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Biomedical subjects

Atsushi Namiki

Publications and source records attributed to Atsushi Namiki.

9 recordsLinked to original sources
PubMed2006

Effect of pravastatin and atorvastatin on glucose metabolism in nondiabetic patients with hypercholesterolemia.

OBJECTIVE: The aim of this study was to assess the effects of hydrophilic pravastatin and lipophilic atorvastatin on glucose metabolism and lipid metabolism in non-diabetic patients with hypercholesterolemia. METHODS: Fasting plasma glucose (FPG), hemoglobin A(1c) (HbA(1c)), total cholesterol (TC), low-density lipoprotein cholesterol (LDLC), high-density lipoprotein cholesterol (HDLC), and triglyceride (TG) levels were determined before and after statin treatment. PATIENTS: A total of 44 nondiabetic patients (FPG < or =125 mg/mL; HbA(1c) <5.8%) undergoing treatment with either pravastatin (n=21) or atorvastatin (n=23) for hypercholesterolemia were investigated. RESULTS: FPG level in the pravastatin but not atorvastatin group was significantly lowered after vs before treatment. Accordingly, the HbA(1c) level in the atorvastatin but not in the pravastatin group was significantly increased. As expected, both TC and LDL-C levels were significantly lowered in both groups. In particular, the TC level in the atorvastatin group was more remarkably and significantly improved than in the pravastatin group. On the other hand, the HDL-C level in the pravastatin group but not in the atorvastatin group was significantly increased after the administration period. The TG level was unaffected in both groups. CONCLUSION: Pravastatin was suggested to act favorably, while atorvastatin adversely, regarding it's effects on glucose metabolism in nondiabetic hypercholesterolemic patients, although atorvastatin exerted more potent cholesterol-lowering effects compared with pravastatin.

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PubMed2005

Intramyocardial injection of fibroblast growth factor-2 plus heparin suppresses cardiac failure progression in rats with hypertensive heart disease.

A reduction of coronary flow reserve has been reported in patients with hypertensive heart disease (HHD), which suggests that myocardial ischemia may contribute to the progression to cardiac failure in HHD. Therefore, we evaluated whether fibroblast growth factor (FGF)-2 and/or heparin, which induce angiogenesis, may affect cardiac function in the setting of HHD. We used Dahl salt sensitive (DS) rats as an HHD model. Direct intramyocardial injection of 100 microg of FGF-2 plus 1.28 microg of heparin (n = 6), 100 microg of FGF-2 (n = 6), 1.28 microg of heparin (n = 6) or saline (n = 6) were performed in 9-week-old rats. Echocardiography was performed to evaluate cardiac function at 9, 11, and 13 weeks of age. Plasma atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) concentrations were measured at 8 and 13 weeks of age. DS rats were killed 4 weeks after myocardial injection (at 13 weeks of age), and myocardial capillary density was assessed by von Willebrand factor staining. Injection of FGF-2 plus heparin significantly decreased left ventricular end-diastolic diameter (P < 0.0001) and left ventricular end-systolic diameter (P < 0.0001), significantly improved the reduction of left ventricular fractional shortening (P = 0.0005), significantly decreased plasma ANP (P < 0.0001) and BNP (P = 0.016) concentrations, and significantly increased myocardial capillary density (P = 0.0002) compared with injection of saline. These findings indicate that intramyocardial injection of FGF-2 plus heparin suppresses the progression of cardiac failure in DS rats. FGF-2 plus heparin administration may be a new therapeutic strategy for the treatment of HHD.

Animals↗
PubMed2004

Hemostatic and fibrinolytic activation is less following cutting balloon angioplasty of the coronary arteries.

Recent studies have shown that percutaneous coronary intervention (PCI) activates systemic hemostatic activity, reflecting platelet activation and thrombin formation in the coronary arteries. The present study compared systemic levels of hemostatic markers induced by plain old balloon angioplasty (POBA), coronary stenting (STENT), and cutting balloon (CB) angioplasty. Sixty-one patients with stable angina pectoris, who underwent elective PCI or diagnostic coronary angiography (CAG) alone, were investigated. Patients who underwent PCI were divided into the POBA group (n = 11), the STENT group (n = 27), and the CB group (n = 11). Patients who underwent CAG alone were assigned to the CAG group (n = 12). Blood samples were collected before, 24 hours after, and 3 days after PCI or CAG. Plasma concentrations of prothrombin fragment 1+2 (F1+2), fibrinopeptide A (FPA), thrombin-antithrombin III complex (TAT), and plasminogen activator inhibitor-1 (PAI-1) were measured. In the CB group, the F1+2 (1.23 +/- 0.4 nmol/L) level 3 days after PCI was significantly smaller than that of the POBA group (2.37 +/- 0.5 nmol/L) (P < 0.05). The FPA (1.81 +/- 0.9 ng/mL), TAT (3.36 +/- 1.2 ng/mL) and PAI-1 (23.0 +/- 4.1 ng/mL) levels in the CB group 3 days after PCI were significantly smaller than those of the POBA group (P < 0.05, respectively) and STENT group (P < 0.05, respectively), but similar to the CAG group. Systemic hemostasis is activated to a greater extent after POBA and stenting than it is after CB angioplasty of the coronary arteries. This may contribute to the favorable long-term outcome of CB angioplasty.

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PubMed2004

Concentrations of hepatocyte growth factor, basic fibroblast growth factor, and vascular endothelial growth factor in pericardial fluid and plasma.

Some angiogenic factors, including hepatocyte growth factor (HGF), basic fibroblast growth factor (bFGF), and vascular endothelial growth factor (VEGF), have been reported to promote angiogenesis and improve myocardial perfusion in experimental models of ischemic heart disease. These factors are produced in various tissues, including myocardium. We measured the concentrations of HGF, bFGF, and VEGF by enzyme-linked immunosorbent assay in plasma and in pericardial fluid sampled during open heart surgery (12 patients with ischemic heart disease and 17 with nonischemic heart disease). HGF levels were significantly higher in plasma than in pericardial fluid (12.0 +/- 1.8 versus 0.26 +/- 0.04 ng/mL, P < 0.0001). On the other hand, bFGF levels were significantly higher in pericardial fluid than in plasma (243.5 +/- 50.9 versus 49.6 +/- 7.8 pg/mL, P = 0.009). VEGF levels were not significantly different between pericardial fluid and plasma (47.2 +/- 17.6 versus 24.5 +/- 3.6 pg/mL, P = 0.23). Concentrations of angiogenic factors in pericardial fluid and in plasma were not significantly different between patients with ischemic and nonischemic heart disease. These results suggest that the production, secretion, and kinetics of HGF, bFGF, and VEGF are different. These angiogenic factors may have different pathophysiologic roles.

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PubMed2003

Lack of insulin receptor substrate-2 causes progressive neointima formation in response to vessel injury.

BACKGROUND: Insulin resistance is associated with atherosclerosis, but its mechanism is unknown. It has been reported that insulin receptor substrate (IRS)-1 deficient (IRS-1-/-) mice showed insulin resistance without type 2 diabetes, whereas the IRS-2 deficient (IRS-2-/-) mice showed insulin resistance with type 2 diabetes. METHODS AND RESULTS: We investigated neointima formation in the IRS-1-/- and IRS-2-/- mice at 8 and 20 weeks. The IRS-2-/- mice showed much greater neointima formation than the IRS-1-/- and wild-type mice at 8 weeks. At 20 weeks, the IRS-2-/- mice had greater neointima formation than the IRS-1-/- mice, which showed more enhanced neointima formation than the wild-type mice. The IRS-1-/- and IRS-2-/- mice had dyslipidemia, hypertension, and insulin resistance. The IRS-2-/- mice had more metabolic abnormalities than the IRS-1-/- mice at 8 and 20 weeks. IRS-2 expression was detected, but IRS-1 expression was not detected in the vessels. CONCLUSIONS: The neointima formation in the IRS-1-/- and IRS-2-/- mice appears to be related to abnormalities induced by the altered metabolic milieu in insulin-resistant states. Moreover, because neointima formation was much greater in the IRS-2-/- mice than in the IRS-1-/- mice at 8 and 20 weeks, it is suggested that a lack of IRS-2 renders the vasculature more susceptible to injury in the abnormal metabolic milieu, and IRS-2 may have a protective effect on neointima formation. We conclude that IRS-2 is protective and retards the development of neointima formation in insulin-resistant states.

Animals↗
PubMed2003

Endothelin-1 concentrations in pericardial fluid are more elevated in patients with ischemic heart disease than in patients with nonischemic heart disease.

There is epidemiologic evidence that the prognosis of patients with nonischemic heart failure is better than that for patients with ischemic heart failure. In addition, studies have revealed that patients with ischemic heart failure show a poorer response to medical therapy. However, the pathophysiologic difference between ischemic and nonischemic heart disease is unclear. To clarify this point, we measured atrial natriuretic peptide, brain natriuretic peptide, angiotensin II, endothelin (ET)-1. interleukin-1beta interleukin-6. tumor necrosis factor (TNF)-alpha soluble TNF receptor I, and soluble TNF receptor II concentrations in plasma and pericardial fluid in patients with ischemic or nonischemic heart disease undergoing cardiac surgery. The pericardial ET-1 concentration in patients with ischemic heart disease was statistically greater than that in patients with nonischemic heart disease (about 1.5-fold), although no difference was found in the plasma ET-1 concentration. These findings suggest that the production and secretion of ET-1 from the myocardium in patients with ischemic heart disease are augmented to a greater extent than in patients with nonischemic heart disease. This result may lead to a greater understanding of the pathophysiology of ischemic heart disease.

Angiotensin II↗
PubMed2002

Left atrial thrombus causing pulmonary embolism by passing through an atrial septal defect.

A 66-year-old woman admitted with dyspnea on exertion had atrial fibrillation and left ventricular dysfunction. Echocardiography revealed an atrial septal defect (ASD) and a soft, easily deformable thrombus in the dilated left atrium. The atrial mass suddenly disappeared on the 10th day after admission, and contrast-enhanced chest computed tomography and pulmonary blood flow scintigraphy showed that the thrombus had detached from the left atrium, floated into the right atrium through the ASD and caused pulmonary embolism. This is the first documented case of a left atrial thrombus causing pulmonary embolism by passing through an ASD. When an ASD is present, it is important to consider not only paradoxical thromboembolism (from the right to the left atrium), but also pulmonary embolism caused by thromboembolism from the left to the right atrium.

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PubMed2002

[Hypertrophic cardiomyopathy with mid-ventricular obstruction complicated with apical left ventricular aneurysm and ventricular tachycardia: a case report].

A 69-year-old man was admitted with palpitations and syncope. His medical history included hypertension and left ventricular hypertrophy. Arterial pulsation was not palpable on admission. Electrocardiography revealed ventricular tachycardia, and cardioversion restored normal sinus rhythm. An electrophysiological study reproducibly induced polymorphic ventricular tachycardia, so a cardioverter defibrillator was implanted. Echocardiography revealed mid-ventricular obstruction and an apical aneurysm, and Doppler color flow imaging showed a diastolic paradoxic jet from the apex toward the base. Coronary angiography showed no stenosis of the extramural coronary arteries. Ventricular tachycardia on admission showed a right bundle branch block pattern and a superior axis deviation, so the arrhythmia was thought to originate from the apical aneurysm. Apical aneurysm can result from elevated intraventricular pressure or relative myocardial ischemia. This is a rare case of hypertrophic cardiomyopathy with mid-ventricular obstruction complicated with apical aneurysm and polymorphic ventricular tachycardia.

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