Mcneillhubbard5568

Even in the case of non-severe AV conduction delay, which causes symptoms, it is essential to investigate possible rare causes of the conduction disorder before considering pacemaker treatment. © 2019 Published by Elsevier Ltd on behalf of Japanese College of Cardiology.We report the case of a 40-year-old veterinary surgeon who was admitted for spiking fevers, arthralgia, and a complete atrioventricular block. Tests revealed an inflammatory syndrome, hepatic cytolysis, neutrophilic leukocytosis, and increased troponin levels. Cardiac magnetic resonance imaging showed a small myocarditis but no tissue abnormality on the conduction pathways. In the absence of evidence-based infection and favorable evolution under broad spectrum antibiotherapy, an adult-onset Still's disease was suspected and corticosteroid therapy administered. Evolution was then impressively favorable, with a persistent sinus heart rhythm 3 days later. Learning objective Febrile conductive disorders occurring during a systemic disorder with negative infection and auto-immunity work-up should lead to consider an adult-onset Still's disease, which can be treated and cured, especially with steroids. Moreover, fever, polyarthritis, neutrophilic leukocytosis, pericarditis, and myocarditis should lead to consideration of adult-onset Still's disease. © 2019 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.This clinical case report describes the simultaneous development of an acute myocardial infarction, stroke, and a massive pulmonary thromboembolism in a 44-year-old patient - a carrier of the thrombophilia gene polymorphisms MTHFR C677T, А1298C, PAI-1 4G/5G, ITGA2 C807T. Multifocal thrombosis was probably due to the initial congenital deficiency of anticoagulants, accompanied by a decrease in antithrombin III and protein C, against the background of their critical consumption in cascade thrombosis, in combination with the carrier of polymorphisms of moderate and low thrombogenic risk. This case is unique in that there is usually a tendency toward clinical thrombosis when the level of antithrombin III is less than 70%. Such patients develop thrombosis at a younger age, and by the age of 35-40 years usually have a verified diagnosis of extremely high-risk hereditary thrombophilia. TGF-beta inhibitor In this case, multifocal thrombosis was accompanied by critically low values of anticoagulants antithrombin III - 3.4%, and protein C - 36.8%. The patient had suffered from epilepsy since childhood and took anticonvulsant drugs that increase the deficit of active folic acid and can lead to hyperhomocysteinemia, which in this case, against the background of an innate decrease in the activity of methyltetrahydrofolate reductase, could have aggravated the situation. . © 2019 Published by Elsevier Ltd on behalf of Japanese College of Cardiology.A 40-year-old male visited our institute complaining of transient loss of consciousness. He had been implanted with an implantable cardioverter defibrillator (ICD) due to idiopathic ventricular fibrillation for secondary prevention. His past genetic screening detected a single nucleotide SCN5A mutation (pR18Q), while neither QT prolongation nor ST segment elevation in the right precordial leads was observed. An interrogation of the ICD revealed that a shock therapy successfully terminated ventricular fibrillation at the time syncope occurred. His electrocardiogram revealed ventricular premature contractions (VPCs) with a short coupling interval of 250 ms. Since the spontaneous occurrence of non-sustained polymorphic ventricular tachycardia following the same VPCs was observed after admission, he was diagnosed with a short-coupled variant of Torsades de Pointes (ScTdP). Contact mapping on the basal inferior right ventricular free wall, exhibiting the earliest activation, revealed pre-potentials preceding the QRS by 30 ms during the VPCs. Radiofrequency ablation was performed to reduce the triggering VPCs. To the best of our knowledge, this is the first report describing a case of ScTdP harboring an SCN5A mutation. The present N-terminally mutated SCN5A was originally reported in relation to Brugada syndrome, whereas the detailed mechanism remains to be elucidated. 〈 Learning objective The fundamental genetic disorders of short-coupled variant of Torsades de Pointes (ScTdP) are not clear. The present case harboring a mutation of SCN5A exhibited no long-QT or Brugada syndrome, which may implicate an unknown mechanism of the development of ScTdP.〉. © 2019 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.Coronary sinus ostial atresia is rare and usually not clinically relevant, but it should be noted in cases of cardiac resynchronization therapy. A rare case of successful left ventricular lead implantation for cardiac resynchronization therapy via the left superior vena cava in a patient with coronary sinus ostial atresia is reported. The persistent left superior vena cava associated with these cases tends to be smaller than usual in its diameter and difficult to identify, since the direction of venous drainage is reversed. Therefore, in the present case, it was useful to use a small-diameter, soft inner catheter as a guiding catheter to perform selective imaging and avoid vascular injury. In addition, it appeared to be important to plan the surgical strategy using prior imaging information, since it would be difficult to obtain the backup needed for lead insertion. 〈 Learning objective Cardiac resynchronization therapy via the left superior vena cava with coronary sinus ostial atresia is generally possible without problems if prior imaging information is available, such as three-dimensional computed tomography and the venous phase of coronary angiography. It is important to determine whether there is a persistent left superior vena cava before the procedure. Thromboprophylaxis remains controversial in this situation.〉. © 2019 Japanese College of Cardiology. Published by Elsevier Ltd.We report the case of a 47-year-old man who was diagnosed with severe right ventricular outflow tract (RVOT) stenosis due to a space-occupying lesion; the diagnosis was made using computed tomography. He underwent mass reduction, pulmonary valve replacement, and RVOT reconstruction with a bovine pericardial patch. The pathological diagnosis was undifferentiated pleomorphic sarcoma originating from the myocardium. As the mass resection was incomplete, he received heavy particle therapy. He did not want to receive adjuvant chemotherapy. Four months later, severe RVOT stenosis recurred because the residual mass had invaded the prosthetic valve in the pulmonic position and one of the cusps was fixed in the closed position. He presented with dyspnea and marked lower leg edema. We performed superior vena cava (SVC) to right pulmonary artery (RPA) shunting as a palliative operation to improve his heart failure symptoms. After surgery, his symptoms improved; his hemodynamics have been stable for one year. SVC-RPA shunting is a palliative operation but can be used to effectively treat severe RVOT stenosis caused by unresectable cardiac tumors.