Circulation Journal
Online ISSN : 1347-4820
Print ISSN : 1346-9843
ISSN-L : 1346-9843
Volume 75, Issue 7
Displaying 1-42 of 42 articles from this issue
Reviews
  • Satoshi Imaizumi, Mohamad Navab, Cecilia Morgantini, Christina Charles ...
    2011 Volume 75 Issue 7 Pages 1533-1538
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: May 28, 2011
    JOURNAL FREE ACCESS
    Although high-density lipoprotein-cholesterol (HDL-C) levels in large epidemiological studies are inversely related to the risk of coronary heart disease (CHD), increasing the level of circulating HDL-C does not necessarily decrease the risk of CHD events, CHD deaths, or mortality. HDL can act as an anti- or a pro-inflammatory molecule, depending on the context and environment. Based on a number of recent studies, it appears that the anti- or pro-inflammatory nature of HDL may be a more sensitive indicator of the presence or absence of atherosclerosis than HDL-C levels. The HDL proteome has been suggested to be a marker, and perhaps a mediator, of CHD. Apolipoprotein A-1 (apoA-I), the major protein in HDL is a selective target for oxidation by myeloperoxidase, which results in impaired HDL function. Improving HDL function through modification of its lipid and/or protein content maybe a therapeutic target for the treatment of CHD and many inflammatory disorders. HDL/apoA-I mimetic peptides may have the ability to modify the lipid and protein content of HDL and convert dysfunctional HDL to functional HDL. This review focuses on recent studies of dysfunctional HDL in animal models and human disease, and the potential of apoA-I mimetic peptides to normalize the composition and function of lipoproteins. (Circ J 2011; 75: 1533-1538)
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  • – Evaluation and Positioning of New Oral Anticoagulant Agents –
    Satoshi Ogawa, Yukihiro Koretsune, Masahiro Yasaka, Yoshifusa Aizawa, ...
    2011 Volume 75 Issue 7 Pages 1539-1547
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: June 09, 2011
    JOURNAL FREE ACCESS
    Atrial fibrillation (AF) is the most common cardiac rhythm disorder and a major risk factor for stroke. For more than 60 years, warfarin has been the only approved anticoagulant for prevention of stroke in patients with AF. Although highly effective, it has many limitations that make its use difficult. Therefore, several novel anticoagulants are under development to overcome the limitations of warfarin, and some of these have entered phase III clinical trials. Dabigatran is an oral, reversible direct thrombin inhibitor approved in Europe and in several other countries for the prevention of venous thromboembolism after elective knee and hip replacement surgery. It has also been approved in the United States and Japan for the prevention of stroke and systemic embolism in patients with nonvalvular AF. In this review, the mechanism of action and pharmacological properties of new anticoagulants are described in detail, and the correct use of dabigatran in clinical practice is discussed. (Circ J 2011; 75: 1539-1547)
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  • – Importance of Clinico-Pathological Correlations –
    Hiroyuki Hao, Hatsue Ishibashi-Ueda, Masahiko Tsujimoto, Yasunori Ueda ...
    2011 Volume 75 Issue 7 Pages 1548-1558
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: May 27, 2011
    JOURNAL FREE ACCESS
    The benefit of drug-eluting stents (DES) is the remarkable reduction in the rates of both restenosis and target lesion revascularization. However, the risk of thrombotic complications extends further in DES-implanted arteries compared with those treated with bare-metal stents (BMS). Moreover, in-stent thrombosis (IST) and delayed arterial healing in DES-treated arteries have been identified by histological examination. At autopsy, proliferation of a monolayer composed of endothelium-like cells over stent struts in DES receiving arteries has been observed; however, these cells are negative for well-accepted endothelial cell markers. An inflammatory reaction against the stent struts is apparent after implantation of BMS and paclitaxel-eluting stents, whereas after sirolimus-eluting stents (SES), minimal inflammation is seen up to 6 months after device implantation. IST and in-stent restenosis, both possibly related to a hypersensitivity phenomena, are peculiar to DES, albeit relatively infrequent. A case of enhanced neointimal hyperplasia at 6 months after SES implantation with massive inflammatory reaction including eosinophils, and fibrin deposition is reported here. Observation of the morphological alterations after DES implantation by imaging techniques may furnish important information, but lack of precise comparative data between vascular imaging and histopathology leads to improper interpretation of imaging. Ex vivo imaging using angioscopy, intravascular ultrasound, and optical coherency tomography of SES implantation is presented and the images are compared with the corresponding pathological section. (Circ J 2011; 75: 1548-1558)
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  • Yukio Ishikawa, Yoko Kawawa, Eiichi Kohda, Kazuyuki Shimada, Toshiharu ...
    2011 Volume 75 Issue 7 Pages 1559-1566
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: March 31, 2011
    JOURNAL FREE ACCESS
    A myocardial bridge (MB), partially covering the coronary artery, is a congenital anatomical variant usually present in the left anterior descending coronary artery (LAD). MB causes coronary heart disease (CHD) by 2 distinct mechanisms influenced by the anatomical properties of the MB, such as its length, thickness, and location. One is direct MB compression of the LAD at cardiac systole, resulting in delayed arterial relaxation at diastole, reduced blood flow reserve, and decreased blood perfusion. The other is enhancement of coronary atherosclerosis causing stenosis of the LAD proximal to the MB, occurring because of endothelial injury arising from the abnormal hemodynamics provoked by retrograde blood flow up toward the left coronary ostium at cardiac systole. The magnitude of the effect of the 2 distinct mechanisms of the MB on LAD blood flow is prescribed by a common root of the MB-muscle mass volume generated by those properties. Furthermore, the anatomical properties of the MB are closely associated with the choice of treatment and therapeutic outcome in CHD patients having an MB. Thus, the anatomical properties of an MB should be considered in the diagnosis and management of CHD patients with this anomaly. (Circ J 2011; 75: 1559-1566)
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Editorials
Original Articles
Arrhythmia/Electrophysiology
  • Tzu-Wei Tseng, Yu-Feng Hu, Chin-Feng Tsai, Hsuan-Ming Tsao, Ching-Tai ...
    2011 Volume 75 Issue 7 Pages 1581-1584
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: April 22, 2011
    JOURNAL FREE ACCESS
    Background: This study aimed to investigate the impact of aging on electrophysiological characteristics in patients with atrioventricular nodal re-entrant tachycardia (AVNRT). Methods and Results: The 2,111 patients who underwent an electrophysiological study and radiofrequency (RF) catheter ablation of AVNRT were enrolled. The patients were divided into 4 groups according to age (group 1: <20 years; group 2: 20-39 years; group 3: 40-59 years; and group 4: ≥60 years). The gender distribution differed with age. The atrio-Hisian interval, and effective refractory periods (ERP) of the right atrium, ventricle, antegrade slow pathway, retrograde slow pathway and fast pathway, and tachycardia cycle length all increased with age. However, a paradoxical change in the fast pathway ERP was noted. The fast pathway ERP was significantly longer in group 2 than in other groups, and was associated with the largest tachycardia window. The response to catecholamines was similar between different age groups. Procedure time, radiation time, and complications did not differ. However, the number of RF impulses was higher in group 2 compared with other groups (7.6±9.3, P=0.04), which might imply a differing complexity during the ablation. Conclusions: Paradoxical aging changes of AVN electrophysiological characteristics were associated with a different atrioventricular nodal conduction property and the number of RF impulses. (Circ J 2011; 75: 1581-1584)
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  • Yasuaki Tanaka, Hiroshi Tada, Sachiko Ito, Shigeto Naito, Koji Higuchi ...
    2011 Volume 75 Issue 7 Pages 1585-1591
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: May 12, 2011
    JOURNAL FREE ACCESS
    Background: The prevalence, gender- and age-related differences, ablation success rate and inter-relationship between the origins of the idiopathic ventricular arrhythmias (I-VA) have not been clarified. Methods and Results: A total of 625 consecutive patients with symptomatic, drug resistant I-VA (315 males and 310 females; mean age, 54±17 years; 218 ventricular tachycardias, 407 premature ventricular contractions) who underwent catheter ablation were studied. The patients were divided into 5 groups based on the VA origin: (1) outflow tract (OT)-VA, consisting of right ventricular (RV) OT-VA and left ventricular (LV) OT-VA; (2) inflow tract (IT)-VA, consisting of tricuspid annulus (TA)-free wall (FW)-VA, IT-septum-VA, and mitral (MA)-FW-VA; (3) LV-inferoseptum-VA; (4) LV-other-VA; and (5) RV-other-VA. RVOT-VA in women were 1.5 times more frequent than in men, while LVOT-VA were more frequent in men. The prevalence of LVOT origin I-VA increased with age compared to that for the RVOT. The mean age of MA-FW-VA patients (62±14 years) was higher than that of TA-FW-VA patients (51±18 years; P=0.03). The ablation success rate for RVOT-VA (88%) was higher than that for LVOT-VA (58%; P<0.0001). A multivariate analysis revealed that the patient age was one of the valuable predictors of a successful ablation (odds ratio=0.97; 95% confidence interval: 0.95-0.99; P=0.007). Conclusions: Distinct gender and age differences were found in the incidence of I-VA according to their site of origin. (Circ J 2011; 75: 1585-1591)
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  • Wen-Chin Ko, Chuang-Ye Hong, Shaw-Min Hou, Chien-Huang Lin, Eng-Thiam ...
    2011 Volume 75 Issue 7 Pages 1592-1600
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: May 17, 2011
    JOURNAL FREE ACCESS
    Background: Atrial fibrosis is a feature of structural remodeling in atrial fibrillation (AF). Connective tissue growth factor (CTGF) is a potent profibrotic factor, but its role of CTGF in AF is not yet fully understood. Methods and Results: Right atrial appendages were obtained from 20 patients who underwent cardiac surgery (10 with sinus rhythm, 10 with AF). The mRNA level, protein level and immunohistochemical staining of CTGF were significantly increased in AF patients. In a porcine AF model, tissue angiotensin II (Ang II) and CTGF levels were significantly upregulated in both atria. In perfused rat hearts, Ang II stimulation increased CTGF expression, which could be inhibited by Ang II type I receptor antagonist. In a cell culture system, both atrial fibroblasts and myocytes were responsible for the increased CTGF expression under Ang II treatment. Ang II type I receptor antagonist could inhibit the Ang II-induced CTGF expression. Treating with recombinant CTGF, atrial fibroblasts expressed an increased level of collagen I. Furthermore, the CTGF level was highly correlated with tissue Ang II content in AF pigs. Conclusions: AF patients and animals exhibited a significantly increased expression of CTGF. Ang II stimulation upregulated CTGF expression in both atrial fibroblasts and myocytes. Ang II-induced CTGF expression might be involved in atrial substrate remodeling. (Circ J 2011; 75: 1592-1600)
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  • Luong Cong Thuc, Yasushi Teshima, Naohiko Takahashi, Satoru Nishio, Ak ...
    2011 Volume 75 Issue 7 Pages 1601-1608
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: May 25, 2011
    JOURNAL FREE ACCESS
    Supplementary material
    Background: Statins are reported to reduce mortality in patients with coronary artery disease and that mortality benefit might be related to the drugs' antiarrhythmic properties. Methods and Results: Male rats were fed with or without pravastatin (0.1mg·kg-1·day-1) for 7 days, and thereafter subjected to 10min of ischemia by coronary artery ligation followed by 20min reperfusion. Treatment with pravastatin reduced the frequency and duration of ventricular tachycardia and fibrillation (VT/VF) and improved the arrhythmia score after reperfusion. To investigate the rapid effects of pravastatin, isolated perfused rat hearts were subjected to 20min of global ischemia followed by 30 or 60min of reperfusion. Treatment with pravastatin (10nmol/L) from 10min before ischemia shortened the total duration of reperfusion-induced VT/VF. Interestingly, pravastatin administered from the beginning of reperfusion also exerted antiarrhythmic effects. These results indicate that pravastatin exerts antiarrhythmic effects not only with daily oral intake but also when administered just before ischemia or even after ischemia. Intracellular calcium ([Ca2+]i) overload and collapse of mitochondrial inner membrane potential (Δψm) are associated with the arrhythmogenesis during ischemia-reperfusion. In cultured cardiomyocytes, pretreatment with pravastatin (10nmol/L) suppressed [Ca2+]i overload and prevented Δψm loss induced by H2O2. Conclusions: Pravastatin attenuated reperfusion-induced lethal ventricular arrhythmias. Inhibition of [Ca2+]i overload and preserving Δψm may be the mechanisms of the observed antiarrhythmic effects of pravastatin. (Circ J 2011; 75: 1601-1608)
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  • – Analysis of Speckle Tracking Echocardiography –
    Katsuji Inoue, Hideki Okayama, Kazuhisa Nishimura, Makoto Saito, Toyof ...
    2011 Volume 75 Issue 7 Pages 1609-1615
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: May 20, 2011
    JOURNAL FREE ACCESS
    Background: Right ventricular (RV) pacing alters left ventricular (LV) mechanical activation, resulting in adverse impacts on LV function. This study was aimed to investigate the acute effect of RV apical (RVA) and septal pacing (RVS) on LV dyssynchrony and function using speckle tracking echocardiography. Methods and Results: The 103 patients (749 years) with symptomatic bradyarrhythmia and preserved LV ejection fraction, and 50 age-matched control subjects were studied. All patients received a permanent pacemaker and were randomly assigned into 2 groups (RVA: n=51, RVS: n=52). After insertion, patients underwent an echocardiographic study during RV pacing. LV dyssynchrony and global strain parameters were analyzed using speckle tracking echocardiography. The QRS width and dyssynchrony indices by longitudinal and radial strain were significantly greater in RVA than in both the control and RVS. The LV longitudinal dyssynchrony index was significantly related to global longitudinal strain (GLS) among 103 patients receiving RV pacing (R2=0.25, P<0.0001). The GLS in RVA were the lowest among the 3 groups (GLS: Control: -18.22.4%, RVA: -14.33.1%, P<0.001 vs. control, RVS: -16.82.7%, P<0.01 vs. RVA). Conclusions: RVA created heterogeneous LV contraction, which resulted in deteriorated LV longitudinal contraction. RVS could be a better pacing alternative in terms of less LV dyssynchrony and better longitudinal function compared to RVA. (Circ J 2011; 75: 1609-1615)
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Cardiovascular Intervention
  • Masahiro Natsuaki, Yutaka Furukawa, Takeshi Morimoto, Yoshihisa Nakaga ...
    2011 Volume 75 Issue 7 Pages 1616-1625
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: April 29, 2011
    JOURNAL FREE ACCESS
    Supplementary material
    Background: Among hemodialysis (HD) patients, those who have diabetes have poorer cardiovascular outcomes than non-diabetic patients, but the impact of diabetes on cardiovascular outcomes has not been fully elucidated in HD patients undergoing coronary revascularization. Methods and Results: We identified 375 HD patients (203 diabetes, 172 non-diabetes) and 9,006 patients without HD (3,455 diabetes, 5,551 non-diabetes) in the database of the CREDO-Kyoto registry of patients undergoing their first coronary revascularization. In non-HD patients, significantly higher risks of death (10.8% vs. 7.7%, P<0.0001; adjusted hazard ratio (HR) 1.29, P<0.0001) and major adverse cardiovascular events (MACE), a composite of death, myocardial infarction and stroke (18.8% vs. 13.3%, P<0.0001; HR 1.36, P<0.0001) were seen in diabetic patients than in non-diabetic patients through 4-year follow-up. Analysis in HD patients showed that the duration of HD before first coronary revascularization was significantly shorter in diabetic patients than in non-diabetic patients (median interval: 858 vs. 2,216 days, P<0.0001). In contrast to the results in non-HD patients, the risks of death (41.9% vs. 39.1%, P=0.75; HR 0.98, P=0.93) and MACE (45.6% vs. 45.8%, P=0.83; HR 0.87, P=0.50) after first revascularization were comparable between diabetic and non-diabetic HD patients. There were significant interactions between HD and diabetes for death and for MACE. Conclusions: HD patients who require coronary revascularization have extremely poor outcomes irrespective of concomitant diabetes. (Circ J 2011; 75: 1616-1625)
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  • – Results From the Multicenter `Korea Stent Thrombosis (KoST)' Registry –
    Kyung Woo Park, Seok-Jae Hwang, Dong-A Kwon, Byung-Hee Oh, Young-Bae P ...
    2011 Volume 75 Issue 7 Pages 1626-1632
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: May 28, 2011
    JOURNAL FREE ACCESS
    Supplementary material
    Background: Previous studies have reported possible predictors of drug-eluting stent thrombosis (ST), but data for Asians are relatively limited. This study was performed to elucidate clinical predictors of ST in Koreans. Methods and Results: From May 2003 to May 2007, consecutive patients presenting with ST were enrolled from 10 cardiovascular centers in Korea. They were compared with 2,192 controls (3,223 lesions) who had received percutaneous coronary intervention with at least 6 months of follow-up without ST. On multivariate analysis, acute myocardial infarction (AMI) as initial diagnosis, drug-eluting stents (DES) in-stent restenosis (ISR), low ejection fraction (EF), small stent diameter, left anterior descending artery intervention, and young age were independent predictors of total ST. When divided into early (ST within 30 days of index procedure) and delayed ST (ST after 30 days of index procedure), low EF, small stent diameter, DES ISR and AMI as initial diagnosis were universal risks for both early and delayed ST. The time from antiplatelet agent discontinuation to ST occurrence was significantly shorter in late compared with very late ST. Conclusions: Predictors of ST may be slightly different for early vs. delayed ST. However, low EF, small stent diameter, DES ISR lesion, and AMI as initial diagnosis were universal risk factors for both early and delayed ST cases. The relationship between antiplatelet agent discontinuation and ST occurrence seems stronger in late compared with very late ST. (Circ J 2011; 75: 1626-1632)
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  • – Comparison of Bare-Metal and Sirolimus-Eluting Stents Using Optical Coherence Tomography –
    Iwao Goto, Tomonori Itoh, Takumi Kimura, Tetsuya Fusazaki, Hiroki Mats ...
    2011 Volume 75 Issue 7 Pages 1633-1640
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: May 28, 2011
    JOURNAL FREE ACCESS
    Background: It has been suggested that sirolimus-eluting stents (SES) provoke a more sustained inflammatory response (IR) in neointimal hyperplasia (NIH). The purpose of this study was to compare morphological vessel characteristics, including post-stent IR in NIH, between patients with SES and bare metal stents (BMS) using optical coherence tomography (OCT). Methods and Results: Thirty-seven patients underwent OCT at their post-stent follow-up. OCT signal-intensity deviation (normalized standard-deviation; OCT-NSD) values in NIH were compared between the 2 groups. In addition, the serum concentration of high-sensitivity C-reactive protein (hs-CRP) was measured. Stent-malapposition rate (1.78% vs. 0.7%; P=0.016), uncovered stent-strut rate (16% vs. 3.7%; P=0.0002), peri-stent ulcer like appearance (PSUA; 50% vs. 0%; P=0.006) were all significantly higher in the SES group than in the BMS group, respectively. The OCT-NSD value was also significantly higher in the SES group than in the BMS group (0.213±0.005 vs. 0.198±0.005; P<0.001), as was the hs-CRP level (2.54±1.89 vs. 0.64±0.3mg/L; P=0.0006). In addition, a significant positive correlation was found between hs-CRP and OCT-NSD (r=0.471; P=0.0025). Conclusions: PSUA-morphology was specific in the SES group, and higher levels of OCT-NSD and hs-CRP after SES implantation suggest sustained IR in NIH compared with following BMS implantation. These different characteristics may be some of the background that promotes thrombus formation as a late-stage post-stent complication of SES. (Circ J 2011; 75: 1633-1640)
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  • Takenori Okada, Hideya Yamamoto, Tomokazu Okimoto, Masaya Otsuka, Ken ...
    2011 Volume 75 Issue 7 Pages 1641-1648
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: May 17, 2011
    JOURNAL FREE ACCESS
    Background: Angiotensin II receptor blockers (ARB) have been shown to reduce cardiovascular events in patients at risk. The effect of valsartan on outcomes after percutaneous coronary interventions (PCI) with bare-metal stents (BMS) was investigated. Methods and Results: The prospective, randomized study included 191 patients at 5 participating institutions, who were randomly assigned to either a 40-80mg valsartan add-on or non-ARB treatment. The primary endpoint was a composite of all-cause death, non-fatal myocardial infarction, and target lesion revascularization (TLR) at 18 months. Enrollment was stopped when the use of drug-eluting stents has been expanded in Japan. No significant differences existed between the groups in terms of primary endpoint (18.9% vs. 24.8%; hazard ratio [HR], 0.84; 95% confidence interval [CI], 0.61-1.14; P=0.26). In the valsartan group, as compared with the non-ARB group, the secondary endpoint of TLR was significantly reduced at a median follow-up 4.4 years; the rate of TLR was from 27.8% to 14.5% (HR, 0.69; 95%CI, 0.49-0.96; P=0.024). Conclusions: Valsartan treatment was not superior to non-ARB treatment in reducing the primary endpoint after PCI at 18 months. The pre-specified secondary endpoint of TLR was lower in the valsartan group, but this needs to be proved statistically with an adequate study sampling. (Circ J 2011; 75: 1641-1648)
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Cardiac Rehabilitation
  • Isao Nishi, Teruo Noguchi, Yoshitaka Iwanaga, Shinichi Furuichi, Naohi ...
    2011 Volume 75 Issue 7 Pages 1649-1655
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: May 25, 2011
    JOURNAL FREE ACCESS
    Background: It remains unclear whether patients with chronic heart failure (CHF) and advanced left ventricular (LV) dysfunction on β-blocker therapy benefit from exercise training (ET). Methods and Results: We studied 45 CHF patients with advanced LV dysfunction [ejection fraction (LVEF) <25%] and impaired exercise tolerance [normalized peak oxygen uptake (PVO2) <70%] receiving a β-blocker: 33 patients participated in a cardiac rehabilitation program with ET (ET group) and 12 did not (inactive control group). Exercise capacity, LV dimension and plasma B-type natriuretic peptide (BNP) were assessed before and after a 3-month study period. At baseline, both groups had markedly reduced LVEF (ET group 18±4% vs. Control group 18±5%, NS) and impaired exercise capacity (normalized PVO2 51±10% vs. 55±9%, NS). Although one patient in the ET group withdrew from the program due to worsening CHF, no serious cardiac events occurred during the ET sessions. After 3 months, the ET group (n=24) had significantly improved PVO2 by 16±15% (1,005±295 to 1,167±397ml/min, P<0.001), while the PVO2 of the control group was unchanged. LV end-diastolic dimension decreased in both groups to a similar extent, but plasma BNP was significantly decreased only in the ET group (432 to 214pg/ml, P<0.05). Conclusions: The data indicate that in CHF patients with advanced LV dysfunction on β-blocker therapy, ET successfully improves exercise capacity and BNP without adversely affecting LV remodeling or causing serious cardiac complications. (Circ J 2011; 75: 1649-1655)
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Cardiovascular Surgery
  • – Comparison of Port-Access and Conventional Standard Approach –
    Arudo Hiraoka, Masahiko Kuinose, Genta Chikazawa, Toshinori Totsugawa, ...
    2011 Volume 75 Issue 7 Pages 1656-1660
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: May 25, 2011
    JOURNAL FREE ACCESS
    Background: In recent years, minimally invasive cardiac surgery has been developed. Thus far, only at our institute has port-access aortic valve replacement (PAVR) been performed in Japan. Herein we review our experiences with PAVR, and evaluate the surgical outcomes. Methods and Results: Between May, 2007 and June, 2010, 37 cases of PAVR were performed. During the same period, 107 patients underwent conventional aortic valve replacement (CAVR) with midline sternotomy. Because we initially selected patients without high risk factors for PAVR, there were some differences in the preoperative demographic data between the CAVR and PAVR groups. Although cardiopulmonary bypass time and cross-clamp time were longer in the PAVR group (139±28 vs. 113±34min; 97±23 vs. 83±24min), there were no significant differences in total operative time between both groups. With regard to the percentage of blood transfusion requirement, postoperative ventilation time, intensive care unit stay and hospital stay the PAVR group had significantly lower outcomes (11 vs. 90; 3.4±1.9h vs. 8.2±16.3h; 1.2±0.6 days vs. 2.5±1.7 days; 11.1±4.3 days vs. 19.7±7.8 days, respectively). There were no significant differences in mortality (1/37), and morbidity between both groups. Conclusions: PAVR a feasible treatment of choice for patients with aortic valve diseases complicated by various preoperative backgrounds. (Circ J 2011; 75: 1656-1660)
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Heart Failure
  • Naoko Kato, Koichiro Kinugawa, Satomi Seki, Taro Shiga, Masaru Hatano, ...
    2011 Volume 75 Issue 7 Pages 1661-1669
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: April 29, 2011
    JOURNAL FREE ACCESS
    Background: Little is known about health-related quality of life (QOL) in Japanese patients with heart failure. The purpose of this study was to identify factors related to QOL using a disease-specific QOL instrument, and to clarify whether QOL independently predicts clinical outcomes among Japanese patients with heart failure. Methods and Results: A total of 114 outpatients with heart failure were enrolled (mean age 64.7±15.8 years; 73.7% males). The Minnesota Living with Heart Failure Questionnaire (MLHFQ) to assess patient's QOL was used. At baseline, depressive symptoms and chronic kidney disease were significantly associated with worse QOL in multiple regression analysis. During a 2-year follow up, patients with a MLHFQ score ≥26, indicating worse QOL, had a higher incidence of the combined endpoint of cardiac death or hospitalization for heart failure, and a higher all-cause mortality than those with a score <26 (25.3% vs. 7.5%, P=0.011; 18.5% vs. 6.4%, P=0.018; respectively). Multivariate Cox proportional hazard models demonstrated that a higher MLHFQ score was significantly associated with increased risks of cardiac events (hazard ratio, 1.02, 95% confidential interval, 1.001-1.05, P=0.038) and of all-cause death (hazard ratio, 1.04, 95% confidential interval, 1.02-1.07, P=0.001). Conclusions: Depressive symptoms and chronic kidney disease are major determinants of impaired QOL, and the MLHFQ score is an independent predictor of both cardiac events and death among Japanese patients with heart failure. (Circ J 2011; 75: 1661-1669)
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Imaging
  • Tomonari Kiriyama, Masahiro Toba, Yoshimitsu Fukushima, Hiromitsu Haya ...
    2011 Volume 75 Issue 7 Pages 1670-1677
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: May 12, 2011
    JOURNAL FREE ACCESS
    Background: The aim of this study was to determine the relationship between the morphological and physiological information of coronary CT angiography (CCTA) and stress myocardial perfusion imaging (S-MPI) from the standpoint of risk stratification of patients with intermediate to high probability of coronary artery disease (CAD). Methods and Results: In total, 51 patients underwent both CCTA and S-MPI as sequential examinations. In each patient, the severity of coronary plaque and stenosis (>50%) and the presence of myocardial perfusion abnormalities were assessed and the prognostic information from the CCTA and S-MPI results was compared. In 30 patients with normal S-MPI, 3 (10%) had only completely normal coronaries and another 3 (10%) had non-obstructive CAD as observed on CCTA. The remaining 24 patients (80%) with normal S-MPI and all 21 patients with abnormal S-MPI study had obstructive CAD. High-risk CAD (defined as obstructive left main trunk (LMT) lesion or 3-vessel disease) was seen in 10 (33%) of 30 patients with normal S-MPI, although it was less frequent than in the 14 (67%) of 21 patients with abnormal S-MPI. Conclusions: A normal S-MPI result can reflect a wide range of coronary atherosclerosis types and severities and, to some extent, involves severe coronary atherosclerosis such as LMT lesion and 3-vessel disease in patients with an intermediate to high probability of CAD. (Circ J 2011; 75: 1670-1677)
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  • Sharon W. Kirschbaum, Koen Nieman, Tirza Springeling, Annick C. Weusti ...
    2011 Volume 75 Issue 7 Pages 1678-1684
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: June 10, 2011
    JOURNAL FREE ACCESS
    Background: To evaluate additional adenosine magnetic resonance perfusion (MRP) imaging in the diagnostic workup of patients with suspected stable angina with computed tomography coronary angiography (CTCA) as first-line diagnostic modality. Methods and Results: Two hundred and thirty symptomatic patients (male, 52%; age, 56 year) with suspected stable angina underwent CTCA. In patients with a stenosis of >50% as visually assessed, MRP was performed and the quantitative myocardial perfusion reserve index (MPRI) was calculated. Coronary flow reserve (CFR) using invasive coronary flow measurements served as the standard of reference. CTCA showed non-significant CAD in 151/230 (66%) patients and significant CAD in 79/230 patients (34%), of whom 50 subsequently underwent MRP and CFR. MRP showed reduced perfusion in 32 patients (64%), which was confirmed by CFR in 27 (84%). All 18 cases of normal MRP (36%) were confirmed by CFR. The positive likelihood ratio of MRP for the presence of functional significant disease in patients with a lesion on CTCA was 4.49 (95% confidence interval [CI] 2.12-9.99). The negative likelihood ratio was 0.05 (95%CI 0.01-0.34). Conclusions: CTCA as first-line diagnostic modality excluded coronary artery disease in a high percentage of patients referred for diagnostic workup of suspected stable angina. MRP made a significant contribution to the detection of functional significant lesions in patients with a positive CTCA. (Circ J 2011; 75: 1678-1684)
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Ischemic Heart Disease
  • Hun-Jun Park, Ju-Yeol Baek, Woo Seung Shin, Dong-Bin Kim, Sung Won Jan ...
    2011 Volume 75 Issue 7 Pages 1685-1690
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: May 17, 2011
    JOURNAL FREE ACCESS
    Background: The roles of soluble and endogenous secretory receptors for advanced glycation endproducts (sRAGE and esRAGE, respectively) in plaque vulnerability are unknown in patients with acute myocardial infarction (AMI). Methods and Results: We enrolled 54 patients with AMI (27 patients had type 2 diabetes mellitus [DM]) who had undergone primary percutaneous coronary intervention, and 54 controls who were matched for age, gender and the presence of DM. Plasma levels of s/esRAGE and matrix metalloproteinase (MMP)-9 were measured at the time of coronary angiography. There were no significant differences in the baseline characteristics of the AMI and control groups, except for the C-reactive protein levels (CRP: 14.1±14.2mg/L vs. 3.7±5.2mg/L, P<0.001). The plasma levels of MMP-9 (28.6±21.4 vs. 14.3±8.5ng/ml P<0.001) and sRAGE (0.61±0.28 vs. 0.41±0.17ng/ml, P<0.001) were higher in the AMI group than in the controls. In multivariate logistic regression analysis, the plasma levels of MMP-9 and sRAGE above the median (odds ratio [OR], 2.39; 95% confidence interval [CI], 1.02-5.58; P=0.044; OR, 2.47; 95%CI, 1.05-5.80; P=0.039, respectively) were independent predictors of AMI, as well as being a current smoker (OR, 2.98; 95%CI, 1.18-7.55; P=0.021) and CRP≥3.0mg/L (OR, 3.08; 95%CI, 1.25-7.59; P=0.015). Conclusions: An elevated plasma level of sRAGE might be independently associated with plaque vulnerability, as well as MMP-9, in patients with AMI. (Circ J 2011; 75: 1685-1690)
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  • Seiji Koga, Satoshi Ikeda, Tomoo Nakata, Tomohiko Yasunaga, Masayoshi ...
    2011 Volume 75 Issue 7 Pages 1691-1695
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: May 11, 2011
    JOURNAL FREE ACCESS
    Background: Although chronic kidney disease is associated with a high prevalence of cardiovascular disease, the relationship between coronary artery spasm and renal dysfunction has not been elucidated. Methods and Results: We evaluated 139 patients with chest pain at rest who had no significant organic stenosis on coronary angiograms and who underwent coronary spasm provocation tests using acetylcholine or ergonovine. The results of the provocation tests revealed that 59 patients had vasospastic angina (VSA), and that 80 did not (non-VSA). We analyzed the association between VSA and renal dysfunction using the estimated glomerular filtration rate (eGFR). The eGFR was significantly lower in the VSA group than in the non-VSA group (P=0.013). The patients were assigned to quartiles (Q) 1, 2, 3 and 4 based on eGFR (ml·min-1·1.73m2) <64.1, 64.1-74.7, 74.8-85.0 and ≥85.1, respectively, in each of which the prevalence of VSA was 57%, 53%, 34% and 26%, respectively. The prevalence of VSA was significantly higher in Q1 than in Q4 (P=0.008). Logistic regression analysis showed that the independent factors associated with the presence of VSA were a lower eGFR (P=0.011) and male gender (P=0.001). Conclusions: Lower levels of eGFR in our study population were significantly and independently associated with a high prevalence of VSA, suggesting that a lower eGFR could be a risk factor for VSA. (Circ J 2011; 75: 1691-1695)
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  • – Randomized Parallel Comparison With β-Blockers –
    Akihiro Nakagomi, Eitaro Kodani, Hitoshi Takano, Takahiro Uchida, Naok ...
    2011 Volume 75 Issue 7 Pages 1696-1705
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: May 17, 2011
    JOURNAL FREE ACCESS
    Background: Beta-blockers (BB) have been widely used in the management of hypertension and acute myocardial infarction (AMI), and both national and international guidelines have recommended them as first-line agents. Calcium channel antagonists (CCA) are also effective in the treatment of hypertension and angina pectoris. However, the efficacy of CCA in the prevention of cardiovascular events in post-myocardial infarction (MI) patients in comparison to that of BB remains unclear. Methods and Results: A total of 120 post-MI patients (71 patients who were at least 1 month after the onset AMI and 49 stable coronary artery disease patients with a history of MI) were randomly assigned to receive a BB (atenolol, 25-50mg/day, n=60) or a CCA (benidipine, 4-8mg/day, n=60). All patients with AMI within the previous 1 month or with vasospastic angina were excluded from the present study. The baseline clinical characteristics were generally similar in the BB and CCA groups. The rate of primary composite outcome was 26.3% in the BB group in comparison to 13.3% in the CCA group, with no significant between-group differences (hazard ratio with the CCA group 0.640, P=0.276). Both treatments were well tolerated with few severe adverse events. Conclusions: CCA treatment was found to be as effective as BB in reducing cardiovascular events in post-MI patients. (Circ J 2011; 75: 1696-1705)
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Molecular Cardiology
  • Yu-Cheng Hsieh, Hung-I Yeh, Shien-Fong Lin, Ya-Wen Hsu, Jin-Long Huang ...
    2011 Volume 75 Issue 7 Pages 1706-1716
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: May 25, 2011
    JOURNAL FREE ACCESS
    Background: Whether connexin43 gap junctions (Cx43 GJs) and spatial heterogeneity of conduction velocity (CV) restitutions are altered in hearts during moderate (MH; 33°C) and severe (SH; 30°C) hypothermia remains unclear. Methods and Results: Using an optical mapping system, ventricular CV was evaluated by S1 pacing in 29 Langendorff-perfused isolated rabbit hearts at baseline (37°C, n=9), 30-min MH (n=6), 30-min SH (n=9), and rewarming (R, 30-min SH followed by 30-min 37°C, n=5). After CV evaluation, myocardium was collected to measure the level and distribution of non-phosphorylated (NP-Cx43) and total (T-Cx43) Cx43 by immunoblotting and immunoconfocal microscopy. In 6 additional hearts, Cx43 GJ remodeling was evaluated at 30-min SH with (n=3) or without (n=3) pretreatment of a protein kinase C (PKC) inhibitor. CV slowing and spatial heterogeneities of CV restitutions were enhanced in MH and SH hearts. NP-Cx43 was downregulated in MH (P=0.002) and SH (P<0.001) hearts. NP-Cx43 levels among 4 different ventricular sites became inhomogeneous in MH (P=0.017) and SH (P=0.046) hearts. However, T-Cx43 levels were unchanged. The percentages of lateralized NP- and T-Cx43 were increased in MH, SH, and R hearts. Pretreatment of PKC inhibitor attenuated SH-induced NP-Cx43 lateralization (P=0.0495). Conclusions: Short-duration (30min) therapeutic hypothermia causes prompt Cx43 GJs remodeling, in which the PKC pathway is involved. Rewarming abolished hypothermia-induced conduction disturbance, while Cx43 GJs lateralization did not completely recover. (Circ J 2011; 75: 1706-1716)
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Myocardial Disease
  • Yoshinori Mano, Toshihisa Anzai, Hidehiro Kaneko, Yuji Nagatomo, Toshi ...
    2011 Volume 75 Issue 7 Pages 1717-1727
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: April 26, 2011
    JOURNAL FREE ACCESS
    Background: C-reactive protein (CRP) is known to be a pathogenic agent in the cardiovascular system. However, the effect of CRP on heart failure has not been elucidated. The effect of human CRP on cardiac dysfunction induced by diabetes mellitus (DM) using human CRP-overexpressing transgenic mice (CRP-Tg) was examined. Methods and Results: DM was induced in male wild-type mice (Wt/DM) and CRP-Tg (CRP/DM) by an injection of streptozotocin. Non-diabetic wild-type mice (Wt/Con) and CRP-Tg (CRP/Con) served as controls. Echocardiography and hemodynamic measurements 6 weeks after injection showed lower fractional shortening and left ventricular (LV) dP/dt max in CRP/DM compared with Wt/DM. Myocardial mRNA levels of interleukin-6, tumor necrosis factor-α, plasminogen activator inhibitor-1, angiotensin type 1 receptor, angiotensinogen, NADPH oxidase subunits (p47phox, gp91phox), glutathione peroxidase-3. and connective tissue growth factor were increased in CRP/DM compared with Wt/DM. Nuclear staining of 8-hydroxydeoxyguanosine was also increased in CRP/DM compared with Wt/DM. CRP/DM was associated with increased terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling positive cells and a higher ratio of Bax/Bcl-2 proteins compared with Wt/DM. The extent of cardiac fibrosis assessed by Sirius red staining and immunohistochemical staining for collagen type 1 was significantly increased in CRP/DM compared with Wt/DM. Conclusions: Overexpression of human CRP exacerbates LV dysfunction and remodeling in diabetic cardiomyopathy, possibly through enhancement of the inflammation, renin-angiotensin system, and oxidative stress. (Circ J 2011; 75: 1717-1727)
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  • – Role of Electrocardiography in Predicting Poor Outcome –
    Jan Steffel, David Hürlimann, Mehdi Namdar, Dragan Despotovic, Ri ...
    2011 Volume 75 Issue 7 Pages 1728-1734
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: May 26, 2011
    JOURNAL FREE ACCESS
    Background: Abnormal baseline electrocardiograms (ECGs) are common in patients with isolated left ventricular noncompaction (IVNC). Whether certain electrocardiographic parameters are associated with a poor clinical outcome, however, remains elusive. The present study was therefore designed to comprehensively assess the predictive value of baseline ECG findings in patients newly diagnosed with IVNC. Methods and Results: 74 patients diagnosed with IVNC were included in the analysis. During follow-up, 8 patients (11%) died of a cardiovascular cause or underwent heart transplantation (primary outcome measure). On univariate analysis, several variables, including repolarization abnormalities (ST segment elevation/depression, T-wave inversion) in the inferior leads (5-year estimator: 67.1±10.7% vs. 98±2.2%; P=0.001), an increase in PQ- (hazard ratio (HR) 1.032, P=0.004) and QTc-duration (HR 1.037, P=0.001), were predictive of cardiovascular death or heart transplantation. On multivariate analysis, only PQ- and QTc-duration and the presence of repolarization abnormalities in the inferior leads remained significantly predictive of a poor outcome. Conclusions: PQ duration, QTc duration, and repolarization abnormalities in the inferior leads are independently predictive of a poor prognosis in IVNC. Further prospective studies are required to conclusively investigate the usefulness of baseline ECG parameters for risk stratification in patients with IVNC. (Circ J 2011; 75: 1728-1734)
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Pediatric Cardiology and Adult Congenital Heart Disease
  • Yiu-fai Cheung, Sophia J Wong, Xue-cun Liang, Eddie WY Cheung
    2011 Volume 75 Issue 7 Pages 1735-1741
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: May 12, 2011
    JOURNAL FREE ACCESS
    Background: This study aimed to test the hypothesis that alteration of left ventricular (LV) torsional mechanics occurs in patients after repair of tetralogy of Fallot (TOF) and is associated with right ventricular (RV) volume overload and changes in LV configuration. Methods and Results: Fifty-five TOF patients aged 19.0±8.1 years and 27 age-matched healthy controls were studied. The LV and RV volumes were measured using 3-dimensional echocardiography while LV geometry was quantified by the diastolic eccentricity index (EI). The LV peak systolic torsion and systolic twisting and diastolic untwisting velocities were determined by speckle tracking. Compared with controls, patients had significantly greater RV end-systolic (P<0.001) and diastolic (P<0.001) volumes and LV diastolic EI (P<0.001). In contrast, LV peak apical rotation (P<0.001), systolic torsion (P=0.004), systolic twisting velocity (P=0.001), and diastolic untwisting velocity (P=0.001) were lower in patients than in controls. For the whole cohort, RV EDV and LV diastolic EI correlated negatively with peak systolic torsion, systolic twisting velocity, and diastolic untwisting velocity (all P≤0.001). Systolic torsion correlated strongly with diastolic untwisting velocity (r=0.72, P<0.001), while systolic twisting velocity correlated with LV ejection fraction (r=0.3, P=0.005). Conclusions: LV torsional mechanics is impaired and is negatively related to RV volume overload and LV eccentricity in patients after TOF repair. (Circ J 2011; 75: 1735-1741)
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Peripheral Vascular Disease
  • Akihiro Tsuji, Norikazu Yamada, Satoshi Ota, Ken Ishikura, Mashio Naka ...
    2011 Volume 75 Issue 7 Pages 1742-1746
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: May 20, 2011
    JOURNAL FREE ACCESS
    Background: The utility of rheolytic thrombectomy as a treatment for proximal deep vein thrombosis (DVT) is not well understood. Methods and Results: Patients with proximal DVT were treated with rheolytic thrombectomy, and the safety and efficacy of the procedure were evaluated. The improvement of venous thrombi was assessed using the venographic segment (VS) score. The rheolytic rate was defined as the percentage thrombus aspiration achieved. We also evaluated whether there were differences in age, aspiration time, D-dimer concentration, or the duration from onset to therapy between the high and low rheolytic rate groups. The mean VS score before thrombectomy was 28.8±7.9 points, and the mean VS score after thrombectomy was 10.4±7.1 points (ie, the VS score was significantly decreased after thrombectomy). There were no major treatment-related adverse complications. The mean duration from onset to rheolytic therapy in the 4 patients with a low rheolytic rate was 13.5±13.2 days, which was much longer than for the 9 patients with a high rheolytic rate (mean duration: 4.0±2.2 days: P=0.045). Conclusions: Rheolytic thrombectomy is safe and effective for treating proximal DVT. The duration from onset to therapy was the only factor that was significantly predictive of the outcome of rheolytic thrombectomy. Rheolytic thrombectomy was especially effective when performed within 1 week of onset. (Circ J 2011; 75: 1742-1746)
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Vascular Medicine
  • Zbynek Strasky, Lenka Vecerova, Jana Rathouska, Martina Slanarova, Eva ...
    2011 Volume 75 Issue 7 Pages 1747-1755
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: May 17, 2011
    JOURNAL FREE ACCESS
    Background: The aim of the study was to evaluate whether cholesterol-rich diet affects transforming growth factor-β-RIII (endoglin) levels in blood and 2 endoglin-related pathways in the aorta of ApoE/LDLR double knockout mice. Methods and Results: Mice were fed either chow diet (CHOW) (n=8) or by 1% cholesterol-rich diet (CHOL) (n=8). Biochemical analysis of cholesterol and endoglin levels in blood, lesion size area, immunohistochemistry and Western blot analysis in mice aortas were performed. Biochemical analysis showed that cholesterol-rich diet resulted in a significant increase of cholesterol and endoglin levels in serum, and increased plaque size in the aorta. In addition, a cholesterol-rich diet significantly decreased the expressions of endoglin by 92%, activin receptor-like kinase (ALK)-1 by 71%, p-Smad2 by 21%, and vascular endothelial growth factor (VEGF) by 37% when compared to CHOW mice, but ALK-5, p-Smad1, and endothelial nitric oxide synthase were not significantly affected. Conclusions: Hypercholesterolemia increases endoglin levels in blood and simultaneously decreases its expression in aorta, together with atherosclerosis protective markers p-Smad2 and VEGF, followed by increased plaque size. Inhibition of endoglin signaling might be one of the mechanisms responsible for the promoting of endothelial dysfunction and atherogenesis. Moreover, the monitoring of endoglin serum levels might represent an attractive blood marker of progression of disease; however, the precise source and role of endoglin in blood serum remains to be elucidated. (Circ J 2011; 75: 1747-1755)
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Controversies in Cardiovascular Medicine
  • – The Cause of Dilated Cardiomyopathy: Genetic or Acquired? (Genetic-Side) –
    Akinori Kimura
    2011 Volume 75 Issue 7 Pages 1756-1765
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: May 27, 2011
    JOURNAL FREE ACCESS
    Dilated cardiomyopathy (DCM) is characterized by dilated ventricles and systolic dysfunction. Its etiology is not fully unraveled, but both extrinsic and intrinsic factors are considered to be involved. The intrinsic factors include genetic variations in the genes (ie, disease-causing mutations and disease-associated polymorphisms), which play key roles in controlling the susceptibility to the disease by affecting the performance, regulation, and/or maintenance of cardiac function. DCM can be classified into 2 types: hereditary and non-hereditary. The genetic variations, or disease-causing mutations, contributing to the pathogenesis of hereditary DCM can be found in various genes, especially those for sarcolemma elements, contractile elements, Z-disc elements, sarcoplasmic elements, and nuclear lamina elements of cardiomyocytes. On the other hand, disease-associated polymorphisms, which control the susceptibility to non-hereditary DCM, may be found in genes expressing not only in cardiomyocytes but also other non-cardiac cells involved in the immune system. Because functional alterations caused by these genetic variations can be classified into several categories, it is necessary to understand the pathogenesis and hence to develop diagnostic and therapeutic strategies for both hereditary and non-hereditary DCM from the viewpoint of genetic factors. (Circ J 2011; 75: 1756-1765)
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  • – The Cause of Dilated Cardiomyopathy: Genetic or Acquired? (Acquired-Side) –
    Tsutomu Yoshikawa
    2011 Volume 75 Issue 7 Pages 1766-1773
    Published: 2011
    Released on J-STAGE: June 24, 2011
    Advance online publication: May 27, 2011
    JOURNAL FREE ACCESS
    Although genetic abnormalities play a pivotal role in the development of dilated cardiomyopathy (DCM), acquired infection and autoimmune abnormalities, or both, appear to be predominant underlying disorders. Of these, viral infection causes target organ damage via perforin produced by suppressor T cells. Thereafter, various antigens released from damaged myocytes are presented on the major histocompatibility complex II, which is expressed in antigen-presenting cells, resulting in activation of both cellular (Th1) and humoral (Th2) immunity. Various antimyocardial antibodies are detected in the serum of patients with DCM and recent findings suggest that at least some of them are directly related to the pathophysiology of DCM. An autoantibody targeting the β1-adrenergic receptor is related to the persistent myocardial damage resulting in DCM and provides the substrate for fatal ventricular arrhythmias. An antibody for the muscarinic M2 receptor is related to atrial fibrillation, an antibody targeting Na-K-ATPase is closely related to sudden cardiac death from fatal ventricular arrhythmias, and an autoantibody for troponin I increases the L-type calcium current and is related to myocardial damage. On the other hand, genetic factors are also involved in susceptibility to viral infection and aberrations of acquired immunity, including antigen presentation and autoantibody production. In conclusion, acquired factors are predominant causes of DCM, although the 2 predisposing factors are also linked to genetic abnormalities. (Circ J 2011; 75: 1766-1773)
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