACKGROUND: Hypo-attenuated leaflet thickening (HALT) in bioprosthetic aortic valve has been studied, but its equivalent in bioprosthetic mitral valve (bMV) remains uncharacterized. We sought to identify the prevalence, hemodynamic characteristics, and significance of anticoagulation therapy in bMV HALT. METHODS: A single-center cross-sectional study of 53 consecutive patients who underwent mitral valve replacement (MVR) with bMV between 2007 and 2017 was conducted. Cardiac-gated contrasted CT scans were obtained. Anticoagulant and antiplatelet therapy use were ascertained at the time of hospital discharge and CT scanning. Patient characteristics, postoperative stroke, and hemodynamic profile by echocardiogram were obtained to descriptively characterize the prevalence and characteristics associated with bMV HALT. RESULTS: Three patients (5.7%) were found to have a HALT on bMV. The mean time from index MVR to CT scan was 3.4 ± 0.8 years in HALT cohort and 3.4 ± 2.7 years in non-HALT cohort. Fifty patients (94.3%) were discharged on warfarin, and 37 patients (69.8%) were on warfarin at the time of CT scans. One patient with HALT was on therapeutic warfarin at the time of the CT scan that identified HALT. All three patients were asymptomatic at the time of CT scan. In patients with HALT, mean transmitral pressure gradient were 8, 5, and 2.7 mmHg, all with trivial or mild mitral regurgitation. CONCLUSIONS: In this study, the prevalence of HALT was low at 5.7%, all presenting without symptoms. One patient presented with HALT while on therapeutic oral anticoagulation, which may suggest thrombotic etiology may not adequately explain HALT.

Neuroprotective effects of peroxisome proliferator-activated receptor γ agonist through activation of Akt and signal transducers and activators of transcription 3 in transient forebrain ischemia.

Peroxisome proliferator-activated receptor γ (PPARγ) belongs to the nuclear hormone receptor family and is a ligand-modulated transcriptional factor. Pioglitazone, a PPARγ ligand of the thiazolidinedione class, exerts several pleiotropic effects including neuroprotection in addition to reducing blood glucose and insulin resistance; however, its mechanism remains obscure. In this study, we examined the PPARγ expression and the protective effects of pioglitazone after transient forebrain ischemia. We focused on Akt and signal transducers and activators of transcription 3 (STAT3), key pathways of prosurvival signaling in ischemic neuronal injury as the mechanisms of pioglitazone's effects. Male Sprague-Dawley rats were given daily oral administration of pioglitazone (0.2, 2 and 20 mg/kg/d) or the vehicle, and transient forebrain ischemia was induced by 5-minute occlusion of bilateral common carotid arteries with hypotension. Western blot and immunohistochemistry revealed that PPARγ expression in the hippocampal CA1 subregion was upregulated 1-8 h after forebrain ischemia, which was observed mainly in pyramidal neurons. Most CA1 neurons were positive for TUNEL staining 5 days after ischemia, and pioglitazone administration reduced TUNEL-positive cells in a dose-dependent manner, with a significant difference in the 20 mg/kg/d group compared with the vehicle. Phosphorylation of Akt (Ser473) and its target, glycogen synthase kinase-3ß (Ser9), was increased after ischemia, and 20 mg/kg/d dose of pioglitazone significantly increased phosphorylation of these proteins. Furthermore, pioglitazone treatment enhanced phosphorylation of STAT3 (Tyr705) after ischemia. These results indicate that pioglitazone attenuates neuronal ischemic injury through the activation of Akt and STAT3 pathways.

Relapse of aortopulmonary window 41 years after patch closure.

In this study, we describe a rare case of a 45-year-old man with a recurrence of aortopulmonary window (APW) 41 years after the initial patch closure for an APW at the age of 4. He presented with persistent cough and exertional dyspnoea. Imagings revealed a recurrence of APW, ascending aorta saccular aneurysm, and severe mitral and tricuspid regurgitation. Re-patch closure, ascending aortic replacement, and mitral and tricuspid annuloplasties were performed, followed by an uneventful postoperative course. The relapse of APW in the remote postoperative period is extremely rare.

Neuroprotective effects of microglial P2Y1 receptors against ischemic neuronal injury.

Extracellular ATP, which is released from damaged cells after ischemia, activates P2 receptors. P2Y1 receptors (P2Y1R) have received considerable attention, especially in astrocytes, because their activation plays a central role in the regulation of neuron-to-glia communication. However, the functions or even existence of P2Y1R in microglia remain unknown, despite the fact that many microglial P2 receptors are involved in several brain diseases. Herein, we demonstrate the presence and functional capability of microglial P2Y1R to provide neuroprotective effects following ischemic stress. Cerebral ischemia resulted in increased microglial P2Y1R expression. The number of injured hippocampal neurons was significantly higher in P2Y1 R knockout (KO) mice than wildtype mice after forebrain ischemia. Propidium iodide (PI) uptake, a marker for dying cells, was significantly higher in P2Y1R KO hippocampal slices compared with wildtype hippocampal slices at 48 h after 40-min oxygen-glucose deprivation (OGD). Furthermore, increased PI uptake following OGD was rescued by ectopic overexpression of P2Y1R in microglia. In summary, these data suggest that microglial P2Y1R mediate neuroprotective effects against ischemic stress and OGD insult.

Efficacy of Endoscopic Fluorescein Video Angiography in Aneurysm Surgery-Novel and Innovative Assessment of Vascular Blood Flow in the Dead Angles of the Microscope.

BACKGROUND: In aneurysm surgery, assessment of the blood flow around the aneurysm is crucial. Recently, intraoperative fluorescence video angiography has been widely adopted for this purpose. However, the observation field of this procedure is limited to the microscopic view, and it is difficult to visualize blood flow obscured by the skull base anatomy, parent arteries, and aneurysm. OBJECTIVE: To demonstrate the efficacy of a new small-caliber endoscopic fluorescence video angiography system employing sodium fluorescein in aneurysm surgery for the first time. METHODS: Eighteen patients with 18 cerebral aneurysms were enrolled in this study. Both microscopic fluorescence angiography and endoscopic fluorescein video angiography were performed before and after clip placement. RESULTS: Endoscopic fluorescein video angiography provided bright fluorescence imaging even with a 2.7-mm-diameter endoscope and clearly revealed blood flow within the vessels in the dead angle areas of the microscope in all 18 aneurysms. Consequently, it revealed information about aneurysmal occlusion and perforator patency in 15 aneurysms (83.3%) that was not obtainable with microscopic fluorescence video angiography. Furthermore, only endoscopic video angiography detected the incomplete clipping in 2 aneurysms and the occlusion of the perforating branches in 3 aneurysms, which led to the reapplication of clips in 2 aneurysms. CONCLUSION: The innovative endoscopic fluorescein video angiography system we developed features a small-caliber endoscope and bright fluorescence images. Because it reveals blood flow in the dead angle areas of the microscope, this novel system could contribute to the safety and long-term effectiveness of aneurysm surgery even in a narrow operative field.

Hypoglossal canal dural arteriovenous fistula embolized under precise anatomical evaluation by selective intra-arterial injection computed tomography angiography.

Dural arteriovenous fistula (DAVF) involving the hypoglossal canal is rare but increasingly reported. To achieve complete obliteration without a procedure-related complication, understanding of the precise anatomy of this DAVF is essential. Here, we describe a 72-year-old man who underwent selective intra-arterial injection computed tomography angiography which allowed us to understand the detailed anatomy of the complex DAVF regarding access routes and the target regions for transvenous embolization (TVE). With the aid of this novel neuroimaging technique successful target TVE was achieved safely and completely.

Cerebral hemodynamic disturbance in dural arteriovenous fistula with retrograde leptomeningeal venous drainage: a prospective study using (123)I-iodoamphetamine single photon emission computed tomography.

OBJECT: The severity of cerebral hemodynamic disturbance caused by retrograde leptomeningeal venous drainage (RLVD) of a dural arteriovenous fistula (dAVF) is related to neurological morbidity and unfavorable outcome. However, the cerebral hemodynamics of this disorder have not been elucidated well. The aim of this study was to assess the relationship between the cerebral venous congestive encephalopathy represented as a high-intensity area (HIA) on T2-weighted MR images and the cerebral hemodynamics examined by (123)I-iodoamphetamine (IMP) single photon emission computed tomography (SPECT), as well as the predictive value of (123)I-IMP SPECT for the development and reversibility of venous congestion encephalopathy. METHODS: Based on the pre- and posttreatment T2 HIAs associated with venous congestion encephalopathy, patients were divided into 3 groups: a normal group, an edema group, and an infarction group. The regional cerebral blood flow (rCBF) at the region with RLVD was analyzed by (123)I-IMP SPECT, and the results were compared among the groups. RESULTS: There were 11, 6, and 3 patients in the normal, edema, and infarction groups, respectively. No patients in the normal group showed any symptoms related to venous congestion. In contrast, all patients in the edema and infarction groups developed neurological symptoms. The rCBF in the edema group was significantly lower than that in the normal group, and significantly higher than that in the infarction group. The cerebral vascular reactivity (CVR) of the infarction group was significantly lower than that of the normal and edema groups. After treatment, the neurological signs disappeared in the edema group, but only partial improvement was seen in the infarction group. The rCBF also significantly increased in the normal and edema groups, but not in the infarction group. CONCLUSIONS: Quantitative rCBF measurement is useful for evaluating hemodynamic disturbance in dAVF with RLVD. The reduction of rCBF was strongly correlated with the severity of venous congestive encephalopathy, and loss of CVR is a reliable indicator of irreversible venous infarction caused by RLVD.

Anchor coil technique for arteriovenous fistula embolization. A technical note.

We describe a case of arteriovenous fistula (AVF) successfully treated by coil embolization with an anchor coil inserted in the varix to facilitate dense packing at the shunting site. AVF of the left anterior choroidal artery (AChoA) draining into the ipsilateral basal vein of Rosenthal was incidentally found in a newborn female. A single detachable coil was inserted as an anchor into the varix adjacent to the shunt, and the microcatheter was pulled back to the shunting point. Three more detachable coils were delivered at the shunting point without migration under the support of the anchor coil, and the AVF was successfully obliterated with preservation of AChoA blood flow. The anchor coil technique can reduce the risk of coil migration and the number of coils required.