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relating to or affecting the atria and ventricles of the heart; "atrioventricular disease" (同)auriculoventricular

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/05/28 20:28:24」(JST)

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1. 心電図チュートリアル：房室ブロック ecg tutorial atrioventricular block
2. 第1度房室ブロック first degree atrioventricular block
3. 第2度房室ブロック：モビッツII型 second degree atrioventricular block mobitz type ii
4. 房室（AV）管欠損の臨床症状、病態生理、および診断 clinical manifestations pathophysiology and diagnosis of atrioventricular av canal defects
5. Management and outcome of heterotaxy (isomerism of the atrial appendages)

English Journal

The variant hERG/R148W associated with LQTS is a mutation that reduces current density on co-expression with the WT.

Mechakra A1, Vincent Y1, Chevalier P2, Millat G3, Ficker E4, Jastrzebski M5, Poulin H6, Pouliot V6, Chahine M6, Christé G7.Author information 1Laboratoire de Neurocardiologie, EA4612, Université Lyon 1, Lyon F-69003, France.2Laboratoire de Neurocardiologie, EA4612, Université Lyon 1, Lyon F-69003, France; Unité de Rythmologie, Centre National de Référence des Troubles du Rythme d'Origine Héréditaire, Hôpital Cardiovasculaire et Pneumologique L. Pradel, Hospices Civils de Lyon, Lyon F-69003, France.3Laboratoire de Neurocardiologie, EA4612, Université Lyon 1, Lyon F-69003, France; Laboratoire de Cardiogénétique, Centre de Biologie Est, Hospices Civils de Lyon, Lyon F-69003, France.4MetroHealth Medical Center, Cleveland, OH, USA.5Department of Cardiology and Hypertension, University Hospital, Kracow, Poland.6Le Centre de Recherche en neuroscience, Institut Universitaire en Santé Mentale de Québec and Department of Medicine, Laval University, Québec, Canada.7Laboratoire de Neurocardiologie, EA4612, Université Lyon 1, Lyon F-69003, France. Electronic address: georges.christe@inserm.fr.AbstractBACKGROUND: A variant of the ether-à-go-go related channel (hERG), p.Arg148Trp (R148W) was found at heterozygous state in two infants who died from sudden infant death syndrome (SIDS), one with documented prolonged QTc and Torsade de Pointes (TdP), and in an adult woman with QTc >500ms, atrioventricular block and TdP. This variant was previously reported in cases of severe ventricular arrhythmia but very rarely in control subjects. Its classification as mutation or polymorphism awaited electrophysiological characterization.
Gene.Gene.2014 Feb 25;536(2):348-56. doi: 10.1016/j.gene.2013.11.072. Epub 2013 Dec 12.
BACKGROUND: A variant of the ether-à-go-go related channel (hERG), p.Arg148Trp (R148W) was found at heterozygous state in two infants who died from sudden infant death syndrome (SIDS), one with documented prolonged QTc and Torsade de Pointes (TdP), and in an adult woman with QTc >500ms, atrioven
PMID 24334129

Human cardiotoxic drugs delivered by soaking and microinjection induce cardiovascular toxicity in zebrafish.

Zhu JJ, Xu YQ, He JH, Yu HP, Huang CJ, Gao JM, Dong QX, Xuan YX, Li CQ.Author information Hunter Biotechnology, Inc., Transfarland, Hangzhou, Zhejiang Province, 311231, China.AbstractCardiovascular toxicity is a major challenge for the pharmaceutical industry and predictive screening models to identify and eliminate pharmaceuticals with the potential to cause cardiovascular toxicity in humans are urgently needed. In this study, taking advantage of the transparency of larval zebrafish, Danio rerio, we assessed cardiovascular toxicity of seven known human cardiotoxic drugs (aspirin, clomipramine hydrochloride, cyclophosphamide, nimodipine, quinidine, terfenadine and verapamil hydrochloride) and two non-cardiovascular toxicity drugs (gentamicin sulphate and tetracycline hydrochloride) in zebrafish using six specific phenotypic endpoints: heart rate, heart rhythm, pericardial edema, circulation, hemorrhage and thrombosis. All the tested drugs were delivered into zebrafish by direct soaking and yolk sac microinjection, respectively, and cardiovascular toxicity was quantitatively or qualitatively assessed at 4 and 24 h post drug treatment. The results showed that aspirin accelerated the zebrafish heart rate (tachycardia), whereas clomipramine hydrochloride, cyclophosphamide, nimodipine, quinidine, terfenadine and verapamil hydrochloride induced bradycardia. Quinidine and terfenadine also caused atrioventricular (AV) block. Nimodipine treatment resulted in atrial arrest with much slower but regular ventricular heart beating. All the tested human cardiotoxic drugs also induced pericardial edema and circulatory disturbance in zebrafish. There was no sign of cardiovascular toxicity in zebrafish treated with non-cardiotoxic drugs gentamicin sulphate and tetracycline hydrochloride. The overall prediction success rate for cardiotoxic drugs and non-cardiotoxic drugs in zebrafish were 100% (9/9) as compared with human results, suggesting that zebrafish is an excellent animal model for rapid in vivo cardiovascular toxicity screening. The procedures we developed in this report for assessing cardiovascular toxicity in zebrafish were suitable for drugs delivered by either soaking or microinjection. Copyright © 2013 John Wiley & Sons, Ltd.
Journal of applied toxicology : JAT.J Appl Toxicol.2014 Feb;34(2):139-48. doi: 10.1002/jat.2843. Epub 2013 Jan 11.
Cardiovascular toxicity is a major challenge for the pharmaceutical industry and predictive screening models to identify and eliminate pharmaceuticals with the potential to cause cardiovascular toxicity in humans are urgently needed. In this study, taking advantage of the transparency of larval zebr
PMID 23307606

The heart and pediatric rheumatology.

Vogel T, Kitcharoensakkul M, Fotis L, Baszis K.Author information Division of Rheumatology, Department of Pediatrics, Washington University School of Medicine, Box 8116, One Children's Place, St Louis, MO 63110, USA; Division of Rheumatology, Department of Medicine, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA.AbstractRecent advances in Kawasaki disease have included attempts to define genes involved in its pathogenesis. There have been recent advances in the studies of rheumatic carditis, leading to a better understanding of the mechanism of the disease. Histologic evaluation of patients with neonatal lupus erythematosus has revealed fibrosis with collagen deposition and calcification of the atrioventricular node. Therapy for cardiac involvement in systemic juvenile idiopathic arthritis should involve treatment of the underlying disease and systemic inflammatory state, and typically includes nonsteroidal antiinflammatory drugs, corticosteroids, disease-modifying drugs, and biologic therapies targeting tumor necrosis factor-alpha, interleukin-1, and interleukin-6.
Rheumatic diseases clinics of North America.Rheum Dis Clin North Am.2014 Feb;40(1):61-85. doi: 10.1016/j.rdc.2013.10.008.
Recent advances in Kawasaki disease have included attempts to define genes involved in its pathogenesis. There have been recent advances in the studies of rheumatic carditis, leading to a better understanding of the mechanism of the disease. Histologic evaluation of patients with neonatal lupus eryt
PMID 24268010

Japanese Journal

Clinical and Electrophysiological Characteristics of Typical Atrioventricular Nodal Reentrant Tachycardia in the Elderly : Changing of Slow Pathway Location With Aging

Alihanoglu Yusuf I.,Yildiz Bekir S.,Kilic Dogu I. [他]
Circulation journal : official journal of the Japanese Circulation Society 79(5), 1031-1036, 2015-05
NAID 40020437062

Fetal Bradyarrhythmia Associated With Congenital Heart Defects : Nationwide Survey in Japan

Miyoshi Takekazu,Maeno Yasuki,Sago Haruhiko [他]
Circulation journal : official journal of the Japanese Circulation Society 79(4), 854-861, 2015-04
NAID 40020412405

障害保障特約給付におけるペースメーカ・植込み型除細動器装着の状況

吉田達郎,尾関全,安達慶
日本保険医学会誌 113(1), 31-39, 2015-03-25
2014年4月,厚生労働省により身体障害認定基準が一部改正され,これまで一律に1級と認定されていた心臓ペースメーカ装着者が,身体活動能力により1級,3級または4級に分類されて認定されることとなった。また,障害認定者の中で,心臓機能障害での新規登録者の増加率が他の障害に比べて高い傾向を示したことから,当社でペースメーカ及び植込み型除細動器などの装着により障害給付金の支払となった事例の解析を行った。心 …
NAID 110009924292