Takeshi Shirayama

Kyoto Prefectural University of Medicine, Kioto, Kyōto, Japan

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Publications (66)164.54 Total impact

  • [show abstract] [hide abstract]
    ABSTRACT: Brugada syndrome (BrS) is an inherited cardiac arrhythmia associated with sudden death due to ventricular fibrillation. Mutations in genes related to the cardiac L-type calcium channel (LTCC) have been reported to be causative of BrS. Generally, mRNA that contains a nonsense mutation is rapidly degraded via its decay pathway, which is known as nonsense-mediated mRNA decay (NMD). Previously, we reported a male BrS patient who carried c.1896G>A (the first nucleotide of CACNA1C exon 14), which caused a synonymous mutation, p.R632R. The present study aimed to examine how this synonymous CACNA1C mutation produces the phenotype of BrS, with special emphasis on the splicing error and NMD phenomena. We extracted mRNA from leukocytes of the proband and his two children and performed RT-PCR. Complementary DNAs (cDNAs) were checked by direct sequencing and quantitative analysis. The subsequent sequence electropherogram of the cDNAs did not show the substitution of the nucleotide identified in the genomic DNA of the proband. In the mRNA quantification analysis, we confirmed that reduction in the CACNA1C expression level was suspected to be caused by NMD. Mutant mRNA with a c.1896G>A substitution may be diminished by NMD, and the resultant decrease in CACNA1C message leads to a novel mechanism for inducing BrS that is distinct from that reported previously.
    Heart rhythm: the official journal of the Heart Rhythm Society 12/2013; · 4.56 Impact Factor
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    ABSTRACT: Data regarding the relationship between systolic blood pressure (SBP) at admission and in-hospital outcome in patients with acute myocardial infarction (AMI) undergoing primary percutaneous coronary intervention (PCI) are still lacking in Japan. A total of 1475 primary PCI-treated AMI patients were classified into quintiles based on admission SBP (<105 mmHg, n=300; 105-125 mmHg, n=294; 126-140 mmHg, n=306; 141-158 mmHg, n=286; and ≥159 mmHg n=289). The patients with SBP<105 mmHg tended to have higher age, previous myocardial infarction, chronic kidney disease (CKD), Killip class≥3 at admission, right coronary artery, left main trunk (LMT), or multivessels as culprit lesions, larger number of diseased vessels, lower Thrombolysis In Myocardial Infarction (TIMI) grade in the infarct-related artery before primary PCI, and higher value of peak creatine phosphokinase concentration. Patients with SBP<105 mmHg had a significantly higher mortality, while mortality was not significantly different among the other quintiles: 24.3% (<105 mmHg), 4.8% (105-125 mmHg), 4.9% (126-140 mmHg), 2.8% (141-158 mmHg), and 5.2% (≥159 mmHg) (p<0.001). On multivariate analysis, Killip class≥3 at admission, LMT or multivessels as culprit lesions, admission SBP<105 mmHg, CKD, and age were the independent positive predictors of in-hospital mortality, whereas admission SBP 141-158 mmHg and TIMI 3 flow after PCI were the negative ones, but admission SBP 105-125 mmHg, admission SBP 126-140 mmHg, and admission SBP≥159 mmHg were not. These results suggest that admission SBP 141-158 mmHg might be correlated with better in-hospital prognosis, whereas admission SBP<105 mmHg was associated with in-hospital death in Japanese AMI patients undergoing primary PCI.
    Journal of Cardiology 04/2012; 60(2):139-44. · 2.30 Impact Factor
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    ABSTRACT: Several clinical studies have demonstrated an inverse relationship between systolic blood pressure (SBP) at admission and in-hospital mortality in patients hospitalized for acute myocardial infarction (AMI). However, data on the relation between admission SBP and in-hospital prognosis in AMI patients are still lacking in Japan. A total of 1211 AMI patients were classified into quintiles based on SBP at hospital admission (<106 mmHg, n = 241; 106-125 mmHg, n = 239; 126-140 mmHg, n = 244; 141-159 mmHg, n = 238; and ≥ 160 mmHg, n = 249). The patients with SBP < 106 mmHg tended to have higher age, Killip class ≥ 3 at admission, right coronary artery, left main trunk, or multivessels as culprit lesions, larger number of diseased vessels, lower Thrombolysis In Myocardial Infarction grade in the infarct-related artery before primary percutaneous coronary intervention (PCI), and higher value of peak creatine phosphokinase concentration. Patients with SBP <106 mmHg had a significantly higher mortality, while mortality was not significantly different among the other quintiles: 25.7% (<106 mmHg), 5.4% (106-125 mmHg), 5.7% (126-140 mmHg), 2.5% (141-159 mmHg), and 5.6% (≥ 160 mmHg) (p<0.001). On multivariate analysis, Killip class ≥ 3 at admission, admission SBP <106 mmHg, and age were the independent positive predictors of in-hospital mortality, whereas admission SBP 141-159 mmHg and primary PCI were the negative ones, but admission SBP 106-125 mmHg, admission SBP 126-140 mmHg, and admission SBP ≥ 160 mmHg were not. These results suggest that admission SBP 141-159 mmHg might be correlated with better in-hospital prognosis, whereas admission SBP <106 mmHg was associated with in-hospital death in Japanese patients hospitalized for AMI.
    Journal of Cardiology 05/2011; 58(1):54-60. · 2.30 Impact Factor
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    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. · 9.74 Impact Factor
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    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
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    ABSTRACT: Predictors of suboptimal coronary flow in the infarct-related artery (IRA) after stent-based primary percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI) have not been fully investigated. Using the AMI-Kyoto Multi-Center Risk Study database, we retrospectively compared clinical manifestations and in-hospital prognosis between AMI patients undergoing stent-based primary PCI with final Thrombolysis In Myocardial Infarction (TIMI) grade < or = 2 in the IRA (nonoptimal group, n=69) and those with final TIMI grade 3 (optimal group, n=1200). The nonoptimal group had higher prevalence of Killip class > or = 3 at admission, higher frequency of mechanical support devices during procedures, larger value of maximal creatine phosphokinase, and a significantly higher in-hospital mortality rate (27.5% for nonoptimal vs. 9.0% for optimal, P<0.001), compared with the optimal group. On multivariate analysis, Killip class > or = 3 at admission was the independent predictor of the final nonoptimal flow (odds ratio 2.33, 95% confidence intervals 1.27-4.26 P=0.006), but TIMI 3 flow before primary PCI and elapsed time (symptom onset-to-admission time)<24h were not. Killip class > or = 3 at admission is an independent predictor of the final nonoptimal flow in AMI patients undergoing primary PCI with stent implantation.
    Journal of Cardiology 03/2010; 55(2):217-23. · 2.30 Impact Factor
  • Journal of Cardiology Cases 01/2010; 1(1).
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    ABSTRACT: Recurrent acute myocardial infarction (AMI) is a disastrous condition with high in-hospital morbidity and mortality. However, the relation between location of previous myocardial infarction (MI) and in-hospital outcome in repeat-AMI patients undergoing primary percutaneous coronary intervention (PCI) remains 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 with previous anterior MI (anterior group, n=151) and those with previous non-anterior MI (non-anterior group, n=157). Clinical backgrounds, angiographic findings, results of primary PCI, and in-hospital outcome did not differ significantly between the two groups. On multivariate analysis, Killip class > or =3 at admission, number of diseased vessels > or =2 or diseased left main trunk at initial coronary angiography, and age were the independent predictors of in-hospital mortality in the recurrent-AMI patients, but not the anterior location of previous MI. These results suggest that among recurrent-AMI patients undergoing primary PCI, in-hospital prognosis mostly depends on the severity of acute heart failure at the onset and the residual myocardial ischemia rather than previous MI sites.
    Journal of Cardiology 01/2010; 55(1):77-83. · 2.30 Impact Factor
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    ABSTRACT: There are more than a few risks of hemorrhage complication in patients with amyloidosis. Although most cases with amyloidosis exhibit minor bleeding manifestations, they can be occasionally associated with life-threatening problems. To our knowledge, there are only a few cases of spontaneous pericardial hematoma associated with amyloidosis. We here report a patient who suddenly died of cardiac tamponade with massive pericardial hematoma 7 years after the diagnosis of familial amyloid polyneuropathy (FAP). A 69-year-old female with FAP with cardiogenic shock was admitted to our emergency room. Although she previously underwent permanent pacemaker implantation for atrial fibrillation with slow ventricular response, electrocardiogram showed a critical pacing failure. Emergent telemetry check revealed a sudden extreme increase of pacing capture threshold in the right ventricle. Maximum pacing voltage could not improve the critical condition, and she died 7 h after arrival. Autopsy showed a massive pericardial hematoma in the right ventricular free wall, and microscopic examination revealed typical amyloid deposition in the arterial wall of the pericardium. In this case, it is assumed that a sudden rupture of fragile pericardial vessels with amyloid deposition led to the lethal pericardial hematoma.
    Amyloid: the international journal of experimental and clinical investigation: the official journal of the International Society of Amyloidosis 12/2009; 16(4):221-5. · 2.12 Impact Factor
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    ABSTRACT: Intracellular Na(+) ([Na(+)](i)) regulation plays a crucial role in the structural, mechanical, and electrical properties of myocardium. It is assumed that the [Na(+)](i) handling system may differ not only between normal and diseased hearts but also regionally within a heart. To gain new insight concerning disease- and region-dependent differences in the [Na(+)](i)-regulatory system, we investigated mRNA expression of Na+ transporters, the principal determinants of [Na(+)](i). Nonischemic pressure-overloaded hypertrophy was created by suprarenal abdominal aortic constriction of 50% for 7 weeks. mRNA abundances of Na(+)-Ca(2+) exchanger (NCX1), Na(+)-H(+) exchanger (NHE1), Na(+)-K(+)-2Cl(-) exchanger (NKCC1) and Na(+), K(+)-ATPase multigene family(alpha(1), alpha(2), alpha(3), and beta(1) isoforms) were measured by the real-time quantitative polymerase chain reaction method. mRNA abundance of all transporters mediating Na(+) influx (NCX1, NHE1, and NKCC1) was significantly upregulated as compared to normal. In contrast, Na(+)-efflux-mediating transporter (Na(+), K(+)-ATPase) mRNA expression was unaltered between normal and hypertrophic hearts. Losartan, an angiotensin II AT1 receptor antagonist, significantly attenuated upregulation of Na(+)-influx-mediating transporters induced by aortic constriction. The onset of Na(+)-influx-mediating transporter upregulation occurred within 5 days following constriction. In normal and hypertrophied hearts, mRNA of all Na(+)-influx-mediating transporters was expressed in order of abundance as: apex > septum approximately free wall of left ventricles. A transmural gradient in expression was also evident in normal hearts (midcardium > endo- and epicardium), which was attenuated under hypertrophic development. Myocardial hypertrophy is associated with significant changes in the spatial distribution and expression levels of Na(+) transporters. The upregulation of Na influx transporters during hypertrophy may contribute to the remodeling process, modulate contractility and promote arrhythmias.
    Heart and Vessels 01/2009; 24(1):54-62. · 2.13 Impact Factor
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    ABSTRACT: Losartan, enalapril and amlodipine reduced the number of premature ventricular contractions (PVCs) in patients with essential hypertension as well as blood pressure. The effect of losartan was the most prominent among the three drugs.
    Journal of human hypertension 11/2008; 23(4):289-91. · 2.80 Impact Factor
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    ABSTRACT: Recurrent acute myocardial infarction (AMI) is a deteriorated condition with high in-hospital morbidity and mortality, but the predictors of in-hospital outcome after primary percutaneous coronary intervention (PCI) for repeat AMI 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 with previous myocardial infarction (MI) (repeat-MI patients, n=235) and those without previous MI (first-MI patients, n=1,550). The repeat-MI patients had higher prevalence of Killip class>or=3 at admission, larger number of diseased vessels, and a significantly higher in-hospital mortality rate than the first-MI patients. On multivariate analysis, number of diseased vessels>or=2 or diseased left main trunk (LMT) on initial coronary angiography was the independent positive predictor of in-hospital mortality in the repeat-MI patients, not in the first-MI patients, whereas acquisition of Thrombolysis In Myocardial Infarction 3 flow in the infarct-related artery immediately after primary PCI and elapsed time<24 h were the negative predictors in the first-MI patients, not in the repeat-MI patients. Number of diseased vessels>or=2 or diseased LMT on initial coronary angiography is an independent risk factor of in-hospital death in recurrent-AMI patients undergoing primary PCI.
    Circulation Journal 08/2008; 72(8):1225-9. · 3.58 Impact Factor
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    ABSTRACT: Several clinical studies have demonstrated an inverse relationship between hospital volume of primary percutaneous coronary interventions (PCI) and in-hospital mortality. However, the relationships among hospital primary PCI volume, angiographic results, and in-hospital prognosis in patients with acute myocardial infarction (AMI) have not been fully investigated in Japan. Using the AMI-Kyoto Multi-Center Risk Study database between January 2000 and December 2005, hospitals were classified into quintiles based on their annual volume of primary PCI. The fifth quintile of hospitals was labeled as high-volume, and the other quintiles were combined and defined as low-volume. Although patients undergoing primary PCI in high-volume hospitals (high-volume group, n=764) had a larger number of diseased vessels at initial coronary angiography and lower Thrombolysis In Myocardial Infarction (TIMI) flow grade in the infarct-related artery before PCI, compared with those in low-volume hospitals (low-volume group, n=1,021), the rates of achieving TIMI flow grade 3 just after PCI in the high-volume group was significantly higher than that in the low-volume group. The overall in-hospital mortality did not differ between the 2 groups. On multivariate analysis, in AMI patients undergoing primary PCI, Killip class >or=3 at admission, multivessel disease or left main trunk (LMT) as culprit lesion, number of diseased vessels >or=2 or diseased LMT, and age were the independent positive predictors of in-hospital mortality, whereas the TIMI flow grade 3 after primary PCI and elapsed time <24 h were the negative ones, but not low-volume hospital. Angiographic results of primary PCI in high-volume hospitals were superior to those in low-volume hospitals, but there was no significant difference in the in-hospital mortality between AMI patients in high-volume hospitals and those in low-volume hospitals.
    Circulation Journal 02/2008; 72(7):1041-6. · 3.58 Impact Factor
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    ABSTRACT: The Na(+)-HCO(3)(-) cotransporter (NBC) plays a key role in intracellular pH (pH(i)) regulation in normal ventricular muscle. However, the state of NBC in nonischemic hypertrophied hearts is unresolved. In this study, we examined functional and molecular properties of NBC in adult rat ventricular myocytes. The cells were enzymatically isolated from both normal and hypertrophied hearts. Ventricular hypertrophy was induced by pressure overload created by suprarenal abdominal aortic constriction of 50% for 7 wk. pH(i) was measured in single cells using the fluorescent pH indicator 2',7'-bis(2-carboxyethyl)5-(6)carboxyfluorescein. Real-time PCR analysis was used to quantitatively assess expression of NBC-encoding mRNA, including SLC4A4 (encoding electrogenic NBC, NBCe1) and SLC4A7 (electroneutral NBC, NBCn1). Our results demonstrate that: 1) mRNA levels of both the electrogenic NBCe1 (SLC4A4) and electroneutral NBCn1 (SLC4A7) forms of NBC were increased by aortic constriction, 2) the onset of NBC upregulation occurred within 3 days after constriction, 3) normal and hypertrophied ventricles displayed regional differences in NBC expression, 4) acid extrusion via NBC (J(NBC)) was increased significantly in hypertrophied myocytes, 5) although acid extrusion via Na(+)/H(+) exchange was also increased in hypertrophied myocytes, the relative enhancement of J(NBC) was larger, 6) membrane depolarization markedly increased J(NBC) in hypertrophied myocytes, and 7) losartan, an ANG II AT(1) receptor antagonist, significantly attenuated the upregulation of both NBCs induced by 3 wk of aortic constriction. Enhanced NBC activity during hypertrophic development provides a mechanism for intracellular Na(+) overload, which may render the ventricles more vulnerable to Ca(2+) overload during ischemia-reperfusion.
    AJP Heart and Circulatory Physiology 09/2007; 293(2):H1254-64. · 3.63 Impact Factor
  • Takeshi Shirayama
    Nippon rinsho. Japanese journal of clinical medicine 09/2007; Suppl 4:513-6.
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    ABSTRACT: The occurrence and the duration of paroxysmal atrial fibrillation (AF) are influenced by vagal tone. Paroxetine, an antidepressant, can modulate vagal tone at the level of the mid-brain and inhibit the vasovagal reflex. In this study, oral paroxetine 10 mg/day was administered to patients with multidrug-resistant paroxysmal AF. Nine consecutive men responded favorably to the drug. In 3 patients, AF resolved completely. One patient could not tolerate the drug because of nausea and nervousness. These preliminary results suggest that paroxetine could be a choice in the pharmacologic treatment of paroxysmal AF.
    The American Journal of Cardiology 07/2006; 97(12):1749-51. · 3.21 Impact Factor
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    ABSTRACT: We investigated the association between sympathetic nerve activity and delayed rectifier potassium current (I(K)) in hypertrophic rat hearts. Left ventricular hypertrophy was induced by a 50% constriction of suprarenal abdominal aorta for 6 weeks. The effects of isoproterenol on action potential duration (APD), I(K), and L-type calcium current (I(Ca)) were investigated using the whole-cell patch clamp technique. In hypertrophic rats, I(K) was decreased by 28.2%, resulting in significant APD(90) (90% repolarization) prolongation (sham: 55 +/- 3.9, hypertrophy: 98 +/- 11 ms, P = 0.01). Isoproterenol (100 nM)-stimulated I(K) was increased by 54.9% +/- 0.10% in sham-operated rats, but not in hypertrophic rats. On the other hand, isoproterenol increased I(Ca) in both sham-operated (77.7% +/- 7.6%) and hypertrophic rats (69.6% +/- 9.7%). Consequently, isoproterenol prolonged further APD in hypertrophic rats (98 +/- 11 vs. 145 +/- 8.6 ms, P < 0.01), but not in sham-operated rats (55 +/- 3.9 vs. 61 +/- 5.6 ms, n.s.). Forskolin (1 microM, an adenylyl cyclase stimulator) did not enhance I(K) in hypertrophic rats, but IBMX (100 microM, a nonselective phosphodiesterase inhibitor) enhanced the current (30.2 +/- 0.05%), as much as in sham-operated rats. We concluded that in hypertrophic hearts, I(K) was not increased by isoproterenol because of the enhanced activity of phosphodiesterase, which leads to excessive APD prolongation.
    The Journal of Physiological Sciences 04/2006; 56(2):173-81. · 1.09 Impact Factor
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    ABSTRACT: A 45-year-old man who had been undergoing maintenance hemodialysis for end-stage renal failure, caused by chronic glomerulonephritis 4 years before, was admitted to our hospital for biventricular pacemaker implantation (BVP). Ten years ago, he was diagnosed with idiopathic dilated cardiomyopathy, and had been suffering from dialysis-related hypotension (DRH) due to low cardiac function over the past year. An electrocardiogram revealed complete left bundle branch block with a QRS duration of 180 ms, and echocardiography showed moderate hypokinesis of the left ventricular wall and systolic asynchronized motion of the septum and free wall. After BVP, the left ventricular ejection fraction had increased from 29% to 40%, and the transmitral rapid left ventricular filling (E wave) and atrial contraction (A wave) ratio (E/A) had improved from 1.3 to 1.0. Before and after BVP, we measured hemodynamic parameters during hemodialysis by successive echocardiography. Before BVP, systemic vascular resistance had decreased, cardiac output had not changed, and hypotension was noted. In contrast, after BVP, cardiac output had increased and systemic vascular resistance had not changed, which caused an increase in blood pressure. We conclude that BVP improved the cardiac function which resulted in an improvement in dialysis-related hypotension (DRH).
    Clinical and Experimental Nephrology 10/2005; 9(3):255-9. · 1.25 Impact Factor
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    ABSTRACT: Hypercholesterolemia is a risk factor for development of coronary artery disease (CAD), however, several reports have suggested that low serum cholesterol is associated with a worse prognosis in patients with congestive heart failure (CHF). The objective of this study was to determine the prognostic value of cholesterol for CHF. The study subjects consisted of 133 consecutive patients hospitalized in our institution for progressive heart failure from April 2000 to March 2003. Thirty-two percent of the patients had CAD. After improvement of congestive heart failure and discharge from the hospital, lipid profiles, including serum total cholesterol (TC), triglycerides, and high and low density lipoprotein cholesterol (HDL, LDL, respectively), were obtained. During the follow-up period (2.3 +/- 0.9 years), 21 patients died. There was a significant difference between survivors and nonsurvivors in HDL (53 +/- 15, 43 +/- 15 mg/dL, P = 0.01), but no differences were observed in other variables. In patients with CAD, survivors had significantly lower TC concentrations (179 +/- 30 versus 246 +/- 55 mg/dL, P = 0.004), although in patients without CAD, survivors had significantly higher TC concentrations (203 +/- 37 versus 170 +/- 40 mg/dL, P = 0.02). Multivariate analysis showed high TC predicted a worse outcome in patients with CAD (odds ratio (OR) = 1.052, 95% confidence interval (CI) 1.002-1.104, P = 0.04), but a better outcome in patients without CAD (OR = 0.972, 95% CI 0.948-0.997, P = 0.03), independent of age, gender, medication, and complications. Thus, low serum cholesterol is associated with an improved outcome in patients with CAD, while it predicts a worse outcome in patients without CAD.
    International Heart Journal 08/2005; 46(4):619-29. · 1.23 Impact Factor
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    ABSTRACT: The aim of this clinical crossover study was to elucidate the effects of atrioventricular (AV) synchronous pacing on cardiac function in patients with sick sinus syndrome (SSS). Thirty SSS patients, each with dual chamber pacemaker (DDD), were enrolled and divided into two groups based on echocardiographic findings. Group A (n = 16) had hypertensive heart disease (wall thickness 11 approximately 12 mm) or mitral or aortic regurgitation (Grade I or II). Group B (n = 14) had no organic heart disease. Three successive 3-month pacing periods were tested. For the first 3 months, long AV delay that achieved > 80% ventricular sensing was chosen. For the next 3 months, AV delay was abbreviated to achieve > 80% ventricular pacing at an optimal AV interval. For the final 3 months, the first setting was resumed. At the end of each period, M mode echocardiography, pulsed-Doppler study, and measurement of plasma brain natriuretic peptide (BNP) level were conducted. In both groups, echocardiographic parameters were not significantly changed during the evaluation. In group A, plasma BNP level was significantly higher at the end of the short AV delay period than at the long AV delay period (P = 0.009), while in group B it did not differ during each period. AV synchronous pacing (> 80% ventricular pacing) in the SSS patients with a DDD pacemaker implanted could increase the ventricular load, and it is better to preserve the spontaneous QRS with the DDD mode with prolonged AV delay in patients with mild hypertensive or valvular disease.
    Pacing and Clinical Electrophysiology 10/2004; 27(9):1212-6. · 1.75 Impact Factor

Publication Stats

350 Citations
164.54 Total Impact Points

Institutions

  • 1988–2013
    • Kyoto Prefectural University of Medicine
      • • Department of Cardiovascular Medicine
      • • Division of Cardiology and Vascular Regenerative Medicine
      • • Department of Medicine
      • • Department of Radiology
      • • Department of Pediatric Internal Medicine
      Kioto, Kyōto, Japan
  • 2008–2012
    • Kyoto Daini Red Cross Hospital
      Kioto, Kyōto, Japan