Circulation Journal
Online ISSN : 1347-4820
Print ISSN : 1346-9843
ISSN-L : 1346-9843
Volume 71 , Issue SupplementA
Showing 1-16 articles out of 16 articles from the selected issue
Special Contribution
  • Sami F. Noujaim, David S. Auerbach, José Jalife
    2007 Volume 71 Issue SupplementA Pages A1-A11
    Published: 2007
    Released: June 25, 2007
    JOURNALS FREE ACCESS
    Ventricular fibrillation (VF) is the leading cause of sudden cardiac death. This brief review addresses issues relevant to the dynamics of the rotors responsible for functional reentry and VF. It also makes an attempt to summarize present-day knowledge of the manner in which the dynamic interplay between inward and outward transmembrane currents and the heterogeneous cardiac structure establish a substrate for the initiation and maintenance of rotors and VF. The fragmentary nature of our current understanding of ionic VF mechanisms does not even allow an approach toward a "Theory of VF". Yet some hope is provided by recently obtained insight into the roles played in VF by some of the sarcolemmal ion channels that control the excitation-recovery process. For example, strong evidence supports the idea that the interplay between the rapid-inward sodium current and the inward-rectifier potassium current controls rotor formation, as well as rotor stability and frequency. Solid evidence also exists for an involvement of L-type calcium current in the control of rotor frequency and in determining VF-to-ventricular tachycardia conversion. Less clear, however, is whether or not time dependent outward currents through voltage-gated potassium channels affect the fibrillatory process. Hopefully, taking advantage of currently available approaches of structural, molecular and cellular biology, together with computational and imaging techniques, will afford us the opportunity to further advance knowledge on VF mechanisms. (Circ J 2007; Suppl A: A-1 - A-11)
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  • Arthur AM Wilde, Hanno L Tan
    2007 Volume 71 Issue SupplementA Pages A12-A19
    Published: 2007
    Released: June 25, 2007
    JOURNALS FREE ACCESS
    Inherited cardiac arrhythmia syndromes have received a lot of attention in recent years, particularly the molecular genetic basis, which has been unraveled to a great extent in the past years. Disease entities have been subdivided based on their causal gene defect, which, indeed, has been shown to impact on disease expression, clinical characteristics, prognosis and treatment. This particularly holds for the long QT syndrome. Studies in other, more recently described, disease entities, such as Brugada syndrome, catecholaminergic polymorphic ventricular arrhythmias and the short QT syndrome, are ongoing. For some of them the heterogenetic nature has just very recently been established. For these reasons, genetic testing has been introduced to clinical practice in several countries, which enables timely treatment of affected individuals and reassurance of those not inheriting the causal gene defect. Presymptomatic testing, however, is not without drawbacks. Psychosocial studies are needed in this field and should be promoted. It is likely that this development will further increase the knowledge of the (patho-) physiology of these disease entities, but also of more common arrhythmia syndromes. (Circ J 2007; Suppl A: A-12 - A-19)
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  • Yi-Jen Chen, Shih-Ann Chen
    2007 Volume 71 Issue SupplementA Pages A20-A25
    Published: 2007
    Released: June 25, 2007
    JOURNALS FREE ACCESS
    The thoracic veins are important foci for the genesis of ectopic atrial tachycardia and play a critical role in the pathophysiology of paroxysmal and permanent atrial fibrillation. The pulmonary veins have the highest arrhythmogenic activity and other venous structures (eg, superior vena cava, coronary sinus and ligament of Marshall) have also been shown arrhythmogenic potential. Thoracic veins contain cardiomyocytes with distinct electrical activities and complex anatomical structures. This review summaries the current understanding of the basic and clinical electrophysiology of thoracic vein arrhythmias. (Circ J 2007; Suppl A: A-20-A-25)
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Invited Review
  • Haruo Honjo, Masatoshi Yamazaki, Kaichiro Kamiya, Itsuo Kodama
    2007 Volume 71 Issue SupplementA Pages A26-A31
    Published: 2007
    Released: June 25, 2007
    JOURNALS FREE ACCESS
    It is well established that spiral wave reentry is the primary mechanism of ventricular tachyarrhythmias (ventricular fibrillation/tachycardia, VF/VT), but information is still limited concerning pharmacological modification of spiral waves by ion channel blockers. In this brief review, the antiarrhythmic and proarrhythmic actions of K+-channel blockade (IKr and I K1) are discussed in terms of spiral wave dynamics, primarily based on recent experimental findings in ventricular preparations perfused in vitro with the aid of high-resolution optical mapping, as well as their related theoretical studies using computer simulation. (Circ J 2007; Suppl A: A-26 - A-31)
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  • Wataru Shimizu, Takeshi Aiba, Shiro Kamakura
    2007 Volume 71 Issue SupplementA Pages A32-A39
    Published: 2007
    Released: June 25, 2007
    JOURNALS FREE ACCESS
    Brugada syndrome is a clinical entity characterized by coved type ST-segment elevation in the right precordial electrocardiographic leads (V1-3) and an episode of ventricular fibrillation in the absence of structural heart disease. Although a number of clinical and experimental reports have elucidated the electrocardiographic, electrophysiologic, cellular, and molecular aspects, several problems remain unsolved. Recently developed high-resolution optical mapping techniques in arterially-perfused wedge preparations enable recording of transmembrane action potentials from 256 sites simultaneously at the epicardial surface, thus providing further advances in the understanding of the cellular mechanism of the specific ST-segment elevation and subsequent ventricular arrhythmias. In this review article, new findings relating to several unresolved problems such as gender difference (male predominance) and ethnic difference (higher incidence in Asian population) are also presented. (Circ J 2007; Suppl A: A-32 - A-39)
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  • Takeshi Yamashita
    2007 Volume 71 Issue SupplementA Pages A40-A44
    Published: 2007
    Released: June 25, 2007
    JOURNALS FREE ACCESS
    Atrial fibrillation (AF), one of the most common arrhythmias, has grown to be an important medical problem in societies with an increasing number of aged people, because AF is strongly associated with the occurrence of severe thromboembolism. Although the processes underlying AF-associated thrombosis have long been believed to be mainly dependent upon the decreased blood flow in the left atrium induced by AF, revisiting the well known Virchow's triad from the basic approach has disclosed that this is too simplistic. Here, the role of 3 important components, abnormalities in the blood flow, blood coagulability, and the endocardial function of the atria, in thrombus formation in the fibrillating atria are discussed. Unraveling the molecular basis of thrombus formation in the atrium could open a new era of a wide variety of management of stroke prevention for AF patients. (Circ J 2007; Suppl A: A-40 - A-44)
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  • Shunichiro Miyoshi, Yukinori Ikegami, Yuji Itabashi, Akira Furuta, Aki ...
    2007 Volume 71 Issue SupplementA Pages A45-A49
    Published: 2007
    Released: June 25, 2007
    JOURNALS FREE ACCESS
    Cardiac stem cell based therapy is a promising therapy for patients with severe heart failure. Many types of stem cells, such as embryonic stem cells, myoblasts, marrow-derived mesenchymal stem cells, circulating endothelial progenitor cells, and cardiac precursor cells etc, are known as cellular sources for cardiac stem cell therapy. Both in the clinical and experimental setting, stem cells are reported, and supposed, to cause some arrhythmogenic adverse effects. In order to overcome these serious adverse effects, it is necessary to know the electrophysiological properties of stem cell-derived cardiomyocytes, and have a profound insight into the mechanisms of arrhythmia to know whether such arrhythmogenic properties of the cells can cause serious arrhythmia in situ. In the present study, recent publications that focus on the electrophysiological aspect of stem cell based therapy are reviewed and, furthermore, a new perspective on cardiac stem cell therapy of arrhythmias is given. (Circ J 2007; Suppl A: A-45 - A-49)
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  • Minoru Horie, Hideki Itoh
    2007 Volume 71 Issue SupplementA Pages A50-A53
    Published: 2007
    Released: June 25, 2007
    JOURNALS FREE ACCESS
    The long and short QT syndromes are heterogeneous diseases characterized by abnormal ventricular repolarization and episodes of syncope and/or life-threatening cardiac arrhythmias. Several disease-causing genes have been identified, including those encoding cardiac ion channel-composing proteins. The clinical determination of genotype offers a striking benefit: diagnosis, prediction of clinical phenotype, risk stratification, clinical and genetic counseling, and introduction of therapy. Genetic testing is of special importance for the genotyped patient's family members to prevent unexpected cardiac death. By means of recently advanced methodology in molecular genetics and electrophysiology it is expected that novel genes responsible for these disease entities will be identified. (Circ J 2007; Suppl A: A-50 - A-53)
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  • Naomasa Makita, Hiroyuki Tsutsui
    2007 Volume 71 Issue SupplementA Pages A54-A60
    Published: 2007
    Released: June 25, 2007
    JOURNALS FREE ACCESS
    Over the past 10 years, remarkable advances have been made in identifying the genes responsible for primary electrical heart diseases, such as congenital long QT syndrome and Brugada syndrome. Basic and clinical studies on these inherited arrhythmias have provided significant insight into the molecular basis of cardiac electrophysiology and the mechanisms of arrhythmias. However, many studies of genotype - phenotype relationships in these diseases have revealed considerable phenotypic variability in individuals from the same kindred carrying the identical disease-associated DNA variant, as is commonly observed in other polygenic disorders. Furthermore, despite rapid progress in understanding the molecular basis of primary electrical heart diseases, there is little insight into the genetics of acquired arrhythmias. Recently, it has been recognized that common genetic polymorphisms in cardiac ion channel and other genes may modify cardiac excitability, which in turn predisposes affected individuals to arrhythmias in the presence of triggering factors, such as electrolyte abnormalities or drugs. This paper reviews the current understanding of the contribution of genetic polymorphisms to the pathophysiology of cardiac arrhythmias. (Circ J 2007; Suppl A: A-54 - A-60)
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  • Masayasu Hiraoka
    2007 Volume 71 Issue SupplementA Pages A61-A68
    Published: 2007
    Released: June 25, 2007
    JOURNALS FREE ACCESS
    The incidence of Brugada syndrome (BS) is relatively high in Japan compared with the rest of the world, ranging between 0.1% and 0.2% in the general population. BS in Japan, as in other countries, is most prevalent in middle-aged men, and has characteristics ECG changes, a high recurrence rate in symptomatic patients, and relatively low incidence of SCN5A mutations. In contrast, both the incidence of a family history of BS and/or sudden cardiac death and the rate of developing cardiac events in asymptomatic patients are less in Japan than in other countries. Increased vagal tone and/or decreased sympathetic activity are suggested as provoking cardiac events. Several factors should be evaluated in risk stratification for recurrence of life-threatening arrhythmias, because there appears to be no single determinant for risk stratification: spontaneous ST elevation of coved-type (Type 1), family history of sudden cardiac death, inducible ventricular tachycardia/ventricular fibrillation and positive late potentials. An implantable cardioverter defibrillator is recommended for patients with aborted sudden cardiac death. (Circ J 2007; Suppl A: A-61 - A-68)
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  • Akira Fujiki, Hiroshi Inoue
    2007 Volume 71 Issue SupplementA Pages A69-A74
    Published: 2007
    Released: June 25, 2007
    JOURNALS FREE ACCESS
    Pharmacological therapy for atrial fibrillation (AF) is difficult because AF induces atrial remodeling. Randomized prospective studies using amiodarone could not show the superiority of rhythm control strategy to rate control strategy for treatment of AF. Bepridil is a multichannel blocker like amiodarone and expected to be effective for termination of AF without exacerbation of extracardiac adverse effects. Efficacy and safety of bepridil in pharmacological cardioversion of long-lasting AF (≥3 months) was assessed. To avoid the risk of excessive QT prolongation, bepridil dosage was limited to ≤200 mg/day and aprindine (class Ib) was added if necessary. Bepridil alone or in combination with aprindine restored sinus rhythm in 69% of patients. No adverse effects necessitating drug termination occurred. The average time to conversion after starting bepridil was 30 days and cardioversion was associated with significant increase in fibrillation cycle length. After cardioversion, atrial contraction recovered faster within 1 week and sinus rhythm was maintained better than conventional electrical cardioversion. The history of drug-resistant AF did not affect efficacy of bepridil. These observations suggest that pharmacological cardioversion of long-lasting AF could become a new therapeutic option. Although the precise mechanism of cardioversion by bepridil is not clear, reversal of the remodeled atria may play an important role. (Circ J 2007; Suppl A: A-69 - A-74)
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  • Koichiro Kumagai
    2007 Volume 71 Issue SupplementA Pages A75-A81
    Published: 2007
    Released: June 25, 2007
    JOURNALS FREE ACCESS
    There are multiple factors for the etiology of atrial fibrillation (AF), including stretch, autonomic imbalance, hyperthyroidism, and inflammation. Of these factors for AF, stretch and inflammation increase the angiotensin II level, thereby inducing calcium over load, and inducing ectopic focal activities that initiate AF. Angiotensin II activates the Erk cascade through the AT1R and induces interstitial fibrosis of the atria, which compromises intra-atrial conduction. Short atrial refractoriness and slow conduction form multiple re-entry, before maintaining AF. Anti-arrhythmic drugs used for downstream therapy can suppress the focal activities and re-entry, but cannot prevent the development of a structural substrate. In contrast, angiotensin-converting enzyme, angiotensin II type 1 receptor blocker and statins might constitute upstream therapy through the prevention of structural remodeling that promotes AF. (Circ J 2007; Suppl A: A-75 - A-81)
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  • Yoshito Iesaka, Kiyoshi Otomo, Yasutoshi Nagata, Kikuya Uno
    2007 Volume 71 Issue SupplementA Pages A82-A89
    Published: 2007
    Released: June 25, 2007
    JOURNALS FREE ACCESS
    Curing atrial fibrillation (AF) by catheter ablation has significantly improved patient morbidity and mortality. The circumferential pulmonary vein isolation technique is established as the principal procedure, with a high cure rate and acceptable safety, for paroxysmal AF, but new adjunctive ablation strategies targeting the AF substrates and sources for long-standing persistent/chronic AF have been developed. These new techniques include linear ablation, complex fractionated atrial electrogram guided ablation, dominant frequency map-guided ablation, ganglionated plexi ablation and disconnection of the coronary sinus and superior vena cava to ablate the AF substrates and sources. The long-term usefulness of the established technique and these innovative adjunctive approaches for the treatment of AF remains to be investigated. (Circ J 2007; Suppl A: A-82 - A-89)
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  • Tsuyoshi Shiga, Hiroshi Kasanuki
    2007 Volume 71 Issue SupplementA Pages A90-A96
    Published: 2007
    Released: June 25, 2007
    JOURNALS FREE ACCESS
    Sudden cardiac death (SCD) accounts for approximately one-third of all deaths in patients with heart failure, and is generally the result of ventricular tachycardia (VT) and/or ventricular fibrillation (VF). The mechanisms of VT/VF associated with heart failure are complex and heterogeneous; they include functional and structural remodeling, as well as neurohormonal activation. The implantable cardioverter-defibrillator is very useful for preventing SCD, but the improvement of outcome is limited in patients with cardiac dysfunction and advanced heart failure. This article reviews the current status of drug therapy for the treatment of VT/VF in patients with heart failure. Chronic β-blocker therapy reduces SCD and improves survival. Angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers and aldosterone antagonists are thought to reduce SCD by preventing ventricular remodeling. Amiodarone is potentially effective for preventing VT/VF in patients at high risk, especially those with nonischemic heart failure. This may be a result of the complex pharmacodynamics of amiodarone, which affects many kinds of ion channels/transporters, as well as thyroid function. The pure class III antiarrhythmic drug, nifekalant, is useful in the emergency treatment of VT/VF. (Circ J 2007; Suppl A: A-90 - A-96)
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  • Masaomi Chinushi, Yoshifusa Aizawa
    2007 Volume 71 Issue SupplementA Pages A97-A105
    Published: 2007
    Released: June 25, 2007
    JOURNALS FREE ACCESS
    Ventricular tachyarrhythmias (VTA), a major cause of sudden cardiac death, require meticulous management in order to prevent recurrent episodes. Recently, non-pharmacological interventions, including radiofrequency catheter ablation and implantable cardioverter defibrillators (ICD), have become important treatments of VTA. Catheter ablation is curative in a relatively high percentage of patients presenting with idiopathic monomorphic ventricular tachycardia (VT). For VT associated with structural heart disease, however, the efficacy of catheter ablation remains limited, and ICD is the first-line therapy. In a subset of patients presenting with recurrent episodes of ventricular fibrillation (VF), catheter ablation is a therapeutic option when the VF is triggered by specific premature ventricular complexes. In Japan, unlike in the United States and Europe, ICD have not yet been accepted as first-line prevention of sudden cardiac death caused by VTA. The efficacy of ICD is occasionally limited by intolerable complications, such as electrical storm, inappropriate shock delivery and infection. Catheter ablation and ICD therapy might need to be combined for problematic cases. (Circ J 2007; Suppl A: A-97 - A-105)
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  • Takanori Ikeda, Satoru Yusu, Kentaro Nakamura, Hideaki Yoshino
    2007 Volume 71 Issue SupplementA Pages A106-A114
    Published: 2007
    Released: June 25, 2007
    JOURNALS FREE ACCESS
    Sudden cardiac death (SCD) is a leading cause of mortality in industrialized countries, and ventricular fibrillation and sustained ventricular tachycardia are the major causes of SCD. Although there are now effective devices and medications that can prevent such serious arrhythmias, it is crucial to have methods of identifying patients at risk. Numerous studies suggest that most patients dying of SCD have coronary artery disease or cardiomyopathy. Functional or electrophysiological measurements are effective in risk stratification. Left ventricular ejection fraction measured by echocardiography or cardiac imaging techniques is the gold standard to detect high-risk patients. Electrophysiological studies have also been used for risk stratification. Noninvasive techniques and measurements, such as T-wave alternans, signal-averaged electrocardiography, nonsustained ventricular tachycardia, heart rate variability, and heart rate turbulence, have been proposed as useful tools in identifying patients at risk for SCD. This article reviews the epidemiology, mechanisms, substrates, and current status of risk stratification of SCD. (Circ J 2007; Suppl A: A-106 - A-114)
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