Takeshi Shirayama

Kyoto Prefectural University of Medicine, Kioto, Kyōto, Japan

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Publications (70)167.69 Total impact

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    ABSTRACT: We here report the angioscopic assessment of inoperable peripheral chronic thromboembolic pulmonary hypertension in an 81-year-old man who was previously diagnosed with the disease. To assess the pathological morphology of the web lesion, pouch defect and band lesion, we used two types of angioscopic catheter: blood flow-maintaining type and blood flow-blocking type. Angioscopy revealed a heterogeneous thrombus that contained white organized thrombus, red fragile thrombus and yellowish thrombus. After three sessions of balloon pulmonary angioplasty, his pulmonary arterial pressure decreased and his symptom of dyspnea on exertion and desaturation were improved. Angioscopy displayed various forms of organized thrombus, and also allowed the detailed observation of lesions that were difficult to be observed by angiography.
    Journal of cardiovascular medicine (Hagerstown, Md.). 07/2014;
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    ABSTRACT: Data regarding clinical efficacy of thrombectomy in patients with acute myocardial infarction (AMI) have been still limited in Japan. Using the AMI-Kyoto Multi-Center Risk Study database, the clinical background characteristics, angiographic findings, primary percutaneous coronary intervention (PCI) results and in-hospital prognoses were retrospectively compared between AMI patients with totally occluded infarct-related artery (IRA) (TIMI flow grade 0) undergoing thrombus aspiration during primary PCI (with-aspiration patients, n = 568) and those without thrombus aspiration (without-aspiration patients, n = 266). The with-aspiration patients were more likely to have higher TIMI grade in the IRA immediately after primary PCI, and had a lower in-hospital mortality rate than the without-aspiration patients. According to a multivariate analysis, thrombectomy as well as stent usage was found to be independent predictor of final TIMI flow grade ≥2 in the IRA, and the final TIMI flow grade ≥2 in the IRA was found to be an independent factor for in-hospital survival. These results suggest that among real-world, unselected Japanese AMI patients with totally occluded IRA on initial coronary angiography, thrombus aspiration is an effective adjunctive therapy during primary PCI to improve final epicardial coronary flow in the IRA, which might lead to better in-hospital prognosis.
    Cardiovascular Intervention and Therapeutics 07/2014;
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    ABSTRACT: Cardiorenal anemia syndrome has recently been receiving greater attention; however, data regarding the relationship between chronic kidney disease (CKD)/anemia on presentation and in-hospital outcome in patients with acute myocardial infarction (AMI) undergoing primary percutaneous coronary intervention (PCI) are still limited in Japan.A total of 1,447 primary PCI-treated AMI patients were classified into 4 groups according to the presence of CKD and/or anemia on hospital admission (with CKD/with anemia n = 222, with CKD/without anemia n = 299, without CKD/with anemia n = 151, without CKD/without anemia n = 775). Angiographic acute results of primary PCI were similar among the 4 groups. The patients with CKD had a significantly higher in-hospital overall mortality rate than the patients without CKD, and in the presence or absence of CKD, patients with anemia tended to have a higher in-hospital mortality rate than the patients without anemia. According to a multivariate analysis, anemia on admission was found to be an independent predictor of in-hospital mortality, whereas admission CKD and admission eGFR were statistically not independent predictors. Moreover, the multivariable adjusted odds ratio of in-hospital death in AMI patients with CKD alone was 1.855 (95% CI 0.929-3.706), and that in AMI patients with CKD/with anemia was 3.384 (95% CI 1.697-6.748).These results suggest that among real-world, unselected Japanese AMI patients undergoing primary PCI, the combination of CKD and anemia on admission confers significant adverse effects on in-hospital mortality.
    International heart journal. 06/2014;
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    ABSTRACT: Objective The predictors of in-hospital outcomes after primary percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) complicated with heart failure or cardiogenic shock at presentation remain unclear. Methods Using the AMI-Kyoto Multi-Center Risk Study database, the clinical background characteristics, angiographic findings, primary PCI results, and in-hospital prognoses were retrospectively compared between primary PCI-treated AMI patients with a Killip class status of ≥2 (Killip 2-4 patients, n=390) and those with a Killip class 1 status (Killip 1 patients, n=1,057). Results The Killip 2-4 patients were more likely to have a higher age and proportion of women and exhibited a higher prevalence of previous myocardial infarction, diabetes mellitus and chronic kidney disease or anemia on admission, lower systolic blood pressure (SBP) values on admission, a higher rate of multivessels or left main trunk as the culprit artery, a larger number of diseased vessels, a 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 Killip 1 patients. According to a multivariate analysis, age was found to be an independent positive predictor of in-hospital mortality, while admission SBP was an independent positive predictor of in-hospital survival in both groups. In contrast, anemia on admission was found to be an independent predictor of in-hospital death, while the TIMI 3 flow in the IRA after PCI was found to be an independent factor for survival in the Killip 2-4 patients, but not the Killip 1 patients. Conclusion Anemia on admission and the final TIMI 3 flow in the IRA are critical determinants of in-hospital death in AMI patients with a Killip class status of ≥2 undergoing primary PCI.
    Internal Medicine 01/2014; 53(9):933-939. · 0.97 Impact Factor
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    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. · 9.81 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
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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
  • Journal of Cardiology Cases 01/2010; 1(1).
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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. · 2.51 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. · 4.01 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

Publication Stats

399 Citations
167.69 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