Circulation Journal
Online ISSN : 1347-4820
Print ISSN : 1346-9843
ISSN-L : 1346-9843
Volume 74 , Issue 1
Showing 1-36 articles out of 36 articles from the selected issue
Massage From the Editor-in-Chief
Reviews
  • Quo Vadis?
    Alexander Breitenstein, Felix C. Tanner, Thomas F. Lüscher
    2010 Volume 74 Issue 1 Pages 3-12
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: December 08, 2009
    JOURNALS FREE ACCESS
    The coagulation cascade represents a system of proteases responsible to maintain vascular integrity and to induce rapid clot formation after vessel injury. Tissue factor (TF), the key initiator of the coagulation cascade, binds to factor VIIa and thereby activates factor IX and factor X, resulting in thrombus formation. Different stimuli enhance TF gene expression in endothelial and vascular smooth muscle cells. In addition to these vascular cells, TF has recently been detected in the bloodstream in circulating cells such as leukocytes and platelets, as a component of microparticles, and as a soluble, alternatively spliced form of TF. Various cardiovascular risk factors like hypertension, diabetes, and dyslipidemia, increase levels of TF. In line with this observation, enhanced vascular TF expression occurs during atherogenesis, particularly in patients with acute coronary syndromes. (Circ J 2010; 74: 3 - 12)
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  • Toru Hosoda, Jan Kajstura, Annarosa Leri, Piero Anversa
    2010 Volume 74 Issue 1 Pages 13-17
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: November 17, 2009
    JOURNALS FREE ACCESS
    The plasticity of bone marrow-derived progenitor cells (BMPCs) and their ability to acquire the myocyte lineage and regenerate dead myocardium after infarction has been challenged. Similarly, although several laboratories have identified cardiac progenitor cells (CPCs), the controversy concerning myocyte regeneration in the adult heart has not been resolved. The therapeutic efficacy of these 2 classes of progenitor cells depends on their ability to (1)survive in the hostile milieu of the damaged heart, (2)engraft within the myocardium and (3)grow and differentiate. BMPCs may have a growth potential that is superior to that of CPCs, but transdifferentiation could affect this characteristic and CPCs may constitute a more powerful form of therapy for cardiac repair. The process of transdifferentiation may alter the growth behavior of BMPCs, which may result in losing part of their capability of dividing through alterations of the telomere-telomerase system, premature cellular senescence and apoptosis. Moreover, myocytes derived from BMPCs may possess inherent limitations in the acquisition of the adult phenotype. The opposite may also be true and BMPCs may retain a stronger regenerative capacity than CPCs, representing the most appropriate cells for the damaged heart even after transdifferentiation. Ultimately, the question to be addressed is whether BMPCs are superior, equal or inferior to CPCs for the regeneration of cardiomyocytes and coronary vessels in acute and chronic ischemic heart failure. (Circ J 2010; 74: 13 - 17)
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  • Li-Wei Lo, Shih-Ann Chen
    2010 Volume 74 Issue 1 Pages 18-23
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: November 18, 2009
    JOURNALS FREE ACCESS
    Atrial fibrillation (AF) is the most common tachyarrhythmia, with a prevalence of 5% in people over the age of 65. Catheter ablation of AF has emerged as an important management choice for drug-refractory symptomatic paroxysmal or persistent AF. Three-dimensional (3D) electroanatomic mapping systems were introduced into catheter ablation of AF more than a decade ago. The 3D tool has the benefit of reducing the radiation exposure time, as well as voltage and fractionation mapping in order to identify the critical substrate during the ablation, prevent the formation of gaps, guide the ablation of post-ablation atrial tachycardia or flutter, and integrate images to improve the safety and long-term success rate. The 3D systems successfully enable safe and tailored radiofrequency ablation of AF in individual patients. (Circ J 2010; 74: 18 - 23)
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  • Their Pathophysiological Background and Clinical Application
    Hirofumi Tomiyama, Akira Yamashina
    2010 Volume 74 Issue 1 Pages 24-33
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: November 17, 2009
    JOURNALS FREE ACCESS
    The arterial wall has 3 layers (ie, the intima, including the endothelium, the media, and the adventitia); each of these layers has individual roles in systemic circulation. The vascular endothelium regulates the vascular tone, hemostasis and/or vascular permeability, and the media is the major determinant of arterial elasticity, which regulates the conduit function (delivery of blood to tissues) and cushioning effect (for generation of continuous blood flow). Failure of these functions results in organ/vascular damage. Several non-invasive methods are currently used to assess vascular dysfunction, including measurement of flow-mediated vasodilatation of the brachial artery induced by reactive hyperemia (FMD), pulse wave velocity (PWV), the augmentation index (AI), and central blood pressure. Endothelial dysfunction, which is assessed by FMD, contributes to the initiation/progression of atherosclerosis. Increased arterial stiffness, which is assessed by the PWV and/or AI, causes increased cardiac afterload, impaired coronary arterial blood supply, atherogenesis and/or microvascular damage. The combination of risk stratification by assessment of conventional risk factors for cardiovascular disease (CVD) with not only a morphological assessment of vascular damage, such as carotid ultrasound examination, but also vascular function tests, may be a useful strategy for the management of CVD and its related risk factors. (Circ J 2010; 74: 24 - 33)
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  • Naoya Matsumoto, Ken Nagao, Atsushi Hirayama, Yuichi Sato
    2010 Volume 74 Issue 1 Pages 34-40
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: December 05, 2009
    JOURNALS FREE ACCESS
    Coronary multislice computed tomography (MSCT) angiography and magnetic resonance angiography (MRA) have emerged as new diagnostic techniques that allow direct visualization of the coronary artery. These new modalities have both advantages and disadvantages concerning radiation exposure, the use of contrast medium, ability of visualizing heavily calcified artery lumens, and spatial and temporal resolution. However, these modalities only provide anatomical information of the coronary artery. Functional assessment of the severity of coronary artery disease (CAD) is essential for the management of patients with known or suspected CAD in practical clinical settings. Myocardial perfusion single-photon emission computed tomography is thought to be the most suitable diagnostic procedure for the determination of therapeutic strategy when coronary MSCT and MRA show significant and also insignificant coronary artery lesions. (Circ J 2010; 74: 34 - 40)
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Editorials
Original Articles
Aortic Disease
  • Tomoko Machino-Ohtsuka, Yoshihiro Seo, Tomoko Ishizu, Yukio Sekiguchi, ...
    2010 Volume 74 Issue 1 Pages 51-58
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: December 05, 2009
    JOURNALS FREE ACCESS
    Background: Cholesterol crystal embolism (CCE) is a serious complication of vascular procedures and based on the clinical features of patients with CCE, the aim of the present study was to establish screening criteria for aortic complex plaques (ACP) at high-risk of CCE. Methods and Results: For the first study, 10 patients diagnosed as having CCE were recruited. They had prior multiple atherosclerotic disease and a high proportion of complex plaques of the carotid artery and aorta. Elevated levels of high-sensitivity C-reactive protein (hs-CRP), eosinophilia, and renal insufficiency were already recognized before CCE diagnosis. The second study prospectively enrolled 102 patients. ACP is related to CCE and predictive criteria of ACP were established. Among 19 patients with ACP, 2 presented with CCE. Multivariate analysis revealed carotid complex plaque, eosinophilia and multiple atherosclerotic risk factors as independent predictors of ACP. The criteria including these factors (multiple atherosclerotic risk factors, carotid complex plaque, hs-CRP ≥0.2 mg/dl, eGFR ≤60 ml · min-1 · 1.73 m-2, eosinophil count ≥400 /μl) could detect patients with ACP with 95% sensitivity, 94% specificity, and 79% positive predictive value. Conclusions: Multiple atherosclerotic risk factors, elevated hs-CRP, renal insufficiency, eosinophilia before CCE diagnosis and carotid complex plaques were features of patients with CCE. Diagnostic criteria including these characteristics effectively predict ACP patients at high-risk of CCE. (Circ J 2010; 74: 51 - 58)
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Arrhythmia/Electrophysiology
  • Sumito Narita, Koji Miyamoto, Takeshi Tsuchiya, Yasutsugu Nagamoto, Ta ...
    2010 Volume 74 Issue 1 Pages 59-65
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: November 18, 2009
    JOURNALS FREE ACCESS
    Background: Atrial tachycardia (AT) is sometimes difficult to eliminate by radiofrequency ablation (RFA), but the EnSite array (EA) visualizes the beat-to-beat virtual activation of any tachycardia. Methods and Results: The 51 patients with 74 ATs (mean age 57±18 years, 28 males) undergoing EA-guided RFA were included; 14 patients had had previous open heart surgery and 5 had organic heart disease. RFA was performed at the AT focus for focal AT (n=48) with an endpoint of AT termination and subsequent non-inducibility. RFA was performed at a critical conducting pathway for reentrant AT (n=26) with creation of a block line in the critical reentry circuit. EA revealed that 57 ATs originated in the right atrium (77%) and 17 originated in the left atrium (23%); all but 1 were successfully eliminated. Fluoroscopic time was 19±11 min, the number of RFA applications was 8±7, and the radiofrequency energy was 10,711±12,655 J. No complications were noted. All but 2 patients were free of any symptoms during a follow-up of 16±9 months. Conclusions: EA-guided RFA is safe and effective for AT, irrespective of its mechanism, sustainability or origin, and regardless of underlying heart disease. (Circ J 2010; 74: 59 - 65)
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  • Shinya Suzuki, Takeshi Yamashita, Takayuki Ohtsuka, Koichi Sagara, Tok ...
    2010 Volume 74 Issue 1 Pages 66-70
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: October 02, 2009
    JOURNALS FREE ACCESS
    Background: Although recent studies have suggested that height and body mass index (BMI) independently affect the prevalence of atrial fibrillation (AF), their combined effects have not been fully examined in Japanese patients. Methods and Results: Patients without organic cardiac diseases, hypertension and diabetes mellitus were screened from a prospective, single hospital-based cohort of the Shinken Database 2004-2007 (n=4,719). Both height and BMI significantly increased the crude rate of AF prevalence and the effects were significant even after adjustment by age, sex and left atrial dimension. The relative risks (RRs) for AF in the height and BMI categories were 2.07 (95% confidence interval [CI] 1.70-2.52) and 1.78 (95%CI 1.46-2.17), respectively, in the highest tertile compared with the lowest tertile. The RRs in the highest combined tertile was high to 2.98 (95%CI 2.07-4.28) compared with the lowest combined tertile, an unignorable figure for AF prevalence in the future. Conclusions: Height and BMI synergistically affected the prevalence of AF in Japanese patients. With respect to the recent increase in body size of the Japanese population, the present study predicts that there will be more occurrences of AF than previously predicted. (Circ J 2010; 74: 66 - 70)
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  • Subanalysis of J-RHYTHM Study
    Yoshiyasu Aizawa, Shun Kohsaka, Shinya Suzuki, Hirotsugu Atarashi, Shi ...
    2010 Volume 74 Issue 1 Pages 71-76
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: December 02, 2009
    JOURNALS FREE ACCESS
    Background: The J-RHYTHM (Japanese Rhythm Management Trial for Atrial Fibrillation) study demonstrated the benefit of rhythm-control compared with rate-control in Japanese patients with paroxysmal atrial fibrillation (AF), according to AF-specific quality of life scores. However, detailed information on prescribed antiarrhythmic agents remains unclear. Methods and Results: Data for 419 patients enrolled in the rhythm-control arm of J-RHYTHM were analyzed. The primary endpoint was defined as a composite of total mortality, cerebral infarction, embolism, bleeding, heart failure, and physical/psychological disability. The secondary endpoint was recurrence of AF. The clinical outcome according to choice of initial antiarrhythmic agent (AA) was assessed by Kaplan-Meier survival curve, and further adjusted by Cox-regression hazard model. The primary endpoint occurred in 16.9%, 6.7%, 15.8% and 23.3% of patients assigned to class Ia, Ib, Ic and III agents (P=0.359). The rate of AF recurrence was significantly higher in patients taking a class III drug (Ia, Ib, Ic, III=20.3, 23.3, 29.1, 50.0%; P=0.002). However, after adjustment for other clinical variables, the choice of AA was not associated with recurrence of AF (class I vs III, P=0.15). Conclusions: The incidence of each endpoint did not differ according to the choice of AA. The class III drugs seemed to lower the sinus rhythm maintenance rate, which might be confounded by other comorbid conditions. (Circ J 2010; 74: 71 - 76)
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Cardiovascular Surgery
  • Ken Nagao, Kimio Kikushima, Kazuhiro Watanabe, Eizo Tachibana, Yoshite ...
    2010 Volume 74 Issue 1 Pages 77-85
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: November 27, 2009
    JOURNALS FREE ACCESS
    Background: Therapeutic hypothermia for comatose survivors of out-of-hospital cardiac arrest has demonstrated neurological benefits. Although early cooling during cardiac arrest enhances efficacy in animal studies, few clinical studies are available. Methods and Results: The 171 patients who failed to respond to conventional cardiopulmonary resuscitation were studied prospectively. Patients underwent emergency cardiopulmonary bypass (CPB) plus intra-aortic balloon pumping, with subsequent percutaneous coronary intervention (PCI) if needed. Mild hypothermia (34°C for 3 days) was induced during cardiac arrest or after return of spontaneous circulation. Of the 171 patients, 21 (12.3%) had a favorable neurological outcome at hospital discharge. An unadjusted rate of favorable outcome decreased in a stepwise fashion for increasing quartiles of collapse-to-34°C interval (P=0.016). An adjusted odds ratio for favorable outcome after collapse-to-CPB interval was 0.89 (95% confidence interval (CI) 0.82-0.97) and after CPB-to-34°C interval, 0.99 (95%CI 0.98-0.99) when collapse-to-34°C interval was divided into 2 components. Favorable neurological accuracy of a collapse-to-CPB interval at a cutoff of 55.5 min and CPB-to-34°C interval at a cutoff of 21.5 min was 85.4% and 89.5%, respectively. Conclusions: Early attainment of a core temperature had neurological benefits for patients with out-of-hospital cardiac arrest who underwent CPB and PCI. (Circ J 2010; 74: 77 - 85)
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  • Osami Honjo, Satoru Osaki, Yasuhiro Kotani, Teiji Akagi, Shunji Sano
    2010 Volume 74 Issue 1 Pages 86-92
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: November 27, 2009
    JOURNALS FREE ACCESS
    Background: To determine diagnosis-based differences in the response of global ventricular performance to modified ultrafiltration (MUF) using transesophageal echocardiography during congenital heart surgery. Methods and Results: The study included 38 children with atrial septal defect (n=10), ventricular septal defect (VSD) (n=8), tetralogy of Fallot (TOF) (n=9), or a single ventricle (n=11). Arteriovenous MUF was performed for 10-15 min after cardiopulmonary bypass (CPB). The myocardial performance index (MPI) of the systemic ventricles and the % change in MPI before and after MUF were assessed. Impairment of MPI was noted at termination of CPB compared with baseline values in the VSD and TOF groups (P<0.05). MUF resulted in an improvement in MPI in all groups (P<0.01). There was a weak correlation between aortic cross-clamping or CPB time, and the degree of improvement in MPI (r= 0.385, P=0.019; r= 0.348, P=0.037, respectively). MUF improved fractional shortening in all groups (P<0.05) and reversed abnormal relaxation in the VSD and TOF groups. Conclusions: Modified ultrafiltration ameliorated MPI in all groups, indicating improved systemic ventricular function with MUF. The MPI recovery rate differed among the groups. MUF may be particularly useful for restoring the global ventricular performance of patients undergoing longer CPB and may have minimal advantages for simple open-heart surgery. (Circ J 2010; 74: 86 - 92)
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Epidemiology
  • Report From the MIYAGI-AMI Registry Study
    Toru Takii, Satoshi Yasuda, Jun Takahashi, Kenta Ito, Nobuyuki Shiba, ...
    2010 Volume 74 Issue 1 Pages 93-100
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: November 27, 2009
    JOURNALS FREE ACCESS
    Background: Worldwide, the rate of aging is highest in Japan, especially the female population. To explore the trends for acute myocardial infarction (AMI) in Japan, the MIYAGI-AMI Registry Study has been conducted for 30 years since 1979, whereby all AMI patients in the Miyagi prefecture are prospectively registered. Methods and Results: In 1979-2008, 22,551 AMI patients (male/female 16,238/6,313) were registered from 43 hospitals. The age-adjusted incidence of AMI (/100,000persons/year) increased from 7.4 in 1979 to 27.0 in 2008 (P<0.001). Although control of coronary risk factors remained insufficient, the rates of ambulance use and primary percutaneous coronary intervention (PCI) have increased, and the overall in-hospital mortality (age-adjusted) has decreased from 20.0% in 1979 to 7.8% in 2008 (P<0.0001). However, the in-hospital mortality remains relatively higher in female than in male patients (12.2% vs 6.3% in 2008). Female patients were characterized by higher age and lower PCI rate. Conclusions: The MIYAGI-AMI Registry Study demonstrates the steady trend of an increasing incidence, but decreasing mortality, for AMI in Japan over the past 30 years, although the female population still remains at higher risk for in-hospital death, despite improvements in the use of ambulances and primary PCI. (Circ J 2010; 74: 93 - 100)
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Heart Failure
  • Bas M. van Dalen, Osama I.I. Soliman, Floris Kauer, Wim B. Vletter, He ...
    2010 Volume 74 Issue 1 Pages 101-108
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: December 07, 2009
    JOURNALS FREE ACCESS
    Background: In order to gain further insight into age-associated changes of left ventricular (LV) diastolic function, the purpose of the current study was to investigate alterations in LV untwisting with ageing. Methods and Results: The study comprised 75 healthy volunteers, classified into 3 groups: age 16-35 (n=25), 36-55 (n=25) and 56-75 (n=25) years. LV untwisting (as a percentage of peak systolic twist) at 5%, 10%, 15% and 50% of diastole, peak diastolic untwisting velocity, time-to-peak diastolic untwisting velocity and untwisting rate (mean untwisting velocity during the time interval from peak systolic twist to mitral valve opening) were assessed using speckle-tracking echocardiography. Untwisting at 5%, 10%, 15% and 50% of diastole decreased with ageing. Although the peak diastolic untwisting velocity and untwisting rate were not significantly different between the age groups, when normalized for LV peak systolic twist, these parameters decreased with advancing age (both P<0.01). Time-to-peak diastolic untwisting velocity increased with ageing (P<0.01). Conclusions: Impairment of the relative peak diastolic untwisting velocity and untwisting rate, resulting in delayed LV untwisting, may help to explain diastolic dysfunction in the elderly. (Circ J 2010; 74: 101 - 108)
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  • Kazuya Isobe, Keiji Kuba, Yasuhiro Maejima, Jun-ichi Suzuki, Shunichir ...
    2010 Volume 74 Issue 1 Pages 109-119
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: December 07, 2009
    JOURNALS FREE ACCESS
    Background: Although therapeutic angiogenesis is a most promising strategy for the treatment of myocardial infarction (MI), it remains unknown if and how endogenous angiogenesis inhibitors, such as endostatin, regulate angiogenesis in MI. In the present study the role of endostatin in left ventricular (LV) remodeling and heart failure was tested in a rat MI model. Methods and Results: When exposed to hypoxia, rat cardiomyocytes showed increased expression of endostatin. After MI induction in the rat MI model, endostatin expression was upregulated in cardiomyocytes, and serum endostatin levels were significantly elevated. Anti-endostatin antibody treatment resulted in significantly higher mortality of MI rats than controls. The MI rats with endostatin neutralization displayed adverse LV remodeling and severe heart failure compared with control MI rats. Although angiogenesis was increased, tissue remodeling and interstitial fibrosis were further exaggerated in post-MI hearts by endostatin neutralization. Furthermore, the expression and protease activity of matrix metalloproteinases -2 and -9, and of angiotensin-converting enzyme were markedly elevated by endostatin neutralization. Conclusions: Neutralization of endostatin worsens the symptoms and outcomes of MI in a rat model. The results imply that endogenous endostatin/collagen XVIII may suppress aberrant LV remodeling and heart failure after MI. (Circ J 2010; 74: 109 - 119)
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  • Hideo Mizutani, Ryuji Okamoto, Nobuyuki Moriki, Katsuhisa Konishi, Mas ...
    2010 Volume 74 Issue 1 Pages 120-128
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: December 07, 2009
    JOURNALS FREE ACCESS
    Background: Phosphorylation of the regulatory light chain of myosin (MLC) has roles in cardiac function. In vitro, myosin phosphatase target subunit 2 (MYPT2) is a strongly suspected regulatory subunit of cardiac myosin phosphatase (MP), but there is no in-vivo evidence regarding the functions of MYPT2 in the heart. Methods and Results: Transgenic mice (Tg) overexpressing MYPT2 were generated using the α-MHC promoter. Tg hearts showed an increased expression of MYPT2 and concomitant increase of the endogenous catalytic subunit of type 1 phosphatase (PP1cδ), resulting in an increase of the MP holoenzyme. The level of phosphorylation of ventricular MLC was reduced. The pCa-tension relationship, using β-escin permeabilized fibers, revealed decreased Ca2+ sensitization of contraction in the Tg heart. LV enlargement with associated impairment of function was observed in the Tg heart and ultrastructural examination showed cardiomyocyte degeneration. Conclusions: Overexpression of MYPT2 and the increase in PP1cδ resulted in an increase of the MP holoenzyme and a decrease in the level of MLC phosphorylation. The latter induced Ca2+ desensitization of contraction and decreased LV contractility, resulting in LV enlargement. Thus, MYPT2 is truly the regulatory subunit of cardiac MP in-vivo and plays a significant role in modulating cardiac function. (Circ J 2010; 74: 120 - 128)
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Hypertension and Circulatory Control
  • Investigation by Nickel Mesh Filtration Technique
    Kyoko Ariyoshi, Toru Maruyama, Keita Odashiro, Koichi Akashi, Takehiko ...
    2010 Volume 74 Issue 1 Pages 129-136
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: December 02, 2009
    JOURNALS FREE ACCESS
    Background: Deformability of erythrocytes plays a key role in the impairment of the microcirculation in hypertension. However, erythrocyte deformability in spontaneously hypertensive rats (SHR) during development of hypertension has not been fully investigated so far. Methods and Results: Erythrocyte filterability (whole cell deformability) was investigated in relation to blood pressure measured by the tail-cuff method in SHR and age-matched Wistar-Kyoto rats (WKY), using a highly sensitive and reproducible nickel mesh filtration technique. Impaired erythrocyte filterability was marked (37.0±17.5%) in prehypertensive young SHR (7 weeks of age) and sustained (51.6±13.3%) in hypertensive mature SHR (18 weeks of age), when compared with that of age-matched WKY (62.1±7.2% in 7 weeks of age, P<0.005, and 71.1±3.9% in 18 weeks of age, P<0.005, respectively). This impairment in SHR could not be explained by the mean corpuscular volume or mean corpuscular hemoglobin concentration of erythrocytes, but the erythrocyte count was significantly (P<0.005) greater in SHR than in the age-matched WKY. Conclusions: Although the precise mechanisms remain to be elucidated, markedly impaired erythrocyte filterability in SHR is considered to contribute to the development and maintenance of genetic hypertension. (Circ J 2010; 74: 129 - 136)
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Imaging
  • So Yeon Kim, Young Soo Lee, Jin Bae Lee, Jae Kean Ryu, Ji Yong Choi, S ...
    2010 Volume 74 Issue 1 Pages 137-141
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: December 05, 2009
    JOURNALS FREE ACCESS
    Background: The myocardial bridge (MB) is an intramural segment of coronary artery that is covered with myocardial tissue. The current diagnostic methods are coronary angiography, intravascular ultrasound and intracoronary Doppler, which are all invasive modalities. In this study, multidetector computed tomography (MDCT) was used to detect and evaluate the anatomical properties of the MB. Methods and Results: The 607 patients with suspected or known coronary artery disease underwent 64-slice MDCT. MB was diagnosed when an intramural segment of coronary artery was visualized on axial and multiplanar reconstruction images. The prevalence, length, myocardial thickness, and location were evaluated. Of the 607 patients, 39 (6.42%) had a MB. In 20 patients (52.6%), the MB was located in the mid left anterior descending artery. The length of tunneled artery was a mean 16.3 mm, from 6.9 mm to 30 mm, and the maximum thickness of the myocardial tissue was between 0.5 mm and 3.9 mm, with a mean of 1.8 mm. The length of the MB correlated significantly with thickness (P=0.049). Conclusions: The incidence of MB and its anatomical properties can be evaluated with MDCT, which might be a useful and noninvasive method of detecting this variant. (Circ J 2010; 74: 137 - 141)
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Ischemic Heart Disease
  • An Integrated Backscatter Intravascular Ultrasound Study
    Naohiro Komura, Kiyoshi Hibi, Ikuyoshi Kusama, Fumiyuki Otsuka, Takayu ...
    2010 Volume 74 Issue 1 Pages 142-147
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: December 02, 2009
    JOURNALS FREE ACCESS
    Background: Ruptured plaque and culprit lesions associated with anterior acute myocardial infarction cluster mainly in the proximal segment of the left anterior descending coronary artery (LAD). This study investigated whether the tissue characteristics of plaque in the proximal LAD differs from that of plaque in the distal LAD as assessed by integrated backscatter (IB)-intravascular ultrasound (IVUS). Methods and Results: IVUS interrogation was used to study 107 non-culprit intermediate plaques in 68 patients with angina pectoris who underwent percutaneous coronary interventions. Proximal and distal segments were defined as <30 mm and ≥30 mm from the ostium, respectively. IB-IVUS images were recorded, and the average percentage values of each plaque component (lipid, fibrosis, dense fibrosis, and calcification) were compared between segments. Plaques in the proximal segment (n=51) had a higher %lipid content (36 vs 19%, P<0.01) and a lower %fibrosis content (57 vs 64%, P<0.01) than did plaques in the distal segment (n=56). Multiple linear regression analysis showed that proximal plaques had a higher %lipid content, independently of other coronary risk factors and plaque burden (P<0.01). Conclusions: The %lipid and %fibrosis contents differ significantly between plaques in the proximal segment and those in the distal segment of the LAD. (Circ J 2010; 74: 142 - 147)
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  • Hiroto Shiraki, Hitoshi Yokozuka, Koji Negishi, Sousin Inoue, Tetsuo T ...
    2010 Volume 74 Issue 1 Pages 148-155
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: December 02, 2009
    JOURNALS FREE ACCESS
    Background: Right ventricular myocardial infarction (RVMI) is the major cause of hypotension and/or shock (HpS) after acute inferior myocardial infarction (inferior AMI). It is, however, unclear how RVMI affects the acute hemodynamic course. Methods and Results: In the present study, 153 patients with inferior AMI caused by right coronary artery occlusion were examined. Associations between in-hospital outcome and HpS before admission (preER-HpS) or HpS after admission (postER-HpS) were assessed using multivariate logistic regression analysis. Multivariate analysis was also conducted to determine a predictor for postER-HpS, including clinical findings in the emergency room as independent variables. HpS developed in 48.4% of patients with inferior AMI. Patients with RVMI more frequently had HpS than their counterparts in the first 6 h after infarction onset. RVMI was, however, not associated with preER-HpS, but was independently with postER-HpS (odds ratio (OR): 10.1; 4.0-27.7), whereas left ventricular failure was associated with preER-HpS, but not with postER-HpS. Furthermore, RVMI (OR: 9.4; 3.6-27.1) identified at presentation predicted postER-HpS. Conclusions: Independent of concomitant left ventricular involvement, RVMI was significantly associated with postER-HpS, but not with preER-HpS. These findings highlight the importance of identifying RVMI immediately after admission in the setting of inferior AMI. (Circ J 2010; 74: 148 - 155)
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Molecular Cardiology
  • Yoshinori Yoshida, Tatsuya Morimoto, Tomohide Takaya, Teruhisa Kawamur ...
    2010 Volume 74 Issue 1 Pages 156-162
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: December 07, 2009
    JOURNALS FREE ACCESS
    Background: Aldosterone exerts its effect by binding to specific mineralocorticoid receptors (MRs). Spironolactone blocks the aldosterone system, which ameliorates heart failure in humans, but the precise molecular mechanisms of MR blockade are unclear. Methods and Results: Neonatal rat cardiomyocytes were stimulated with phenylephrine (PE), aldosterone, and/or spironolactone. The association of the MR with p300, a transcriptional coactivator of GATA4 required for hypertrophic responses, was examined. MR and p300 synergistically activated GATA4-dependent atrial natriuretic factor (ANF) promoter activities. The stimulation of cardiomyocytes with PE induced translocation of the MRs into the nuclei and markedly increased the association of MRs with p300. Compatible with the synergistic activation by the MR and p300, aldosterone further augmented the PE-induced increase in cell size and induction of ANF gene transcription. Blockade of MR activation by spironolactone inhibited the PE-induced nuclear translocation of MRs and hypertrophic responses. Conclusions: For the first time it has been demonstrated that the aldosterone/MR system associates with the p300/GATA4 transcriptional pathway during the hypertrophic response of cardiomyocytes, and may provide a mechanism of the beneficial effects of aldosterone-blocking agents in heart failure therapy in humans. (Circ J 2010; 74: 156 - 162)
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Myocardial Disease
  • Yosuke Kato, Mitsunori Iwase, Sahoko Ichihara, Hiroaki Kanazawa, Katsu ...
    2010 Volume 74 Issue 1 Pages 163-170
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: November 27, 2009
    JOURNALS FREE ACCESS
    Background: Growth hormone-releasing peptide (GHRP) may act directly on the myocardium and improve left ventricular (LV) function, suggesting a potential new approach to the treatment of cardiomyopathic hearts. The present study tested the hypothesis that the beneficial cardiac effects of GHRP might include attenuation of myocardial oxidative stress. Methods and Results: Dilated cardiomyopathic TO-2 hamsters were injected with GHRP-2 (1 mg/kg) or saline from 6 to 12 weeks of age. F1B hamsters served as controls. Untreated TO-2 hamsters progressively developed LV dilation, wall thinning, and systolic dysfunction between 6 and 12 weeks of age. Marked myocardial fibrosis was apparent in untreated hamsters at 12 weeks of age in comparison with F1B controls. The ratio of reduced to oxidized glutathione (GSH/GSSG) was decreased and the concentration of 4-hydroxynonenal (4-HNE) was increased in the hearts of untreated TO-2 hamsters. Treatment with GHRP-2 attenuated the progression of LV remodeling and dysfunction, as well as myocardial fibrosis, in TO-2 hamsters. GHRP-2 also inhibited both the decrease in the GSH/GSSG ratio and the increase in the concentration of 4-HNE in the hearts of TO-2 hamsters. Conclusions: GHRP-2 can suppress the increase in the level of myocardial oxidative stress, leading to attenuation of progressive LV remodeling and dysfunction in dilated cardiomyopathic hamsters. (Circ J 2010; 74: 163 - 170)
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Pediatric Cardiology and Adult Congenital Heart Disease
  • Masanori Mizuno, Yuko Takeba, Naoki Matsumoto, Yoshimitsu Tsuzuki, Ken ...
    2010 Volume 74 Issue 1 Pages 171-180
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: December 02, 2009
    JOURNALS FREE ACCESS
    Background: Previous study has demonstrated the increase of several cardiac function-related proteins, including creatine kinase (CK) as an important enzyme in the process of ATP synthesis in the fetal heart of rats administered glucocorticoid (GC) antenatally. In the present study the effect of antenatal GC administration on the CK expression in fetal and neonatal hearts was demonstrated. Methods and Results: Dexamethasone was administered to pregnant rats on days 19 and 20 of gestation. The mRNA levels of the CK isoforms, CK-M and Mi-CK, in 21-day-old fetal and 1-day-old neonatal hearts were significantly increased after antenatal GC administration. CK protein levels were also increased in both cultured cardiomyocytes and the mitochondria of the hearts. Uptake of 5, 5', 6, 6'-tetrachloro-1, 1', 3, 3'-tetraethyl-benzimidazolocarbocyanine iodide by mitochondria was significantly increased. An increased ATP level accompanied the CK increase in the neonatal hearts. Furthermore, in vitro these effects were mediated though the GC receptor of cardiomyocytes. Peroxisome proliferator-activated receptor γ as the upstream transcription factor of CK was significantly increased in fetal hearts. Conclusions: These results suggest that antenatal GC administration accelerates ATP synthesis through increased CK and may contribute to maturation of the premature heart so that it is ready for preterm delivery. (Circ J 2010; 74: 171 - 180)
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Peripheral Vascular Disease
  • Miranda Fong, Masuhiro Yoshitake, Junichi Kambayashi, Yongge Liu
    2010 Volume 74 Issue 1 Pages 181-187
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: December 05, 2009
    JOURNALS FREE ACCESS
    Background: The mechanisms underlying the ability of cilostazol to improve walking distance in patients with intermittent claudication (IC) are not fully understood, but may be related to its phosphodiesterase type 3 (PDE3) and adenosine uptake inhibition. In the present study the effect of cilostazol on blood flow and interstitial adenosine concentration was compared with that of the PDE3 inhibitor, milrinone, and the adenosine uptake inhibitor, draflazine. Methods and Results: Rabbit gastrocnemius muscle blood flow was measured under resting, contracting and ischemic conditions. Interstitial adenosine was sampled by microdialysis. None of the drugs affected tissue blood flow at rest. Blood flow in electrically stimulated muscle was 2- to 3-fold higher in vehicle-, milrinone- and draflazine-treated animals. However, cilostazol caused an 8-fold increase. Ligation of the femoral artery decreased blood flow in the stimulated muscle in all groups to a similar degree. Cilostazol and draflazine increased the dialysate adenosine concentration during the first 10 min of muscle contraction, but had no effect during ischemia, most likely because of the high AMP deaminase activity in skeletal muscle. Conclusions: Cilostazol increases blood flow in the gastrocnemius muscle during contraction and it is this effect that may be partially responsible for the improved walking distance in IC patients. (Circ J 2010; 74: 181 - 187)
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Regenerative Medicine
  • Bernhard Schlechta, Dominik Wiedemann, Clemens Kittinger, Anita Jandro ...
    2010 Volume 74 Issue 1 Pages 188-194
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: November 19, 2009
    JOURNALS FREE ACCESS
    Background: Umbilical cord blood (UCB) is a source of human hematopoietic precursor cells (HPCs), a stem cell (SC) type that has been used in several trials for myocardial repair. A certain minimal number of cells is required for measurable regeneration and a major challenge of SC-based regenerative therapy constitutes ex-vivo expansion of the primitive cell compartment. The aim of this study was to investigate the ex-vivo expansion potential of UCB-derived HPCs and the ability of these expanded cells to migrate to the site of damage and improve ventricular function in a rodent model of myocardial infarction (MI). Methods and Results: UCB-derived HPCs, defined by coexpression of CD133 and CD34, were expanded using various cytokine combinations. MI was induced by left anterior descending artery ligation in nude rats. Cells were injected intravenously 2 days after infarction. The combination of SC factor, thrombopoietin, flt3-ligand and interleukin-6 was found to be the most effective for inducing proliferation of HPCs. The migratory capacity of expanded HPCs was similar to that of non-expanded HPCs and improvement of ejection fraction was significant in both groups, with a relative increase of >60%. Conclusions: UCB-derived HPCs can be reproducibly expanded ex-vivo and retain their potential to improve cardiac function post-MI. (Circ J 2010; 74: 188 - 194)
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Vascular Medicine
  • Osamu Yoshida, Takahisa Kondo, Yasuko Kureishi-Bando, Tomonori Sugiura ...
    2010 Volume 74 Issue 1 Pages 195-202
    Published: 2010
    Released: December 25, 2009
    [Advance publication] Released: November 19, 2009
    JOURNALS FREE ACCESS
    Background: Smoking is a major cardiovascular risk factor, leading to endothelial dysfunction. The present study investigated the hypothesis that pitavastatin, an HMG-CoA reductase inhibitor, may improve endothelial function in chronic smokers via its antioxidant properties. Methods and Results: The 30 male chronic smokers who exhibited mild hypercholesterolemia at the time of physical check-up were enrolled and randomized to the pitavastatin group (2 mg/day, n=15) or the untreated control group (n=15). Before and after the 4-week treatment period, endothelium-dependent flow-mediated dilation (FMD) and endothelium-independent dilation by glyceryl trinitrate (GTD) were examined, and the FMD/GTD ratio was calculated. The pitavastatin group showed a significant restoration of endothelial function (percent change in FMD: +49.6% vs +1.4%; percent change in FMD/GTD ratio: +26.6% vs 4.5%, P<0.05 respectively), and a significant reduction in oxidative stress levels (malondialdehyde-low-density lipoprotein-cholesterol: 16.6% vs +7.5%; free radical activity: 1.8% vs +9.7%, P<0.05 respectively) compared with the control group. Pitavastatin had no effect on the number of circulating CD34+CD133+ progenitor cells, endothelial progenitor cells, or the MMP-2, MMP-9 and VEGF levels. In vitro oxidative stress monitoring assay revealed that pitavastatin protected endothelial cells against oxidative stress. Conclusions: Pitavastatin restores endothelial function, even in chronic smokers, possibly through its antioxidative properties. (Circ J 2010; 74: 195 - 202)
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