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The total right ventricular (RV) exclusion procedure for isolated congestive RV failure, in which most of the dilated right atrium (RA) and RV wall is resected, was first reported by Sano et al in 2002.1 This procedure improves the cardiac index2 and suppresses supraventricular/ventricular tachyarrhythmia. Using this procedure with an extracardiac conduit, we successfully treated severe heart failure characterized by a markedly dilated right heart lacking tricuspid leaflets and by recurrent tachyarrhythmia, 17 years after the patient had undergone initial definitive intracardiac repair including RV outflow tract plasty. A 22-year-old woman presented with general fatigue, dyspnea, palpitations, and loss of appetite of 6 months’ duration caused by low cardiac output. She was admitted to the University of Tokyo Hospital to undergo surgery to improve her low cardiac output. She was cyanotic at birth after an uneventful pregnancy and caesarian delivery. Cardiac catheterization performed when she was 47 days old revealed pulmonary atresia with atrial septal defect and patent ductus arteriosus. A Blalock-Taussig anastomosis was established. Subsequently, she was diagnosed with absent tricuspid valve, pulmonary atresia, and atrial septal defect. These were definitively treated surgically in 1990 when the patient was 5 years old via RV outflow tract plasty and atrial septal defect closure. Intraoperative findings included weak RV contraction and an anterior RV wall almost totally lacking myocardium. Five years after the operation, she suffered from ventricular tachycardia originating from the RV wall, which was treated by electrical cardioversion and subsequent administration of oral antiarrhythmic medication. Six months before admission, dyspnea …

Summary In this paper, we propose an algorithm that optimizes the ventricular fiber structure of the human heart. A number of histological studies and diffusion tensor magnetic resonance imaging analyses have revealed that the myocardial fiber forms a right-handed helix at the endocardium. However, the fiber formation changes its orientation as a function of transmural depth, becoming a left-handed helix at the epicardium. To determine how nature can construct such a structure, which obtains surprising pumping performance, we introduce macroscopic modeling of the branching structure of cardiac myocytes in our finite element ventricular model and utilize this in an optimization process. We put a set of multidirectional fibers around a central fiber orientation at each point of the ventricle walls and simulate heartbeats by generating contraction forces along each of these directions. We examine two optimization processes using the workloads or impulses measured in these directions to update the central fiber orientation. Both processes improve the pumping performance towards an optimal value within several tens of heartbeats, starting from an almost-flat fiber orientation. However, compared with the workload optimization, the impulse optimization produces better agreement with experimental studies on transmural changes of fiber helix angle, streamline patterns of characteristic helical structures, and temporal changes in strain. Furthermore, the impulse optimization is robust under geometrical changes of the heart and tends to homogenize various mechanical factors such as the stretch and stretch rate along the fiber orientation, the contraction force, and energy consumption. Copyright © 2015 John Wiley & Sons, Ltd.

Electrocardiogram (ECG) is one of the most basic examinations in the clinical medicine. Although frequently used, the interpretation of a standard 12-lead ECG is sometimes difficult for not only beginners but also clinical cardiologists. Vectorcardiogram (VCG) had been frequently used for describing three-dimensional movement of cardiac electrical activity before 1990s, which was thereafter rarely used in the clinical settings due to its complexity and time-consuming nature. However, VCG still has many features including: (1) easy for spatial understanding, (2) chronologically normalized, and (3) easy for quantitative analysis. For several years, we have collaborated with Fukuda Denshi Co., Ltd. and have established the novel vectorcardiographic descriptor of ventricular electrical activation, which digitally converts standard 12-lead ECG waveforms into “synthesized” VCG QRS-loop drawing. This novel vectorcardiographic descriptor can help us to understand the abnormality of QRS complex such as bundle branch blocks, ventricular hypertrophies, and myocardial injury: adding this synthesized VCG report to conventional 12-lead ECG report, healthcare providers and students are able to diagnose abnormality of QRS complex in ECG more effectively and accurately. Now this system can be optionally installed into the conventional ECG system (Fukuda Denshi Co., Ltd., Japan). This descriptor has great potential to clinical efficacy as well as medical education, and can make us revisit the VCG.

It is well known that disasters have great impact on the onset and frequency of arrhythmia in the patients with heart disease. On March 11 we experienced the unexpected the huge earthquake and tsunami waves. Moreover, the following Fukushima nuclear power plant accident caused severe anxiety to radiation exposure. These tremendous disasters caused strong mental as well as physical stress on the people living in not only the disaster area but also surrounding districts including Tokyo. To evaluate the impact of these disasters on the cardiovascular events, we compared arrhythmic events in the patients with pacemaker or ICD implanted in the University of Tokyo Hospital. Most of the patients had little events before and also after the earthquake, resulting in no significant difference. However, when we focused on the patients who had experienced relatively frequent arrhythmia before the earthquake, tachyarrhythmia events and AF burden were increased after the earthquake in the subset of our study population. Therefore, the strong stress has serious impact on arrhythmic events, which can at least partially contribute to the increase of major cardiovascular events.

Pathologic stressors disrupt cellular homeostasis and cause various diseases, mediated by stress-responsive epigenetic gene regulatory mechanism. Glycelaldehyde-3-phosphate dehydrogenase (GAPDH) is a classic cytosolic glycolytic enzyme, but has been shown to translocate to the nucleus under stress