The Japan Society of Gynecologic Oncology (JSGO) guideline for the treatment of uterine body neoplasm are revised from the 2018 guideline. This guideline aimed to provide standardized care for uterine body neoplasm, indicate appropriate current treatment methods for uterine body neoplasm, minimize variances in treatment methods among institutions, improve disease prognosis and treatment safety, reduce the economic and psychosomatic burden on patients by promoting the performance of appropriate treatment, and enhance mutual understanding between patients and healthcare professionals. The guidelines were prepared through the consensus of the JSGO guideline committee, based on a careful review of evidence from the literature searches and the medical health insurance system and actual clinical practice situations in Japan. The main features of the 2023 revision are as follows: 1) The Guidelines Formulation Committee members were asked to understand Minds' medical guideline development method in advance. 2) The clinical question (CQ) was changed to Patient, Intervention, Comparison, Outcome format as much as possible. 3) Introduced the "body of evidence," which summarizes the results of research reports collected for the CQs by outcome and study design, and the strength of evidence for each body of evidence was rated from levels A to D. 4) Introduction of systematic reviews in some CQs. 5) The strength of evidence, the balance of benefits and harms, value and hope for patients, and clinical applicability were considered while drafting recommendations. Herein, we present the English version of the JSGO guidelines 2023 for the treatment of uterine body neoplasm.

The patient was a 49-year-old male who had undergone total arch replacement with Elephant trunk procedure for acute aortic dissection Stanford type A at another institution. Eight months post-surgery, he presented with hematuria and jaundice. Mechanical hemolysis by grafts was considered, and he was referred to our hospital. Subsequently, we conducted transesophageal echocardiography, which revealed the inversion of felt strips at the proximal anastomosis site, accompanied by blood turbulence at the same site. Consequently, we established a diagnosis of mechanical hemolysis attributed to the inversion of the inner felt strip within the anastomosis, prompting a redo surgery. The utilization of felt strips for reinforcing the anastomosis has become a prevalent technique in ascending aortic replacement for acute aortic dissection. This technique serves to mitigate hemorrhage from the anastomosis and counteract the formation of pseudoaneurysms. In this study, we report an uncommon complication caused by the presence of felt strips within the anastomosis.

Ventricular septal rupture (VSR) has been a lethal complication after acute myocardial infarction. It occurs mostly within one week following onset of myocardial infarction. Medical managements and percutaneous defect closure are still of limited value. Surgical closure of VSR has been developed since the first report in 1957, however the recent STS database reported high surgical mortality of 54.2% in cases within 7 days following onset of myocardial infarction. Posterior VSR has been reported worse surgical mortality than anterior VSR. A novel procedure, the extended sandwich patch (ESP) method via the right ventricle (RV) incision was proposed and developed for overcoming these weaknesses. ESP method starts with the incision close to the culprit artery and the left ventricle (LV) is reached through the defect. After sufficient debridement of the necrotic myocardium, an octagonal fabric patch sized 6 centimeter is introduced into the LV. About eight transmural anchoring sutures are placed inside-out. The second fabric patch is placed on the RV septum and felt pledgetts on the free wall of LV. Before the final closure of the ESP, glue is placed into the defect. The RV incision is then simply closed. Low mortality and least the shunt recurrence were reported by our group. This life-saving procedure seems promising to employ for VSR closure even in cases within 7 days following onset of myocardial infarction or in the posterior type. To improve clinical outcomes of VSR, it is crucial to perform VSR closure with the secure method prior to developing multi-organ failure due to the deteriorating heart failure.

The left atrium and left atrial appendage have unique genetic anatomical and physiological features. Recently, advances in diagnostic imaging technology have provided much new knowledge. Clinically, the risk of developing atrial fibrillation increases with age. In order to reduce the public health burden such as cerebral infarction caused by atrial fibrillation, we need to find some predictive risk factors and preventive strategies for cerebral infarction and more effective treatments. The new concept of atrial myopathy has emerged, and animal models and human studies have revealed close interactions between atrial myopathy, atrial fibrillation, and stroke through various mechanisms. Structural and electrical remodeling such as fibrosis and deterioration of the balance of autonomic nerves and complicated interactions between these mechanisms lead to deterioration of atrial fibrillation and a continuous vicious cycle, and finally thrombosis in the left atrial appendage. Although anticoagulant therapy for patients with atrial fibrillation is strongly recommended, it is difficult for many patients to continue optimal treatment. In the nearly future, it will be important to understand the anatomy and physiology of the left atrial appendage and to understand the shape changes, size and the changes of autonomic function, and thrombus formation conditions associated with LAA remodeling during atrial fibrillation, and then we should provide early therapeutic intervention.

The surgical outcome is worse when VSP is attempted soon after myocardial infarction due to the more poor general condition, preoperative cardiogenic shock, fragile infarcted myocardial tissue. We successfully rescued a 80-year cardiopulmonary arrest patient who was suffering from subacute postinfarcted VSP complicated by the left ventricular aneurysm. The VSP was closed with the sandwich patch technique approached from both ventricles. The left ventricular aneurysm was repaired with endoventricular circular patch plasty.

Some 50% of patients who undergo cardiac surgery will have heparin-induced thrombocytopenia (HIT) antibodies, only 1% will develop typical clinical HIT. Especially delayed-onset HIT is not well-known and extremely rare. A 83-year-old man underwent aortic valve replacement (AVR) with a bioprosthetic valve (Mitroflow 21 mm) and pulmonary vein isolation (PVI). Intravenous unfractionated heparin (8,000 I.U./day) was administered for 5 days after surgery. He had a good recovery and was discharged to home with a platelet count of 100,600/μl on POD 15 on warfarin. On POD 18, he was readmitted to our hospital due to cerebral infarction with hemiparesis. As MRI revealed a multiple left hemispheric infarction, the presence of cardiogenic cerebral infarction was suspected. Continuous intravenous administration of unfractionated heparin (15,000 I.U./day) was started. On POD 24, the platelet count fell to 27,000/μl, and a contrast CT scan revealed a giant thrombus in the aortic arch. He was found to have HIT antibodies, supporting a diagnosis of HIT. After cessation of heparin therapy and administration of vitamin K antagonist, argatroban was administered. He recovered neurologically and was discharged on POD 58. He remains well at 3 years follow up. If a patient has an unexplained and severe thrombocytopenia after cardiovascular surgery, delayed-onset HIT should be taken into consideration.

Triple-vessel disease of coronary artery was recognized in the examination of a 78-year-old man when hemodialysis was introduced for diabetic nephropathy. Percutaneous coronary intervention (PCI) was performed as initial treatment for the lesion of the right coronary artery. Contrast CT was performed because of persistent fever from the first day after the PCI. Since the tumor occupying the inside of the left atrium which was not found before PCI we were concerned about the failure of the hemodynamics and decided to treat it surgically. Surgery was performed with off-pump coronary artery bypass grafting, followed by left atrial mass removal surgery under cardiac arrest using cardio-pulmonary bypass. When examining the interior of the left atrium with a right lateral incision of the left atrium, the tumor was found to be on the posterior wall. This surface was smooth, and there was no endometriosis or hematoma. After incising the left atrial adventitia, old hematoma was found in the inside of the left atrium muscle layer, and it was removed as much as possible. The left atrial tumor was actually an intramural hematoma, based on image findings and macroscopic findings. Searching for the cause retrospectively, it was thought that the wire which was displaced during PCI was the cause of bleeding. We confirmed that there was no recurrence of left atrial intramural hematoma on an outpatient visit on the 113th postoperative day. We report a rare case of removing left atrial intramural hematoma under cardiac arrest which appeared after PCI.

Congenital quadricuspid aortic valve is a very rare malformation. Most cases have been discovered as an incidental finding at aortic valve surgery or at autopsy. It frequently evolves to aortic regurgitation, which can manifest in adulthood and may require surgical treatment. A 66-year-old man was admitted because of dysprea. Echocardiogram revealed aortic regurgitation, mitral regurgitation, and tricuspid regurgitation. We performed aortic valve replacement, mitral annuloplasty, and tricuspid annuloplasty successfully. The aortic valve showed one large, two intermediate and one smaller cusp, which were classified as typed by Hurwitz's classification. An accessory cusp was situated between the right and left coronary cusps. No coronary abnormality was involved. The postoperative course was uneventful and he is doing well 6 months after operation.

In the presence of Leriche syndrome, the lower extremities are perfused by collateral flow from internal mammary arteries. If an internal mammary artery graft is used in coronary artery surgery, an acute ischemic limb will develop postoperatively. A 52-year-old man was admitted to our department with bilateral claudication. Multidetector row computed tomography with contrast showed total occlusion of the infrarenal abdominal aorta and rich collateral flow to the lower extremities from internal mammary arteries. Cardiac angiography revealed three-vessel disease. Simultaneous coronary artery bypass grafting and an ascending aorto-bifemoral bypass were performed without cardiopulmonary bypass. Postoperative computed tomography angiography showed that grafts to the coronary and bifemoral arteries were patent. This combined procedure is useful for patients with coronary artery disease and aortoiliac occlusive disease. This procedure without cardiopulmonary bypass has not previously been reported.

A 62-year-old woman with idiopathic thrombocytopenic purpura (ITP) was admitted to undergo cardiac surgery for aortic stenosis, angina pectoris, and paroxysmal atrial fibrillation. A bleeding tendency was expected due to the dramatic decrease in platelets during cardiopulmonary bypass. We performed high-dose transvenous gammaglobulin infusion (400mg/kg/day) for 5 consecutive days immediately before surgery. The gammaglobulin therapy caused steady increase of thrombocytes from 4 days after surgery, even though the platelet count showed no significant change preoperatively. The postoperative course was satisfactory with neither a bleeding tendency nor wound infection. High-dose transvenous gammaglobulin therapy is thus useful for perioperative patients with accompanying ITP, who are often under medication with steroids. This therapy is also effective for prevention of infection.