Hiroaki Matsubara

Kyoto Prefectural University of Medicine, Kyoto, Kyoto-fu, Japan

Are you Hiroaki Matsubara?

Claim your profile

Publications (349)1532.85 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: The objective of the present study was to examine whether baseline electrocardiographically diagnosed left ventricular hypertrophy (ECG-LVH) influenced the angiotensin II receptor blocker (ARB) valsartan add-on effects on the cardio-cerebrovascular morbidity and mortality in the high-risk hypertensive patients who participated in the KYOTO HEART Study. The primary endpoint was the same as in the main study: a composite of defined cardiovascular and cerebrovascular events. The median follow-up period was 3.27 years. The study group was divided into 2 groups according to the presence of ECG-LVH: with LVH, n=803; without LVH, n=2,228. The primary endpoint events occurred more frequently in patients with LVH than in patients without LVH (9.3% vs. 7.3%; hazard ratio [HR], 1.33; 95% confidence interval [CI]: 1.01-1.75). Valsartan add-on significantly decreased the occurrence of primary endpoint events in both LVH-positive patients (5.8% vs. 12.9%; HR, 0.45; 95%CI: 0.28-0.72) and LVH-negative patients (5.5% vs. 9.2%; HR, 0.59; 95%CI: 0.44-0.81) compared with non-ARB treatment. The reduction in combined cardiovascular events (composite of acute myocardial infarction, angina pectoris, and heart failure) due to valsartan treatment in patients with LVH was significantly larger than that in patients without LVH (P<0.0001). Changes in blood pressure during the follow-up period did not differ significantly among the study subgroups. High-risk hypertensive patients with ECG-LVH might gain more cardiovascular benefits from valsartan add-on treatment, compared with patients without ECG-LVH.
    Circulation Journal 03/2011; 75(4):806-14. · 3.58 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: In this study, we report the comparative result of long-term clinical prognoses for patients with no-option critical limb ischemia (CLI) caused by arteriosclerosis obliterans, who are implanted with autologous bone marrow mononuclear cells (BMMNC; n=74) or G-CSF-mobilized (M)-PBMNC (n=111), as no information is available on how the two treatments compare in terms of long-term prognosis, such as survival or amputation. We performed pooled analysis using data from two previous cohort studies. All patients had disease of Fontaine classification III or IV. The endpoints were OS and amputation-free survival (AFS). After adjustment for history of dialysis and Fontaine classification, there was no significant difference between the two treatments with respect to OS (hazard ratio (HR)=1.49; 95% confidence interval (CI)=0.74-3.03, P=0.26) or AFS (HR=0.96; 95% CI=0.61-1.51, P=0.87). The negative prognostic factors affecting OS or AFS were the small number of CD34-positive cells collected, history of dialysis, Fontaine classification, male sex and older age. These results suggest that there was no significant difference in long-term prognosis between patients treated with BMMNC and those treated with M-PBMNC. The number of CD34-positive cells collected was an important prognostic factor for amputation and death.
    Bone marrow transplantation 02/2011; 46(2):278-84. · 3.00 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: A necropsy study of patients with hypertrophic cardiomyopathy (HCM) who died at a young age exhibited marked disarray and fibrosis in the mid-wall layer of the left ventricular (LV) myocardium. We assessed ultrasonic tissue characteristics in the three layers of the ventricular septum (VS), and correlated the result with long-term prognosis in HCM. The magnitude of cyclic variation of integrated backscatter (CV-IB) was calculated in the three layers of the VS and the whole aspect of the LV posterior wall in 58 non-obstructive HCM patients and 20 healthy controls. All HCM patients were prospectively followed for an average period of 7.1 years for the occurrence of cardiac death or hospitalization due to heart failure. Each CV-IB of four regions was lower in HCM patients than in controls (all P < 0.01). CV-IB of the VS mid-wall layer was lower in 14 HCM patients with cardiac events than in patients without (5.4 ± 0.6 vs. 7.4 ± 0.5 dB, P = 0.033) although CV-IB of three other regions did not differ between the two groups. The optical cut-off point of %CV-IB <90%, i.e. the ratio of CV-IB in the VS mid-wall layer to the mean value in the layers on both sides, was an independent predictor of cardiac events (hazard ratio, 6.12; 95% confidence interval, 1.62-66.6; P = 0.013), with a positive predictive value of 44% and particularly with a high negative predictive value of 91%. Patients with non-obstructive HCM are not likely to undergo cardiac events in the near future, when the CV-IB value is not significantly lower in the VS mid-wall layer than in the layers on both sides.
    European Heart Journal – Cardiovascular Imaging 02/2011; 12(2):90-7. · 2.39 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: S100A12 is an endogenous receptor ligand for advanced glycation end products. Cardiovascular disease remains a major cause of morbidity and mortality in patients with chronic kidney disease. In this study, we report cross-sectional data on 550 hemodialysis patients and assess the relationship between plasma S100A12 level and cardiovascular disease. Design, SETTING, PARTICIPANTS, & MEASUREMENTS: A cross-sectional study of 550 maintenance hemodialysis patients was conducted. We investigated the past history of cardiovascular disease and quantified the plasma level of S100A12 protein in all participants. Plasma S100A12 level was higher in hemodialysis patients with cardiovascular disease (n=197; 33.8 ± 28.1 ng/ml) than in those without it (n=353; 20.2 ± 16.1 ng/ml; P<0.001). In multivariate logistic regression analysis, the plasma S100A12 level (odds ratio [OR], 1.28; 95% confidence interval [CI], 1.13 to 1.44; P<0.001) was identified as an independent factor associated with the prevalence of cardiovascular disease. The other factors associated with the prevalence of cardiovascular diseases were the presence of diabetes mellitus (OR, 2.81; 95% CI, 1.79 to 4.41; P < 0.001) and high-sensitivity CRP level (OR, 1.02; 95% CI, 1.00 to 1.05; P=0.046). Furthermore, the plasma S100A12 level (OR, 1.30; 95% CI, 1.09 to 1.54; P=0.004) was significantly associated with cardiovascular disease even in hemodialysis patients without diabetes mellitus (n=348). These results suggest that the plasma S100A12 protein level is strongly associated with the prevalence of cardiovascular disease in hemodialysis patients.
    Clinical Journal of the American Society of Nephrology 02/2011; 6(4):718-23. · 5.07 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Primary percutaneous coronary intervention (PCI) for ST-elevated myocardial infarction (STEMI) results in dramatically improved clinical outcomes when performed in a timely manner. Although guidelines for STEMI patients recommend PCI should be performed by experienced operators with acceptable PCI volume, cardiologists in a local area must perform primary PCI at their own hospitals. This study evaluated the effects of cardiologist experience on outcomes for STEMI patients in a local area in Japan.Between April 2007 and March 2010, 140 consecutive STEMI patients were admitted to our hospital and 121 of these patients received primary PCI. STEMI patients undergoing primary PCI were divided into two groups according to the operator's experience as a cardiologist. We retrospectively analyzed their clinical backgrounds, PCI findings, in-hospital outcomes, and drug administration at discharge.There were no significant differences in any clinical characteristics, angiographic findings, or PCI procedures between the two groups. Clinical outcomes of the two groups were similar, except for the length of hospital stay (21.1 ± 5.8 versus 15.5 ± 9.7; P = 0.0255). The frequency of administration of drugs such as β-blockers (59.1% versus 34.0%; P = 0.0086), aldosterone blockade (10.4% versus 25.5%; P = 0.0334), and nicorandil (76.1% versus 25.5%; P = < 0.0001) was different between the two groups.The clinical outcomes of STEMI patients in this study were satisfactory and almost equivalent when compared according to the experience of the attending cardiologist. The present findings suggest the important clinical implication that younger cardiologists who have experienced PCI procedures to a certain extent can safely perform primary PCI and contribute to better prognoses of STEMI patients.
    International Heart Journal 01/2011; 52(3):127-30. · 1.23 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: S100A12 is an endogenous ligand of the receptor for advanced glycation end products (RAGE). Plasma S100A12 levels are high in end-stage renal disease (ESRD) patients undergoing maintenance hemodialysis (HD). Peripheral arterial disease (PAD) is common in HD patients and is associated with increased cardiovascular morbidity and mortality rates in this population. To date, however, no study has specifically assessed the relationship between plasma S100A12 and PAD in HD patients. We conducted a cross-sectional study of 152 HD patients in our affiliated hospital. We investigated PAD history and patient characteristics and quantified plasma S100A12 levels in all participants. HD patients with PAD (n = 26; 21.9 [13.6-33.4] ng/ml) showed significantly higher plasma S100A12 levels than HD patients without PAD (n = 126; 11.8 [7.5-17.6]ng/ml; p < 0.001). In multivariate logistic regression analysis, the plasma S100A12 level (odds ratio [OR] 5.71; 95% confidence interval [CI] 1.29-25.3; p = 0.022) was identified as an independent factor associated with PAD prevalence. Another factor associated with PAD prevalence was the ankle-brachial index (OR 0.54; 95% CI 0.40-0.74; p < 0.001). These results suggest that plasma S100A12 levels are strongly associated with PAD prevalence in ESRD patients undergoing HD.
    Nephron extra. 01/2011; 1(1):242-50.
  • Makoto Ariyoshi, Jun Shiraishi, Hiroaki Matsubara
    Internal Medicine 01/2011; 50(19):2237-8. · 0.97 Impact Factor
  • Source
    D G A Burton, H Matsubara, K Ikeda
    [Show abstract] [Hide abstract]
    ABSTRACT: The accumulation of senescent cells within tissues can potentially lead to biological dysfunction and manifestation of disease associated with ageing. The majority of senescent cells display a commonly altered secretome similar to a wound healing response (termed the senescence-associated secretory phenotype or SASP), which could have deleterious implications on the tissue microenvironment. However, senescent cells also appear to have a cell-type (or even cell-strain) exclusive senescent phenotype (CESP), an area of research that is underexplored. One such CESP is the pro-calcificatory phenotype recently reported in senescent vascular smooth muscle cells (VSMCs). Senescent VSMCs have been shown to overexpress genes and proteins (including RUNX-2, alkaline phosphatase (ALP), type I collagen and BMP-2) associated with osteoblasts, leading to partial osteoblastic transdifferentiation. As such, it has been suggested that senescent VSMCs contribute to cardiovascular dysfunction through induction of vascular calcification. This review discusses recent findings on VSMC senescence and their potential role in the pathophysiology of vascular calcification.
    Experimental gerontology 11/2010; 45(11):819-24. · 3.34 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Experience of primary percutaneous coronary intervention (PCI) for young adults with acute myocardial infarction (AMI) due to sequelae of Kawasaki disease (KD) has been extremely limited. In the present report on three young adults (two males and one female; age 20-35 years) with AMI, we performed primary PCI and intravascular ultrasound imaging (IVUS). Case 1 underwent thrombectomy alone in the proximal left circumflex coronary artery, and subsequent IVUS depicted a large aneurysm with an asymmetrically intimal thickening and a residual thrombus in the culprit. Case 2 underwent balloon dilation with adjunctive intracoronary thrombolysis in the proximal left anterior descending coronary artery (LAD), and IVUS during follow-up coronary angiography (CAG) delineated a regressed giant aneurysm with a markedly intimal thickening in the culprit. Case 3, with past history highly suggesting KD, underwent balloon dilation in the proximal LAD, and follow-up CAG as well as IVUS revealed a neoaneurysmal formation in the culprit. In all of the patients, PCI was angiographically effective at the acute phase without complication. Follow-up CAG performed 3-6 months after the procedure revealed no restenosis in all three cases, but a new coronary aneurysm still remained in case 3. Although case 1 and case 2 had no obvious history of KD, the vessel wall morphology from IVUS closely resembled the coronary sequelae after KD, suggesting that they might have antecedent incomplete KD. These cases suggest that primary PCI against coronary sequelae of KD in young AMI patients might be safe and effective in the short term.
    Heart and Vessels 11/2010; 26(1):117-24. · 2.13 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Erythropoietin (EPO) enhances re-endothelialization and anti-apoptotic action. Larger clinical studies to examine the effects of high-dose EPO are in progress in patients with acute myocardial infarction (AMI). The aim of this multi-center pilot study was to investigate the effect of `low-dose EPO' (6,000 IU during percutaneous coronary intervention (PCI), 24 h and 48 h) in 35 patients with a first ST-elevated AMI undergoing PCI who was randomly assigned to EPO or placebo (saline) treatment. Neointimal volume, cardiac function and infarct size were examined in the acute phase and 6 months later (ClinicalTrials.gov identifier: NCT00423020). No significant regression in in-stent neointimal volume was observed, whereas left ventricular (LV) ejection fraction was significantly improved (49.2% to 55.7%, P=0.003) and LV end-systolic volume was decreased in the EPO group (47.7 ml to 39.0 ml, P=0.036). LV end-diastolic volume tended to be reduced from 90.2% to 84.5% (P=0.159), whereas in the control group it was inversely increased (91.7% to 93.7%, P=0.385). Infarction sizes were significantly reduced by 38.5% (P=0.003) but not in the control group (23.7%, P=0.051). Hemoglobin, peak creatine kinase values, and CD34(+)/CD133(+)/CD45(dim) endothelial progenitors showed no significant changes. No adverse events were observed during study periods. This is a first study demonstrating that short-term `low-dose' EPO to PCI-treated AMI patients did not prevent neointimal hyperplasia but rather improved cardiac function and infarct size without any clinical adverse effects.
    Circulation Journal 11/2010; 74(11):2365-71. · 3.58 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Members of the fibroblast growth factor (FGF) family have been clinically applied to the treatment of ischemic diseases because of their strong angiogenic actions. Although tissue ischemia is predominantly caused by atherosclerosis, the roles of endothelial FGF receptors (FGF-Rs) in atherosclerosis remain obscure. We generated endothelial cell (EC)-targeted constitutively active FGF-R2-overexpressing mice, using the Tie2 promoter (Tie2-FGF-R2-Tg), and crossed them with apolipoprotein E (ApoE)-deficient mice (ApoE-KO) to generate Tie2-FGF-R2-Tg/ApoE-deficient mice (Tie2-FGF-R2-Tg/ApoE-KO). After being fed a Western diet for 8 wk, the Tie2-FGF-R2-Tg/ApoE-KO demonstrated 2.0-fold greater atherosclerotic lesion area on the luminal surfaces of the aortas than the ApoE-KO (P < 0.01). The level of p21(Cip1) protein, a cell cycle inhibitor, in the FGF-R2-overexpressing EC was 2.5-fold greater than that in the wild-type (WT) EC at the baseline (P < 0.01). FGF-R2 overexpression in the EC resulted in increased expression of VCAM-1 and ICAM-1, acceleration of apoptosis, and decreased proliferative activity, all of which were normalized by small interfering RNA (siRNA)-mediated knockdown of p21(Cip1) (75% reduction in protein level, P < 0.01). Furthermore, the expression of PDGF-B and Egr-1, a PDGF/p21(Cip1)-inducible transcription factor, in the aortic endothelium of Tie2-FGF-R2-Tg/ApoE-KO was significantly greater than that in ApoE-KO. The proliferation of vascular smooth muscle cells in the aortic media of Tie2-FGF-R2-Tg/ApoE-KO was 2.0-fold higher than that in ApoE-KO (P < 0.01). Thus our study reveals that endothelial FGF-R2 signaling aggravates atherosclerosis by promoting p21(Cip1)-mediated EC dysfunction and cautions against the use of FGF for therapeutic angiogenesis in the setting of atherosclerosis.
    AJP Heart and Circulatory Physiology 10/2010; 300(1):H154-61. · 4.01 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Bioenergetic homeostasis is altered in heart failure and may play an important role in pathogenesis. p53 has been implicated in heart failure, and although its role in regulating tumorigenesis is well characterized, its activities on cellular metabolism are just beginning to be understood. We investigated the role of p53 and its transcriptional target gene TP53-induced glycolysis and apoptosis regulator (TIGAR) in myocardial energy metabolism under conditions simulating ischemia that can lead to heart failure. Expression of p53 and TIGAR was markedly upregulated after myocardial infarction, and apoptotic myocytes were decreased by 42% in p53-deficient mouse hearts compared with those in wild-type mice. To examine the effect of p53 on energy metabolism, cardiac myocytes were exposed to hypoxia. Hypoxia induced p53 and TIGAR expression in a p53-dependent manner. Knockdown of p53 or TIGAR increased glycolysis with elevated fructose-2,6-bisphosphate levels and reduced myocyte apoptosis. Hypoxic stress decreased phosphocreatine content and the mitochondrial membrane potential of myocytes without changes in ATP content, the effects of which were prevented by the knockdown of TIGAR. Inhibition of glycolysis by 2-deoxyglucose blocked these bioenergetic effects and TIGAR siRNA-mediated prevention of apoptosis, and, in contrast, overexpression of TIGAR reduced glucose utilization and increased apoptosis. Our data demonstrate that p53 and TIGAR inhibit glycolysis in hypoxic myocytes and that inhibition of glycolysis is closely involved in apoptosis, suggesting that p53 and TIGAR are significant mediators of cellular energy homeostasis and cell death under ischemic stress.
    AJP Heart and Circulatory Physiology 10/2010; 299(6):H1908-16. · 4.01 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Vascular calcification is an important risk factor for cardiovascular diseases. Here, we investigated a role of dedifferentiated vascular smooth muscle cells (VSMCs) in the atherosclerotic intimal calcification. We prepared human cultured VSMCs in either redifferentiatiated or dedifferentiated state and analyzed the gene expressions of bone-calcification regulatory factors. Expression of bone morphogenetic protein-2 (BMP-2), a potent initiator for osteoblast differentiation, was significantly enhanced in dedifferentiated VSMCs. Furthermore, endogenous BMP-2 antagonists, such as noggin, chordin, and matrix gamma-carboxyglutamic acid protein, were all downregulated in the dedifferentiated VSMCs. Conditioned medium from dedifferentiated VSMCs, but not from redifferentiated VSMCs, stimulated the osteoblastic differentiation of the mesenchymal progenitor C2C12 cells, which was abolished by BMP-2 knockdown. In atherosclerotic intima from apolipoprotein (apo)E-deficient mice, αSM-actin-positive cells, presumably dedifferentiated VSMCs, expressed BMP-2. We generated BMP-2-transgenic mice using αSM-actin promoter and crossed them with apoE-deficient mice (BMP-2-transgenic/apoE-knockout). Significantly accelerated atherosclerotic intimal calcification was detected in BMP-2-transgenic/apoE-knockout mice, although serum lipid concentration and atherosclerotic plaque size were not different from those in apoE-knockout mice. Enhanced calcification appeared to be associated with the frequent emergence of osteoblast-like cells in atherosclerotic intima in BMP-2-transgenic/apoE-knockout mice. Our findings collectively demonstrate an important role of dedifferentiated VSMCs in the pathophysiology of atherosclerotic calcification through activating paracrine BMP-2 osteogenic signals.
    Arteriosclerosis Thrombosis and Vascular Biology 10/2010; 30(10):1908-15. · 6.34 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Klotho is a circulating protein, and Klotho deficiency disturbs endothelial integrity, but the molecular mechanism is not fully clarified. We report that vascular endothelium in Klotho-deficient mice showed hyperpermeability with increased apoptosis and down-regulation of vascular endothelial (VE)-cadherin because of an increase in VEGF-mediated internal calcium concentration ([Ca(2+)]i) influx and hyperactivation of Ca(2+)-dependent proteases. Immunohistochemical analysis, the pull-down assay using Klotho-fixed agarose, and FRET confocal imaging confirmed that Klotho protein binds directly to VEGF receptor 2 (VEGFR-2) and endothelial, transient-receptor potential canonical Ca(2+) channel 1 (TRPC-1) and strengthens the association to promote their cointernalization. An in vitro mutagenesis study revealed that the second hydrolase domain of Klotho interacts with sixth and seventh Ig domains of VEGFR-2 and the third extracellular loop of TRPC-1. In Klotho-deficient endothelial cells, VEGF-mediated internalization of the VEGFR-2/TRPC-1 complex was impaired, and surface TRPC-1 expression increased 2.2-fold; these effects were reversed by supplementation of Klotho protein. VEGF-mediated elevation of [Ca(2+)]i was sustained at higher levels in an extracellular Ca(2+)-dependent manner, and normalization of TRCP-1 expression restored the abnormal [Ca(2+)]i handling. These findings provide evidence that Klotho protein is associated with VEGFR-2/TRPC-1 in causing cointernalization, thus regulating TRPC-1-mediated Ca(2+) entry to maintain endothelial integrity.
    Proceedings of the National Academy of Sciences 10/2010; 107(45):19308-13. · 9.81 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Though restenosis after drug-eluting stent implantation is still observed, the factors affecting post-sirolimus-eluting stent restenosis (re-restenosis) have not been fully determined. We evaluated the long-term angiographic outcomes and examined background factors affecting re-restenosis. We enrolled 51 patients with 68 sirolimus-eluting stent (SES) restenosis lesions who underwent target lesion revascularization (TLR) and angiographic follow-up studies. Re-restenosis was observed in 29 of 68 restenosis lesions, and the rate was 42.6%. Study subjects were divided into two groups: a re-restenosis (Re-R) group (20 patients) with 29 lesions and a restenosis (R) group (31 patients) with 39 lesions with no re-restenosis. There were no differences in age, sex, coronary risk factors, past history, or medications between the two groups. Re-restenosis was observed more frequently in the right coronary artery (Re-R group vs. R group; 65.5 vs. 33.3%, P = 0.009). The incidence of stent fracture was higher in the Re-R group (Re-R group vs. R group; 48.3 vs. 12.8%, P = 0.003). QCA results showed that the initial lesion length at the time of first coronary intervention was significantly longer in the Re-R group (Re-R group vs. R group; 21.6 ± 3.37 vs. 12.6 ± 4.98 mm, P = 0.049). The rate of re-restenosis was 47.1% when treated with POBA alone, while it was 36.7% with SES treatment. In multivariate analysis, the initial lesion length at the time of first coronary intervention (odds ratio = 1.64, 95% CI 1.29-2.06, P < 0.001) and stent fracture (odds ratio = 12.42, 95% CI 1.89-81.4, P = 0.009) were independent predictors of re-restenosis. This study demonstrates that recurrent restenosis with SES treatment is associated with lesion length and stent fracture, a finding that is beneficial in the management of restenosis after SES implantation.
    Heart and Vessels 10/2010; 26(2):168-75. · 2.13 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Prolonged pre-hospital time for acute myocardial infarction (AMI) is associated with decreased indication for primary percutaneous coronary intervention (PCI). However, the efficacy of primary PCI in AMI patients with prolonged pre-hospital time has not been fully investigated in Japan. A total of 3010 consecutive AMI patients admitted to AMI-Kyoto Multi-Center Risk Study Group hospitals were retrospectively analyzed, and the clinical characteristics and in-hospital prognosis of these patients were reviewed. Patients with pre-hospital delay [elapsed time (ET)>12 h] had a lower frequency of Killip≥3 (9.3%) and less frequently received primary PCI (77.7%) compared with patients with ET≤12 h. In the ET>12 h group, older patients or patients with MI history tended to be complicated by heart failure. Primary PCI was performed for patients with ET>12 h, irrespective of the severity of heart failure [Killip 1 (78.7%) vs Killip≥2 (74.0%); p=0.3827]. On multivariate logistic regression analysis, age [odds ratio (OR) 1.053], MI history (OR 2.860), Killip≥2 (OR 10.235), and multi-vessels or left main coronary artery as culprit (OR 11.712) were significant independent positive predictors of in-hospital mortality for patients with ET>12 h. Practice of primary PCI was not a significant negative predictor for patients with ET>12 h (OR 0.812), but it was for patients with ET≤12 h (OR 0.425). These findings indicate that patients with ET>12 h have a less severe condition and less frequently receive primary PCI compared with patients with ET≤12 h. Although primary PCI is often performed for these patients irrespective of the severity of heart failure, no preferable effect of primary PCI on the in-hospital mortality is demonstrated. In contrary, practice of primary PCI is a significant negative predictor of in-hospital mortality for patients with ET≤12 h.
    Journal of Cardiology 09/2010; 56(2):204-10. · 2.30 Impact Factor
  • International journal of cardiology 09/2010; 148(3):359-61. · 6.18 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Predictors of in-hospital outcome after primary percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) requiring mechanical support devices such as intra-aortic balloon pumping (IABP) and/or percutaneous cardiopulmonary support (PCPS) remain unclear. Using the AMI-Kyoto Multi-Center Risk Study database, clinical background, angiographic findings, results of primary PCI, and in-hospital prognosis were retrospectively compared between primary PCI-treated AMI patients requiring mechanical assist devices (with-IABP/PCPS patients, n=275) and those without (without-IABP/PCPS patients, n=1,510). The with-IABP/PCPS patients were more likely to have a larger number of diseased vessels, lower Thrombolysis In Myocardial Infarction (TIMI) grade in the infarct-related artery (IRA) before/after primary PCI, and a significantly higher in-hospital mortality rate than the without-IABP/PCPS patients. On multivariate analysis, the number of diseased vessels > or =2 or diseased left main trunk (LMT) at initial coronary angiography (CAG) was the independent positive predictor of the in-hospital mortality in the with-IABP/PCPS patients, not in the without-IABP/PCPS patients, whereas acquisition of TIMI 3 flow in the IRA immediately after primary PCI was the negative predictor in the without-IABP/PCPS patients, not in the with-IABP/PCPS patients. The number of diseased vessels > or =2 or diseased LMT at initial CAG is an independent risk factor of in-hospital death in primary PCI-treated AMI patients requiring mechanical support devices.
    Circulation Journal 04/2010; 74(6):1152-7. · 3.58 Impact Factor
  • Tetsuro Kusaba, Yasukiyo Mori, Hiroaki Matsubara
    Kidney International 04/2010; 77(7):649-50. · 8.52 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: An attenuated heart rate response to exercise, termed chronotropic incompetence (CI), has been reported to be an independent predictor of cardiovascular mortality. We examined the change in autonomic function during exercise testing and correlated the results with CI. Exercise testing using a bicycle ergometer was performed in 172 patients who had no evidence of cardiac disease. Chronotropic incompetence was defined as the failure to achieve 85% of the age-predicted maximum heart rate, heart rate reserve <80%, or chronotropic response index <0.80. We analysed the relationship between CI and the change in two components of heart rate variability during exercise testing: high-frequency (HF) component (0.15-0.40 Hz) as an index of vagal modulation and the ratio of low-frequency (LF) component (0.04-0.15 Hz) to HF component as an index of sympathovagal balance. Heart rate variability indexes before exercise were similar in patients with and without CI. Percentage changes after exercise in the ratio of LF to HF component were higher in patients with CI than in those without CI (84 +/- 15 vs. 41 +/- 16%, P < 0.05), whereas percentage changes in an HF component were similar in the two groups. Our data suggested that CI in patients without structural heart disease was mainly caused by a pathophysiological condition in which sympathetic activation was not well translated into heart rate increase. Further study is needed to determine the post-synaptic sensitivity of the beta-adrenergic receptor pathway in relation to CI.
    Europace 04/2010; 12(4):561-6. · 2.77 Impact Factor

Publication Stats

8k Citations
1,532.85 Total Impact Points


  • 2004–2013
    • Kyoto Prefectural University of Medicine
      • • Department of Cardiovascular Medicine
      • • Division of Cardiology and Vascular Regenerative Medicine
      Kyoto, Kyoto-fu, Japan
  • 2012
    • Nagoya Second Red Cross Hospital
      Nagoya, Aichi, Japan
  • 2006–2012
    • Kyoto Daini Red Cross Hospital
      Kioto, Kyōto, Japan
  • 2011
    • Asahikawa Medical University
      Asakhigava, Hokkaidō, Japan
  • 1987–2011
    • Kansai Medical University
      • • Second Department of Internal Medicine
      • • Medical School
      Moriguchi, Ōsaka, Japan
    • Tokyo Institute of Technology
      Edo, Tōkyō, Japan
  • 2010
    • Sakurakai Takahashi Hospital
      Kōbe, Hyōgo, Japan
  • 2008–2010
    • Kyoto Pharmaceutical University
      • • Division of Pathological Sciences
      • • Laboratory of Clinical Pharmacology
      Kioto, Kyōto, Japan
  • 2009
    • Kyoto University
      • Department of Experimental Therapeutics
      Kyoto, Kyoto-fu, Japan
  • 2007–2009
    • Kokura Memorial Hospital
      • Department of Cardiology
      Kitakyūshū, Fukuoka, Japan
  • 1986–2008
    • National Cerebral and Cardiovascular Center
      • Department of Cardiovascular Medicine
      Ōsaka, Ōsaka, Japan
  • 2004–2007
    • Maizuru Mutual Hospital
      Kioto, Kyōto, Japan
  • 2003–2004
    • Asahi University
      Gihu, Gifu, Japan
  • 2001
    • Hiroshima University
      • Faculty of Medicine
      Hiroshima-shi, Hiroshima-ken, Japan
  • 1998
    • Harvard Medical School
      Boston, Massachusetts, United States