Circulation Journal
Online ISSN : 1347-4820
Print ISSN : 1346-9843
ISSN-L : 1346-9843
Volume 75, Issue 6
Displaying 1-39 of 39 articles from this issue
Reviews
  • – Approach to Therapy –
    Antonio Curcio, Daniele Torella, Ciro Indolfi
    2011 Volume 75 Issue 6 Pages 1287-1296
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 29, 2011
    JOURNAL FREE ACCESS
    Bare metal stents (BMS) successfully prevented abrupt artery closure and reduced the restenosis rate compared with balloon angioplasty. This review summarizes laboratory and recent clinical investigations concerning neointimal formation and endothelial regeneration after vascular injury. BMS efficacy was severely hampered by proliferating vascular smooth muscle cells (VSMCs), and the resultant neointimal hyperplasia, which is the only mechanism responsible for restenosis after metal stent placement. The advent of drug-eluting stents (DES) in 2002 have since then revolutionized interventional cardiology. By using the stent struts as a platform coated with polymers to elute drugs targeting VSMC proliferation, a substantial attenuation of in-stent restenosis is feasible. As with any medical innovation this technology still has restrictive factors, and novel approaches are promoted to improve the safety and efficacy of DES. Indeed, the antiproliferative properties of DES impair and/or delay endothelialization, hence leading to late stent thrombosis. Improvements in percutaneous coronary intervention procedures include the use of the so-called gsecond-generation DESh, together with new coating technologies, bioabsorbable stents, and non-drug-based stent coatings. Particular emphasis will be placed on the concept that endothelial regeneration might be pursued as well as reduction of VSMC proliferation to allow stable successful revascularization after DES deployment. (Circ J 2011; 75: 1287-1296)
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  • – Refocus on the Electrical Substrate –
    Marc Strik, Sylvain Ploux, Kevin Vernooy, Frits W. Prinzen
    2011 Volume 75 Issue 6 Pages 1297-1304
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 29, 2011
    JOURNAL FREE ACCESS
    Cardiac resynchronization therapy (CRT) is an established treatment for selected heart failure patients with conduction disease. Many studies aimed at quantifying mechanical dyssynchrony in CRT candidates when it became apparent that 30-50% of CRT recipients showed no improvement after implantation. As these, often echocardiography-based, measurements have not yet succeeded in estimating the mechanical substrate in an accurate and reproducible manner, interest in electrical substrate has renewed. In this review, current knowledge concerning electrical substrate in CRT candidates will be explored and applied to current CRT practice, highlighting why the electrical substrate is both essential and sufficient for successful CRT. Finally, novel ways to better measure and treat the electrical substrate are discussed. (Circ J 2011; 75: 1297-1304)
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  • – An Inflammatory Disease –
    Sophie E. P. New, Elena Aikawa
    2011 Volume 75 Issue 6 Pages 1305-1313
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: May 12, 2011
    JOURNAL FREE ACCESS
    Cardiovascular calcification is an independent risk factor for cardiovascular morbidity and mortality. This disease of dysregulated metabolism is no longer viewed as a passive degenerative disease, but instead as an active process triggered by pro-inflammatory cues. Furthermore, a positive feedback loop of calcification and inflammation is hypothesized to drive disease progression in arterial calcification. Both calcific aortic valve disease and atherosclerotic arterial calcification may possess similar underlying mechanisms. Early histopathological studies first highlighted the contribution of inflammation to cardiovascular calcification by demonstrating the accumulation of macrophages and T lymphocytes in `early' lesions within the aortic valves and arteries. A series of in vitro work followed, which gave a mechanistic insight into the stimulation of smooth muscle cells to undergo osteogenic differentiation and mineralization. The emergence of novel technology, in the form of animal models and more recently molecular imaging, has enabled accelerated progression of this field, by providing strong evidence regarding the concept of this disorder as an inflammatory disease. Although there are still gaps in our knowledge of the mechanisms behind this disorder, this review discusses the various studies that have helped form the concept of the inflammation-dependent cardiovascular calcification paradigm. (Circ J 2011; 75: 1305-1313)
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Editorials
Original Articles
Arrhythmia/Electrophysiology
  • – A Report From the J-RHYTHM Registry –
    Hirotsugu Atarashi, Hiroshi Inoue, Ken Okumura, Takeshi Yamashita, Nao ...
    2011 Volume 75 Issue 6 Pages 1328-1333
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 05, 2011
    JOURNAL FREE ACCESS
    Background: Underuse and an inadequate range for the international normalized ratio (INR) for warfarin use are still problems in the management of the patients with atrial fibrillation (AF) in Japan. Methods and Results: From January to July 2009, a total of 7,937 AF patients [5,468 men (68.6±10.0 years) and 2,469 women (72.2±9.0 years)] were registered from 158 institutions for the J-RHYTHM Registry. Overall, 34.2% of the patients were over the age of 75. The associated cardiovascular diagnoses were hypertension in 59.1%, coronary artery disease in 10.1%, cardiomyopathy in 8.3%, valvular heart disease in 13.7% and artificial cardiac valves in 3.1% of the patients. The type of AF was paroxysmal in 37.1%, persistent in 14.4%, and permanent in 48.5%. Overall, 87.3% of patients were taking warfarin (2.9±1.2mg/day), of whom 66.0% had an INR between 1.6 and 2.6, and 35.4% were in the INR range from 2.0 to 3.0 at the time of registration. Aspirin was prescribed in 22.3% of cases. The CHADS2 score was 0 in 15.7% of patients, 1 in 34.0%, and ≥2 in 50.3%. Conclusions: At present, warfarin is used extensively in patients with AF whose stroke risk is relatively low (ie, in Japan) and half of them had CHADS2 scores of 0 to 1 (UMIN Clinical Trials Registry UMIN000001569). (Circ J 2011; 75: 1328-1333)
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  • Tsuyoshi Shiga, Atsushi Suzuki, Miyoko Naganuma, Fumitaka Hosaka, Mori ...
    2011 Volume 75 Issue 6 Pages 1334-1342
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 12, 2011
    JOURNAL FREE ACCESS
    Background: It is unknown whether bepridil improves cardiovascular events in atrial fibrillation (AF) patients, so this study evaluated the clinical outcome in paroxysmal or persistent AF patients receiving bepridil. Methods and Results: We conducted a cohort study of 284 consecutive patients who received bepridil for AF (25% female, 5913 years) with a median follow-up period of 17 months (4-157 months). A total of 135 (48%) patients had structural heart disease, and 231 patients (81%) had previously received class I or class III antiarrhythmic drugs. The cumulative rates for cardiovascular events were 2.4%, 8.1%, and 10.1% at 1, 3, and 5 years, respectively. The cumulative rates for a composite of mortality, cerebral infarction, systemic embolism, major bleeding and heart failure were 9.7%, 18.2%, and 29.6% at 1, 3, and 5 years, respectively. The probability of progression to permanent AF was 23.5% at 5 years. Sudden death occurred in a patient with a prior myocardial infarction who was taking 200mg daily, and torsade de pointes (Tdp) occurred in two patients without structural heart disease taking 200mg daily. Excessive corrected QT interval prolongation (>0.50s) was observed when plasma concentrations were higher than 800ng/ml. Conclusions: Bepridil might not improve the clinical outcome in refractory AF patients. Bepridil-related adverse events, including QT prolongation and Tdp, occurred in a dose- and concentration-dependent manner. (Circ J 2011; 75: 1334-1342)
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  • Masahito Miura, Masanori Hirose, Hideaki Endoh, Yuji Wakayama, Yoshina ...
    2011 Volume 75 Issue 6 Pages 1343-1349
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 02, 2011
    JOURNAL FREE ACCESS
    Supplementary material
    Background: Triggered arrhythmias arise from delayed afterdepolarizations (DADs), with Ca2+ waves playing an important role in their formation. In ventricular hypertrophy, however, it remains unclear how Ca2+ waves change their propagation features and affect arrhythmogenesis. We addressed this important issue in a rat model of hypertrophy. Methods and Results: Rats were given a subcutaneous injection of 60mg/kg monocrotaline (MCT-rats) or solvent (Ctr-rats). After 4 weeks, MCT-rats showed high right ventricular (RV) pressure and RV hypertrophy. Trabeculae were dissected from 36 right ventricles. The force was measured using a silicon strain gauge and regional intracellular Ca2+ ([Ca2+]i) was determined using microinjected fura-2. Reproducible Ca2+ waves were induced by stimulus trains (2Hz, 7.5s). MCT-rats showed a higher diastolic [Ca2+]i and faster and larger Ca2+ waves (P<0.01). The velocity and amplitude of Ca2+ waves were correlated with the diastolic [Ca2+]i both in the Ctr- and MCT-rats. The velocity of Ca2+ waves in the MCT-rats was larger at the given amplitude of Ca2+ waves than that in the Ctr-rats (P<0.01). The amplitude of DADs was correlated with the velocity and amplitude of Ca2+ waves in the Ctr- and MCT-rats. Conclusions: The results suggest that an increase in diastolic [Ca2+]i and an increase in Ca2+ sensitivity of the sarcoplasmic reticulum Ca2+ release channel accelerate Ca2+ waves in ventricular hypertrophy, thereby causing arrhythmogenesis. (Circ J 2011; 75: 1343-1349)
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Cardiovascular Intervention
  • – Possible Role of Inflammatory Cytokines in the Development of Stent Thrombosis From the Korea Stent Thrombosis Registry –
    Seok-Jae Hwang, Kyung Woo Park, Dong-A Kwon, Hyun-Jae Kang, Bon-Kwon K ...
    2011 Volume 75 Issue 6 Pages 1350-1357
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 18, 2011
    JOURNAL FREE ACCESS
    Background: Inflammation might contribute to the development of stent thrombosis (ST). The association between inflammatory cytokine concentrations and drug-eluting ST were evaluated. Methods and Results: Among the 123 ST patients enrolled in the multicenter Korea Stent Thrombosis registry, plasma samples were available in 41 patients. The patients' clinical characteristics and plasma concentrations of monocyte chemoattractant protein-1, tumor necrosis factor-alpha, and interleukin (IL)-6 were compared with 81 matched controls. Although the concentrations of 3 cytokines were higher in the ST group, they did not have significant differences. When divided into quartiles, the proportion of patients with the highest quartile of IL-6 was higher in the ST group than in the control group (44% vs. 16%, P=0.001), and the highest IL-6 quartile was an independent predictor of ST for both early (adjusted hazard ratio [HR] 6.96; 95% confidence interval [CI] 1.75-27.66) and late ST (adjusted HR 4.71; 95%CI 1.06-20.92). In addition, the highest IL-6 quartile was an independent predictor of ST in those on clopidogrel (adjusted HR 7.70; 95%CI 1.97-30.13) but not in those who were off clopidogrel. Conclusions: Highest IL-6 quartile was associated with ST, especially in clopidogrel users regardless of the time of ST, suggesting the involvement of inflammatory cytokines in ST. (Circ J 2011; 75: 1350-1357)
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  • Shunsuke Funakoshi, Yutaka Furukawa, Natsuhiko Ehara, Takeshi Morimoto ...
    2011 Volume 75 Issue 6 Pages 1358-1367
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 12, 2011
    JOURNAL FREE ACCESS
    Supplementary material
    Background: Limited data are available for gender-based differences in patients undergoing coronary revascularization. This study aimed to identify gender-based differences in risk factor profiles and outcomes among Japanese patients undergoing coronary revascularization. Methods and Results: The subjects consisted of 2,845 women and 6,843 men who underwent first percutaneous coronary intervention or coronary artery bypass grafting in 2000-2002. The outcome measures were all-cause death, major adverse cardiovascular events (MACE) as the composite of cardiovascular death, myocardial infarction and stroke, and any coronary revascularization. The females were older than the males and more frequently had histories of heart failure, diabetes, hypertension, chronic kidney disease, anemia, and dyslipidemia. Unadjusted survival analysis revealed a significantly lower incidence of any revascularization in women (at 3 years: 28.2% vs. 31.2%, P=0.0037), although no significant gender-based differences were shown in the incidence of all-cause death (at 3 years: 8.8% vs. 8.5%, P=0.37) or MACE (at 3 years: 12.0% vs. 11.5%, P=0.61). Multivariate analysis revealed that female gender was associated with significantly lower risks of any revascularization (relative risk=0.93, 95% confidence interval [CI]=0.88-0.99, P=0.014) and all-cause death (relative risk=0.86, 95%CI=0.77-0.96, P=0.005). Conclusions: In Japanese patients undergoing first coronary revascularization, the coronary risk factor burden appeared greater in women than in men. Despite the greater modifiable risk factor accumulation, female gender was associated with a lower incidence of repeated revascularization relative to male gender. (Circ J 2011; 75: 1358-1367)
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Cardiac Rehabilitation
  • – The JMS Cohort Study –
    Yosuke Shibata, Shinya Hayasaka, Tomoyo Yamada, Toshiyuki Ojima, Shizu ...
    2011 Volume 75 Issue 6 Pages 1368-1372
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 15, 2011
    JOURNAL FREE ACCESS
    Background: Although many population-based studies have reported an association between physical activity and cardiovascular disease (CVD) among healthy populations, the association among CVD survivors has been less reported. We examined the relationship between physical activity and CVD risk among survivors. Methods and Results: This was a prospective cohort study of 12,490 Japanese participants, including 754 individual CVD survivors. Between April 1992 and July 1995, a baseline survey was conducted in 12 communities in Japan. The mean follow-up period was 11.9 years, during which time 74 individuals had non-fatal CVD and 51 cases were fatal CVD. Among CVD survivors, analysis was performed after exclusion of participants with a history of cancer and those who died within the first 2 years of follow-up. Physical activity was analyzed in tertiles (low, moderate and heavy), and the hazard ratios (HRs) were calculated for non-fatal or fatal CVD among CVD survivors. After setting the low group as the reference, the HRs for non-fatal CVD in the moderate and heavy groups were 0.61 (95% confidence interval: 0.30-1.24) and 0.50 (0.20-1.25) (P for trend=0.059), respectively, and the HRs for fatal CVD were 0.75 (0.33-1.69) and 0.18 (0.04-0.83) (P for trend=0.026), respectively. Conclusions: Physical activity reduced the risk of CVD, both fatal and non-fatal events, among CVD survivors. (Circ J 2011; 75: 1368-1372)
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Cardiovascular Surgery
  • Mitsumasa Hata, Isamu Yoshitake, Shinji Wakui, Satoshi Unosawa, Haruka ...
    2011 Volume 75 Issue 6 Pages 1373-1377
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: March 31, 2011
    JOURNAL FREE ACCESS
    Background: The aim of the present study was to assess the long-term graft patency rate of the radial artery (RA), in comparison to the saphenous vein (SV) in patients harvested for both vessels. Methods and Results: RA and SV were concomitantly used for coronary artery bypass grafting in 318 patients in an 8-year period from January 2002 to March 2010. During follow-up, graft patency was assessed on angiography or multi-slice computed tomography in 192 of these patients. Cumulative graft patency rates were compared between RA and SV. Independent predictors for graft failure were examined for both vessels. Cumulative graft patency rates at 8 years were 74.3% in RA and 64.7% in SV, respectively. There was no significant difference between these types of grafts. Independent predictors of late RA graft failure were native coronary stenosis <75% and peripheral vascular disease (PVD). Independent predictors of late SV graft failure were use of only one anti-platelet agent and low-density lipoprotein cholesterol/high-density lipoprotein cholesterol ratio >2.5. Cardiovascular event-free and actuarial survival rates at 8 years in this series were 81.2% and 89.7%, respectively. Conclusions: Cumulative graft patency rates between RA and SV were similar at 8 years. RA performed more poorly in patients with target vessel stenosis <75% and in those complicated by PVD. Aggressive anti-platelet therapy and strict lipid control may be important in maintaining long-term patency of SV. Circ J 2011; 75: 1373-1377)
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  • – A Propensity Matched Analysis of Outcomes –
    Mahboob Alam, Sahar Siddiqui, Vei-Vei Lee, McArthur A. Elayda, Vijay N ...
    2011 Volume 75 Issue 6 Pages 1378-1385
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 18, 2011
    JOURNAL FREE ACCESS
    Background: There is conflicting data regarding the impact of obesity on morbidity and mortality in patients undergoing isolated coronary artery bypass grafting (CABG). Methods and Results: Retrospective cohort analysis of patients who underwent CABG from January 1, 1995, through July 31, 2010 was performed. Patients were classified as obese or non-obese (body mass index ≥30.0kg/m2 and <30.0kg/m2, respectively). The primary outcome was in-hospital mortality. Secondary outcomes included postoperative respiratory failure, postoperative stroke, postoperative myocardial infarction, sternal and leg wound infections, postoperative atrial fibrillation, postoperative ventricular tachycardia, postoperative renal failure and length of hospital stay. Propensity-matched stepwise multivariable logistic regression was performed. Of 13,115 patients, 4,619 (35.2%) were obese. In the propensity-matched logistic regression models (n=8,442), obesity was not associated with postoperative mortality (odds ratio=1.13, 95% confidence interval 0.86-1.48). However, obesity was associated with postoperative respiratory failure, postoperative renal insufficiency, sternal wound infection, and leg wound infection. Obesity was also associated with a decreased risk of postoperative bleeding and re-operation from bleeding. Conclusions: Obesity was associated with an increased risk of postoperative respiratory failure, postoperative renal failure, and surgical site infections. However, obesity was not associated with in-hospital mortality in patients undergoing CABG. (Circ J 2011; 75: 1378-1385)
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Heart Failure
  • Sayaka Kurokawa, Shinichi Niwano, Hiroe Niwano, Shoko Ishikawa, Jun Ki ...
    2011 Volume 75 Issue 6 Pages 1386-1393
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 16, 2011
    JOURNAL FREE ACCESS
    Background: Although oxidative stress is considered to promote arrhythmogenic substrates in diseased model animals, it is difficult to evaluate its primary role. In this study, we evaluated the promotion of arrhythmogenic substrates in the primary hyperoxidative state. Methods and Results: Sprague-Dawley rats were treated with L-buthionine-sulfoximine (BSO, 30mmol·L-1·day-1) for 14 days. On day 7 or 14, the serum levels of derivatives of reactive oxygen metabolites (d-ROM) were measured, and immune staining of 8-hydroxy-2'-deoxyguanosine (8OHdG) was performed to assess oxidative stress. The ventricular effective refractory period (ERP), monophasic action potential duration (MAPD), and the inducibility of ventricular arrhythmia were also evaluated. BSO rats exhibited higher serum d-ROM and clearer 8OHdG staining than the controls. The inducibility of ventricular arrhythmia was higher in the BSO rats than in the controls. The ERP was shorter in the BSO rats than the control (day 14, 32±1 vs. 36±1ms, P<0.05), whereas the MAPD90 was longer in the BSO rats (day 14, 76±5 vs. 55±4ms, P<0.05). The mRNA levels of Kv4.2, erg, and SERCA2a were downregulated in the BSO rats (P<0.05), and Western blot analysis exhibited the downregulation of erg and SERCA2 expression in the BSO rats (P<0.05). Conclusions: Systemic oxidative stress might be one of the primary factors promoting cardiac electrophysiological remodeling and increasing the inducibility of arrhythmia independently of major organ disorders. (Circ J 2011; 75: 1386-1393)
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  • Naoko Ishibashi, In-Sam Park, Tadashi Waragai, Tadahiro Yoshikawa, Yas ...
    2011 Volume 75 Issue 6 Pages 1394-1399
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: March 22, 2011
    JOURNAL FREE ACCESS
    Background: The effect of carvedilol on heart failure (HF) in patients with a functionally univentricular heart (UVH) remains unclear. Methods and Results: Carvedilol was used to treat HF in 51 patients with a UVH, classified into 3 groups: after the Fontan operation (F), after the bidirectional Glenn operation (G), and patients who had not undergone Fontan or Glenn operation (NF). Carvedilol therapy was started at a mean age of 10±12 years (range: 1 month to 34 years). The initial and maximum doses of carvedilol were 0.04±0.03 and 0.42±0.29mg·kg-1·day-1, respectively. After a mean follow-up of 11 months, the cardiothoracic ratio improved from 60±8 to 58±8% (P<0.01), and the dosage of furosemide was reduced from 1.4±0.9 to 0.7±0.7mg·kg-1·day-1 (P<0.01). The ejection fraction also improved from 35±12 to 40±11% (P<0.05), and this improvement was prominent in the F group (from 35±15 to 45±9%; P<0.05). Clinical signs, symptoms, and New York Heart Association functional class also improved. Conclusions: Carvedilol may play an important role in treating HF associated with a UVH. (Circ J 2011; 75: 1394-1399)
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  • Toshihiko Kubo, Eduardo R Azevedo, Gary E Newton, Peter Picton, John D ...
    2011 Volume 75 Issue 6 Pages 1400-1408
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 26, 2011
    JOURNAL FREE ACCESS
    Background: Muscle sympathetic nerve firing rate increases as chronic heart failure (CHF) progresses, yet its oscillation, particularly within the frequency range encompassing 0.13Hz, diminishes. The current study tested the hypothesis that chronic therapy with lipophilic β-adrenoceptor antagonists augments the modulation of muscle sympathetic nerve activity variability (MSNAV) at this frequency range. Methods and Results: In 21 CHF angiotensin converting enzyme (ACE) inhibitor-treated patients (age: 53±2, ejection fraction: 20±2%), MSNA was recorded before and after 4 months of β-blockade with either metoprolol (up to 50mg b.i.d.) or carvedilol (up to 25mg b.i.d.). Harmonic MSNAV was assessed by coarse graining spectral analysis. Both drugs lowered heart rate similarly (-13±2 beats/min; P<0.001) but neither affected MSNA burst frequency (-7±4 bursts/min, not significant). Before β-blockade, harmonic MSNA power in the region encompassing 0.13Hz was essentially absent. Beta-blockade increased the mean values for total power (from 0.00 to 0.50Hz; 5.2±0.8 to 6.8±1.2U2; P<0.001) and for harmonic MSNA spectral power across the 0.1-0.22Hz frequency range (from 0.48±0.10 to 1.50±0.32U2, F=12.2; P<0.001). Both carvedilol and metoprolol had a similar effect. Conclusions: In patients with CHF receiving ACE inhibitors, adding a β-adrenoceptor antagonist restores low and high frequency harmonic oscillations in MSNA. Beta-1 antagonism is sufficient to achieve this response. Augmented modulation of sympathetic outflow could contribute to the beneficial effects of β-blockade in CHF on sudden death and disease progression. (Circ J 2011; 75: 1400-1408)
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Hypertension and Circulatory Control
  • – Possible Role for Cardiovascular Remodeling in Spontaneously Hypertensive Rats –
    Jie Han, Dong-Mei Jiang, Chang-Qing Du, Shen-Jiang Hu
    2011 Volume 75 Issue 6 Pages 1409-1417
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: March 31, 2011
    JOURNAL FREE ACCESS
    Background: The mevalonate pathway is an important metabolic pathway that plays a key role in multiple cellular processes. The aim of this study was to define whether the enzyme expression in mevalonate pathway changes during cardiovascular remodelling in spontaneously hypertensive rats (SHR). Methods and Results: Hearts and thoracic aortas were removed for the study of cardiovascular remodeling in SHR and Wistar-Kyoto rats (WKY). The protein expression of the enzymes in hearts, aortas and livers was analyzed by western blot. The histological measurements showed that the mass and the size of cardiomyocytes, the media thickness and the media cross-sectional area (MCSA) of the thoracic aorta were all increased in SHR since 3 weeks of age. In the heart, there was overexpression of some enzymes, including 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR), farnesyl diphosphate synthase (FDPS), and geranylgeranyltransferase type I (GGTase-I), and downregulation of squalene synthetase (SQS) in SHR since 3 weeks of age. In the aorta, besides similar expressions of HMGR, SQS, FDPS and GGTase-I as in the heart, there was upregulation of farnesyltransferase α at 16 and 25 weeks of age and of farnesyltransferase β in 25-weeks-old SHR. Western blot demonstrated overexpression of HMGR and downregulation of SQS in SHR livers at all ages tested. Conclusions: The cardiovascular remodeling of SHR preceded the development of hypertension, and altered expression of several key enzymes in the mevalonate pathway may play a potential pathophysiological role in cardiovascular remodeling. (Circ J 2011; 75: 1409-1417)
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  • Kunio Yufu, Naohiko Takahashi, Norihiro Okada, Osamu Wakisaka, Tetsuji ...
    2011 Volume 75 Issue 6 Pages 1418-1423
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 09, 2011
    JOURNAL FREE ACCESS
    Background: Cardiovascular autonomic neuropathy is a major complication in patients with diabetes mellitus (DM), and baroreflex sensitivity (BRS) reportedly can predict cardiovascular prognosis in type 2 DM patients. The hypothesis that cardiovascular events are associated with gender differences in BRS was tested in the present study. Methods and Results: From 1998, we have evaluated BRS by phenylephrine methods in 185 consecutive type 2 DM patients. The long-term prognostic value of BRS was compared between 91 female (5812 years) and 94 male patients (5811 years). There was no significant difference in age or severity and duration of DM between the 2 groups. When compared to male, the BRS value in female patients was significantly lower (9.266.0 vs. 5.975.0ms/mmHg, P<0.0001). During a mean of 62.7 months of follow-up, 16 female patients developed cardiovascular events (17.6%) including stroke, acute myocardial infarction, angina pectoris requiring percutaneous coronary intervention or coronary artery bypass grafting and congestive heart failure requiring admission, while only 4 male patients developed events (4.3%, P<0.005). In females, the Kaplan-Meier curves revealed that those with depressed BRS (<6ms/mmHg) had a higher incidence of cardiovascular events than those with preserved BRS (P<0.05), but this relationship was not observed in male patients. Conclusions: Although the reason why females had a more depressed BRS remains unclear, our findings demonstrated that a depressed BRS value can accurately predict cardiovascular events, especially in female patients with type 2 DM. (Circ J 2011; 75: 1418-1423)
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Imaging
  • Mashio Nakamura, Yoshiaki Okano, Hiroki Minamiguchi, Mitsuru Munemasa, ...
    2011 Volume 75 Issue 6 Pages 1424-1432
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 22, 2011
    JOURNAL FREE ACCESS
    Background: Unfractionated heparin (UFH) is the standard drug for the initial treatment of pulmonary embolism (PE) and deep vein thrombosis (DVT) in Japan, whereas fondaparinux is the standard drug in Europe and the United States. Here, we examine the efficacy and safety of fondaparinux in Japanese patients. Methods and Results: In 2 randomized, open-label, multicenter studies, 80 Japanese patients with acute PE or DVT received either subcutaneous fondaparinux or intravenous UFH as a non-comparative reference, in a 3:1 ratio, for 5-10 days. Concomitant warfarin therapy was continued until Day 90. Multidetector-row computed tomography-based assessment showed that 57.9% and 45.9% of the patients with acute PE and acute proximal DVT had proximal DVT and PE as a complication, respectively. There was no recurrence of symptomatic venous thromboembolism. In the fondaparinux group, the respective improvement rates at the end of the initial treatment and follow-up periods were 71.4% and 86.8% for 42 patients with PE, and 57.8% and 83.3% for 46 patients with DVT; similar results were noted in the UFH group. One patient in the fondaparinux group experienced major bleeding during the initial treatment, but no such episode in the UFH group. Conclusions: Once-daily, subcutaneous fondaparinux is as effective and safe without monitoring as adjusted-dose intravenous UFH for the initial treatment of acute PE and DVT in Japanese patients. (Circ J 2011; 75: 1424-1432)
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Ischemic Heart Disease
  • – Time-Dependent Comparison With Other Biomarkers –
    Nobuaki Kobayashi, Noritake Hata, Noriaki Kume, Yoshihiko Seino, Toru ...
    2011 Volume 75 Issue 6 Pages 1433-1439
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: March 30, 2011
    JOURNAL FREE ACCESS
    Background: The diagnostic sensitivity of myocardial necrosis markers, such as creatine kinase-MB (CK-MB), cardiac troponins, myoglobin and heart-type fatty acid-binding protein (H-FABP) for the earliest stage of ST-elevation myocardial infarction (STEMI), remains insufficient. We compared a new biomarker of plaque vulnerability (soluble lectin-like oxidized low-density lipoprotein receptor-1, sLOX-1) with other biomarkers at the earliest stage of STEMI. Methods and Results: Plasma sLOX-1 levels were measured in 125 STEMI, 44 non-STEMI (NSTEMI) and 125 non-acute myocardial infarction (non-AMI) patients and were significantly (P<0.0001) higher in the STEMI and NSTEMI than in the non-AMI patients (median, 25th and 75th percentiles: 241.0, 132.3 and 472.2 vs. 147.3, 92.9 and 262.4 vs. 64.3, 54.4 and 84.3pg/ml, respectively). At the optimal cut-off value of 91.0pg/ml, sLOX-1 discriminated STEMI from non-AMI with 89.6% sensitivity and 82.4% specificity. Time-dependent changes in sLOX-1, H-FABP, myoglobin, troponin T and CK-MB were analyzed in 27 STEMI patients. Elevated plasma sLOX-1 levels persisted for 24h after admission, whereas other markers were not elevated at the time of admission and peaked at ≥2h thereafter. The diagnostic sensitivity of sLOX-1, H-FABP, myoglobin, troponin T and CK-MB for STEMI upon admission (89min after onset) was 93%, 78%, 70%, 56% and 33%, respectively. Conclusions: Plasma sLOX-1 diagnosed the early stages of STEMI more accurately than H-FABP, myoglobin, troponin T and CK-MB. (Circ J 2011; 75: 1433-1439)
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  • Myung Hwan Bae, Jang Hoon Lee, Sang Hyuk Lee, Sun Hee Park, Dong Heon ...
    2011 Volume 75 Issue 6 Pages 1440-1447
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 16, 2011
    JOURNAL FREE ACCESS
    Background: There are limited data regarding the prognostic value of serum uric acid (UA) after acute myocardial infarction (AMI). We investigated whether UA predicts the prognosis independently and whether it has an incremental value to other factors, including N-terminal Pro-B-type natriuretic peptide (NT-ProBNP), in patients with AMI. Methods and Results: This study included 850 patients with AMI who were enrolled in the Korea AMI Registry from a single center. A major adverse cardiovascular event (MACE) was defined as a composite of death, recurrent myocardial infarction, and revascularization. During 6-month follow-up, MACE developed in 109 (12.8%). UA was higher in patients with MACE than in those without MACE (6.5±2.4mg/dl vs. 5.4±1.8mg/dl, P<0.001). In the Cox-proportional hazard model, UA (hazard ratio [HR] 1.297, 95% confidence interval [CI] 1.075-1.565, P=0.007) was an independent predictor for 6-month MACE in addition to log NT-ProBNP (HR 2.362, 95%CI 1.007-5.539, P=0.048), heart rate (HR 1.028, 95%CI 1.009-1.047, P=0.004) and 3-vessel disease (HR 3.278, 95%CI 1.378 to 7.797, P=0.007). UA had incremental prognostic value to conventional risk factors (chi-square=8, P=0.005), and to the combination of conventional factors and NT-ProBNP (chi-square=10, P=0.002). Conclusions: UA is an independent predictor of short-term prognosis and has incremental value to NT-ProBNP in patients with AMI. (Circ J 2011; 75: 1440-1447)
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  • Atsushi Hirayama, Satoshi Saito, Yasunori Ueda, Tadateru Takayama, Jun ...
    2011 Volume 75 Issue 6 Pages 1448-1454
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 19, 2011
    JOURNAL FREE ACCESS
    Background: The aim of this study was to compare the effect of atorvastatin treatment on high-grade yellow coronary plaques (grade ≥2, group H) vs. low-grade yellow plaques (grade ≤1, group L). Methods and Results: Twenty-nine hypercholesterolemic patients with coronary heart disease were treated with atorvastatin (10-20mg/day) for 80 weeks and were divided into 2 groups by baseline plaque color grade. The angioscopic plaque grade and the vessel, plaque, and luminal volumes were measured by intravascular ultrasound at baseline and in weeks 28 and 80. The plaque color grade decreased significantly from baseline to weeks 28 and 80 in group H (2.27±0.48, 1.47±0.75, and 1.55±0.86, respectively), but not significantly in group L (0.90±0.31, 0.83±0.61, and 0.89±0.56, respectively). The plaque volume of group HP was greater than that of group LP (respectively 158.0±45.8 vs. 107.5±21.9mm3 at baseline, 144.5±41.1 vs. 97.5±24.8mm3 in week 28, and 128.8±31.5 vs. 87.9±31.5mm3 in week 80 (P<0.001 by ANCOVA between groups). Conclusions: The plaque-stabilizing effect of atorvastatin was stronger for more vulnerable plaques with a higher color grade, although regression of plaque during atorvastatin therapy was noted irrespective of plaque vulnerability. (Circ J 2011; 75: 1448-1454)
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Pediatric Cardiology and Adult Congenital Heart Disease
  • Ryota Ebata, Jun Abe, Kumi Yasukawa, Hiromichi Hamada, Kouji Higashi, ...
    2011 Volume 75 Issue 6 Pages 1455-1462
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 12, 2011
    JOURNAL FREE ACCESS
    Background: Kawasaki disease (KD) is characterized by systemic vasculitis with tissue edema. During the healing process of inflammation, lymphangiogenesis is essential for reducing tissue edema. One potential responsible candidate for the induction of lymphangiogenesis in the healing process of acute KD is vascular endothelial growth factor-D (VEGF-D). Methods and Results: Sequential changes in serum VEGF-D levels in patients with acute KD (n=47) using an enzyme-linked immunosorbent assay were investigated. Cross-sectional areas of lymphatic vessels and VEGF-D protein expression were evaluated immunohistochemically in cardiac tissues of patients (n=6) who died of KD. Regulation of VEGF-D messenger RNA (mRNA) expression in cultured fibroblasts was assessed using quantitative real-time polymerase chain reaction. Serum VEGF-D levels increased after intravenous immunoglobulin therapy in patients with acute KD (P<0.001). In addition, they were significantly lower in patients with coronary artery lesions (CAL) than in those without CAL (P<0.05). The cross-sectional areas of lymphatic vessels in cardiac tissues were enlarged in patients with acute KD. VEGF-D protein was detected on the endothelium of the enlarged lymphatic vessels. In vitro, tumor necrosis factor- significantly down-regulated VEGF-D mRNA expression in cultured fibroblasts (P=0.004). Conclusions: This study indicates that the production of VEGF-D increases and is related to lymphangiogenesis in patients with acute KD. In addition, low VEGF-D production appears to be associated with the development of CAL. (Circ J 2011; 75: 1455-1462)
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  • HaiQiong Huang, Peng Zhang, Zhen Wang, Feng Tang, Zhen Jiang
    2011 Volume 75 Issue 6 Pages 1463-1471
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 17, 2011
    JOURNAL FREE ACCESS
    Background: It is unclear why some patients, who undergo complete repair or palliative surgery for congenital heart disease (CHD), still develop irreversible pulmonary artery hypertension (PAH). There is no consensus to preoperationally assess the reversible and irreversible pulmonary vasculopathy seen in PAH. Methods and Results: The peri-operative pulmonary hemodynamic data of 16 CHD patients (reversible PAH, n=6; irreversible PAH, n=10) were analyzed. The lung biopsies were also performed during surgery for defining histopathological characteristics as well as immunohistochemical expression of endothelin-1 (ET-1), endothelin-1 receptors (ETR), and its downstream signaling markers in the small pulmonary arteries and arterioles. Neointimal formation and neoangiogenesis was characterized by increased intimal layer immunoreactivity for α-SMA, Factor VIII, CD34, and VEGF. Neointimal formation was found in 90% of patients and neoangiogenesis was found in 80% of patients with irreversible PAH. Neither was present in the reversible PAH group and the control group. Expression of ET-1 and ETR in the neointimal layer of the pulmonary arterioles was upregulated in irreversible PAH, and immunoreactivity of phospho-Akt, phospho-ERK1/2, and phospho-mTOR was also increased in irreversible PAH. Conclusions: Increased expression of ET-1, ETR, and activation of signaling pathways were observed in the pulmonary arteries and arterioles of irreversible PAH patients associated with CHD. Activation of these pathways might in turn lead to neointimal formation and neoangiogenesis and thus might contribute to irreversible pulmonary vascular abnormalities. (Circ J 2011; 75: 1463-1471)
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Peripheral Vascular Disease
  • – An Important Risk Factor for Venous Thromboembolism –
    Satoshi Ota, Norikazu Yamada, Yoshito Ogihara, Akihiro Tsuji, Ken Ishi ...
    2011 Volume 75 Issue 6 Pages 1472-1475
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 17, 2011
    JOURNAL FREE ACCESS
    Background: Elevated levels of Factor VIII (FVIII) have been suggested as important for the pathogenesis of venous thromboembolism (VTE). The objective of this study was to explore the association between elevated FVIII level and VTE in Japan. Methods and Results: 68 patients with objectively documented VTE and 40 controls were included. In the patients, the FVIII level was measured for a mean follow-up period of 52.6 months (3-348 months) after the onset of VTE, in order to avoid an acute-phase response. The VTE patients had a higher mean FVIII level than the controls (154.5±55.8IU/dl vs. 114.3±16.0IU/dl, P<0.0001). According to multivariate analysis, FVIII levels above the 50th percentile (124IU/dl) conferred an odds ratio of 4.9 (95% confidence intervals (CI) 1.9-12.4; P<0.001) and those above the 75th percentile (150IU/dl) conferred an odds ratio of 31.9 (95%CI 4.0-252.3; P<0.001). Conclusions: Elevated plasma FVIII level is a risk factors for VTE in Japanese people, and FVIII levels above the 75th percentile are associated with a significant odds ratio for the occurrence of VTE. (Circ J 2011; 75: 1472-1475)
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Regenerative Medicine
  • Hui Xu, Yue-Jin Yang, Hai-Yan Qian, Yi-Da Tang, Hong Wang, Qian Zhang
    2011 Volume 75 Issue 6 Pages 1476-1485
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 19, 2011
    JOURNAL FREE ACCESS
    Background: Widespread death of implanted cells hampers the development of stem cell therapy for acute myocardial infarction (AMI). Our previous studies indicated that statins can protect implanted mesenchymal stem cells (MSCs) against the post-infarct microenvironment, thus increasing the therapeutic effect. However, the underlying mechanisms are unclear. The JAK-STAT pathway participates in regulation of stress responses of the myocardium to various insults. This study aimed to detect whether rosuvastatin (ROSU) facilitates the survival, engraftment, and differentiation of allogeneic bone marrow-derived MSCs in the post-infarct heart via the JAK-STAT signaling pathway. Methods and Results: Female Sprague-Dawley rats were randomized into 5 groups: AMI (control), ROSU gavage (group R), MSCs transplantation (group M), MSCs and ROSU (group M+R), or MSCs, ROSU and a JAK2 inhibitor AG-490 (group M+R+AG). MSCs from male rats were injected into the myocardium 1 week after AMI. Cardiac function and histology, as well as the expression of Y-chromosomal genes and JAK-STAT signaling proteins, were examined at 4 weeks after transplantation. Better functional recovery, increased survival and differentiation of MSCs occurred in group M+R. Furthermore, phosphorylation of JAK2 and STAT3 was higher in group M+R. The effects of ROSU, as well as of activated JAK-STAT proteins, could be attenuated by AG-490. Conclusions: ROSU treatment improves the efficacy of stem cell transplantation in infarcted hearts by activation of the JAK2-STAT3 signaling pathway. (Circ J 2011; 75: 1476-1485)
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Vascular Medicine
  • Zhi-Yong Li, Tjun Y Tang, Fan Jiang, Yun Zhang, Jonathan H Gillard
    2011 Volume 75 Issue 6 Pages 1486-1492
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 12, 2011
    JOURNAL FREE ACCESS
    Background: Inflammation and biomechanical factors have been associated with the development of vulnerable atherosclerotic plaques. Lipid-lowering therapy has been shown to be effective in stabilizing them by reducing plaque inflammation. Its effect on arterial wall strain, however, remains unknown. The aim of the present study was to investigate the role of high- and low-dose lipid-lowering therapy using an HMG-CoA reductase inhibitor, atorvastatin, on arterial wall strain. Methods and Results: Forty patients with carotid stenosis >40% were successfully followed up during the Atorvastatin Therapy: Effects on Reduction Of Macrophage Activity (ATHEROMA; ISRCTN64894118) Trial. All patients had plaque inflammation as shown by intraplaque accumulation of ultrasmall super paramagnetic particles of iron oxide on magnetic resonance imaging at baseline. Structural analysis was performed and change of strain was compared between high- and low-dose statin at 0 and 12 weeks. There was no significant difference in strain between the 2 groups at baseline (P=0.6). At 12 weeks, the maximum strain was significantly lower in the 80-mg group than in the 10-mg group (0.0850.033 vs. 0.1690.084; P=0.001). A significant reduction (26%) of maximum strain was observed in the 80-mg group at 12 weeks (0.0180.02; P=0.01). Conclusions: Aggressive lipid-lowering therapy is associated with a significant reduction in arterial wall strain. The reduction in biomechanical strain may be associated with reductions in plaque inflammatory burden. (Circ J 2011; 75: 1486-1492)
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  • – The PATROL Trial –
    Keijiro Saku, Bo Zhang, Keita Noda, The PATROL Trial Investigators
    2011 Volume 75 Issue 6 Pages 1493-1505
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 15, 2011
    JOURNAL FREE ACCESS
    Background: Atorvastatin, rosuvastatin and pitavastatin are available for intensive, aggressive low-density lipoprotein cholesterol (LDL-C)-lowering therapy in clinical practice. The objective of the Randomized Head-to-Head Comparison of Pitavastatin, Atorvastatin, and Rosuvastatin for Safety and Efficacy (Quantity and Quality of LDL) (PATROL) Trial was to compare the safety and efficacy of atorvastatin, rosuvastatin and pitavastatin head to head in patients with hypercholesterolemia. This is the first prospective randomized multi-center trial to compare these strong statins (UMIN Registration No: 000000586). Methods and Results: Patients with risk factors for coronary artery disease and elevated LDL-C levels were randomized to receive atorvastatin (10mg/day), rosuvastatin (2.5mg/day), or pitavastatin (2mg/day) for 16 weeks. Safety was assessed in terms of adverse event rates, including abnormal clinical laboratory variables related to liver and kidney function and skeletal muscle. Efficacy was assessed by the changes in the levels and patterns of lipoproteins. Three hundred and two patients (from 51 centers) were enrolled, and these 3 strong statins equally reduced LDL-C and LDL particles, as well as fast-migrating LDL (modified LDL) by 40-45%. Newly developed pitavastatin was non-inferior to the other 2 statins in lowering LDL-C. There were no differences in the rate of adverse drug reactions among the 3 groups, but HbA1c was increased while uric acid was decreased in the atorvastatin and rosuvastatin groups. Conclusions: The safety and efficacy of these 3 strong statins are equal. It is suggested that the use of these 3 statins be completely dependent on physician discretion based on patient background. (Circ J 2011; 75: 1493-1505)
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  • Nader Ghaffari, Christine Ball, Jennifer A Kennedy, Irene Stafford, Jo ...
    2011 Volume 75 Issue 6 Pages 1506-1514
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 29, 2011
    JOURNAL FREE ACCESS
    Background: Statins have been shown to inhibit conduit vessel constrictor responses via the endothelial nitric oxide (NO) pathway. Clinical studies have implicated an effect in microvascular resistance vessels; however, direct effects of therapeutically relevant statin concentrations have not been examined. We examined the effect of acute pravastatin pretreatment on vasoconstrictor responsiveness of isolated rat mesenteric small vessels. Methods and Results: Pravastatin (112nmol/L) pretreatment for 60min reduced both the potency and maximal constrictor responses to phenylephrine, thromboxane (U46619) and serotonin in small vessels. This effect was abolished by endothelial denudation, NO synthase (NOS) inhibition with N-ω-nitro-L-arginine methyl ester (L-NAME 300μmol/L) and Akt inhibition (Akt1/2 kinase inhibitor 500nmol/L), confirming an endothelium-dependent mechanism and implicating a NO-mediated effect via the Akt pathway. Maximal superoxide scavenging with polyethylene glycol-superoxide dismutase (PEG-SOD), 150U/ml did not influence phenylephrine constrictor responses but potentiated pravastatin's effect, suggesting that the statin did not increase NO bioavailability merely via an antioxidant mechanism. In contrast, pravastatin did not affect endothelin-1 (ET-1) constrictor responses. However, after pre-incubation with a selective endothelin-B (ETB) receptor antagonist (BQ788 3μmol/L) pravastatin inhibited ET-1 constriction, suggesting that its effect is via the same mechanistic pathway as the ETB receptor. Conclusions: In small vessels, pravastatin inhibits constrictor responses by increasing endothelial NO bioavailability via the Akt pathway. Furthermore, ETB receptor blockade unmasks this effect in ET-1 constrictor responses. (Circ J 2011; 75: 1506-1514)
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Controversies in Cardiovascular Medicine
  • – Does MDCT Accurately Estimate Plaque Vulnerability? (Pro) –
    Sei Komatsu, Atsuko Imai, Kazuhisa Kodama
    2011 Volume 75 Issue 6 Pages 1515-1521
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 29, 2011
    JOURNAL FREE ACCESS
    Over the past decade, multidetector row computed tomography (MDCT) has become the most reliable and established of the noninvasive examination techniques for detecting coronary heart disease. Now MDCT is chasing intravascular ultrasound (IVUS) in terms of spatial resolution. Among the components of vulnerable plaque, MDCT may detect lipid-rich plaque, the lipid pool, and calcified spots using computed tomography number. Plaque components are detected by MDCT with high accuracy compared with IVUS and angioscopy when assessing vulnerable plaque. The TWINS study and TOGETHAR trial demonstrated that angioscopic loss of yellow color occurred independently of volumetric plaque change by statin therapy. These 2 studies showed that plaque stabilization and regression reflect independent processes mediated by different mechanisms and time course. Noncalcified plaque and/or low-density plaque was found to be the strongest predictor of cardiac events, regardless of lesion severity, and act as a potential marker of plaque vulnerability. MDCT may be an effective tool for early triage of patients with chest pain who have a normal ECG and cardiac enzymes in the emergency department. MDCT has the potential ability to analyze coronary plaque quantitatively and qualitatively if some problems are resolved. MDCT may become an essential tool for detecting and preventing coronary artery disease in the future. (Circ J 2011; 75: 1515-1521)
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  • – Does MDCT Accurately Estimate Plaque Vulnerability? (Con) –
    Masahiro Higashi
    2011 Volume 75 Issue 6 Pages 1522-1528
    Published: 2011
    Released on J-STAGE: May 25, 2011
    Advance online publication: April 29, 2011
    JOURNAL FREE ACCESS
    As a result of the advent and advances of multidetector row computed tomography (MDCT), coronary computed tomography (CT) has become popular and is performed at many institutions. Coronary CT is useful for diagnosing cases of moderate risk of coronary artery disease. On the other hand, it has been shown that most cardiac infarctions (≈70%) occur from mild to moderate stenoses (ie, ≤50%). Thus, conventional cardiac angiographic findings alone cannot predict developing cardiac infarction. The mechanism by which ruptured plaque and subsequent thrombus leads to developing cardiac infarction has been shown, so determining which plaque tended to rupture, the so-called "vulnerable plaque", and treatment of it are in the spotlight. Coronary CT can visualize and evaluate non-invasively not only the lumen but also the arterial wall. The findings that are suspicious for vulnerable plaque on coronary CT are low-density plaque, positive remodeling, and spotty calcification. However, CT is restricted in its resolution (temporal, spatial and contrast resolution). The diagnosis of vulnerable plaque by CT is still challenging. This report demonstrates the present conditions and problems for the characterization of the plaque using coronary CT. (Circ J 2011; 75: 1522-1528)
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Images in Cardiovascular Medicine
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