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Biomedical subjects

Takanori Yasu

Publications and source records attributed to Takanori Yasu.

At least 19 recordsLinked to original sources
PubMed2006

Association of hyperadiponectinemia with severity of ventricular dysfunction in congestive heart failure.

BACKGROUND: Adiponectin, which is a collagen-like plasma protein produced by adipose tissue, has anti-atherogenic and anti-inflammatory effects. Plasma adiponectin levels in patients with congestive heart failure (CHF) were determined, as well as relationships between the plasma levels of adiponectin and other hormones. METHODS AND RESULTS: The study group comprised 90 patients with CHF and 20 control subjects, who were divided into 4 subgroups according to New York Heart Association (NYHA) functional class. Plasma levels of adiponectin, tumor necrosis factor (TNF)-alpha and brain natriuretic peptide (BNP) and cardiac hemodynamics were determined. Plasma adiponectin levels were significantly increased according to the severity of NYHA class in the patients with CHF; control: 6.2+/-1.0; NYHA I: 8.5+/-1.9, NYHA II: 12.0+/-2.2, NYHA III: 13.0+/-2.7, NYHA IV: 14.9+/-2.7 microg/ml (p=0.0008). Similarly, plasma BNP levels were significantly increased in accordance with the NYHA class. Plasma adiponectin levels correlated positively with BNP (r=0.40, p=0.0002) and TNF-alpha (r=0.49, p=0.0001), and correlated negatively with cardiac index (r=-0.27, p=0.05). In 24 of 46 patients in the NYHA III and IV subgroups, according to the prompt improvement in cardiac function, levels of both plasma adiponectin and BNP were significantly reduced (p<0.0001). CONCLUSION: Plasma adiponectin levels increased according to the severity of CHF and, moreover, they correlated with the plasma levels of BNP and TNF-alpha. These results indicate that augmented release of adiponectin is involved in the pathogenesis of CHF and further study is needed to elucidate its exact role.

Adiponectin↗
PubMed2006

Close association of regional interleukin-6 levels in the infarct-related culprit coronary artery with restenosis in acute myocardial infarction.

BACKGROUND: The involvement of interleukin (IL)-6 in restenosis of the recanalized coronary artery after the percutaneous coronary intervention (PCI) was examined. METHODS AND RESULTS: There were 40 patients enrolled in the study who had acute myocardial infarction and whose infarct-related coronary arteries were treated by new thrombectomy devices and stenting. Blood samples were collected from the culprit coronary artery before and immediately after the maneuver of the PCI. Restenosis was defined as residual stenosis because it accounted for more than 50% at the follow-up coronary angiography. Plasma IL-6 levels in the infarct-related coronary artery were 12.8 and 13.2 pg/ml before and after the initial maneuver of the PCI, respectively, values that were significantly greater than that of 7.2 pg/ml in the peripheral vein (p<0.0001). The levels of IL-6 in the pre- and the post-stage of PCI were significantly greater in the patients with restenosis than those without restenosis. The plasma IL-6 levels in the post-stage of PCI had significant correlations with late loss and loss index. CONCLUSIONS: The present study findings indicate that plasma IL-6 levels in the culprit coronary artery at the post-stage of PCI are closely associated with the future restenosis of the revasculized coronary artery in acute myocardial infarction.

Acute Disease↗
PubMed2006

Acute mitral regurgitation due to ruptured chordae tendineae in a patient with hypertrophic obstructive cardiomyopathy: a case report.

A 63-year-old woman had been followed up for hypertrophic obstructive cardiomyopathy with 85 mmHg of left ventricular outflow tract pressure gradient over 7 years. She was hospitalized because of acute dyspnea and syncope. On admission, echocardiography revealed severe mitral regurgitation with ruptured chordae tendineae at the medial scallop of the posterior mitral leaflet. Mitral valve replacement was successfully performed and her symptoms improved to 28 mmHg of left ventricular outflow tract pressure gradient. In patients with hypertrophic obstructive cardiomyopathy, elevated left ventricular systolic pressure and systolic anterior motion of the mitral leaflets may lead to mucoid degeneration in the chordae tendineae. Rupture of the mitral chordae tendineae should be considered in the differential diagnosis of acutely deteriorated mitral regurgitation in patients with hypertrophic obstructive cardiomyopathy, because this is a rare but critical complication.

Acute Disease↗
PubMed2006

Successfully treated massive pulmonary thromboembolism and thrombus in the right atrium due to diffuse malignant lymphoma: a case report.

A 40-year-old man presented with massive pulmonary embolism related to diffuse large B cell lymphoma. His hemodynamic state worsened rapidly to shock after sudden onset of dyspnea. Echocardiography and thoracic computed tomography indicated pulmonary thromboembolism due to deep venous thromboembolism, associated with a mass in the anterior mediastinum and a 5 x 8 cm mass in the left pelvis compressing the left femoral vein. He underwent emergent surgery to remove a huge thrombus from the right atrium through the bilateral pulmonary arteries. Soon after this surgery, his hemodynamic state recovered and excision of the left cervical lymph node revealed diffuse large B cell lymphoma. Venous compression by the lymphoma mass had caused hemostasis and thrombus formation in the present case.

Adult↗
PubMed2005

Relation of atherothrombosis burden and volume detected by intravascular ultrasound to angiographic no-reflow phenomenon during stent implantation in patients with acute myocardial infarction.

This study investigated the mechanism of occurrence of the no-reflow phenomenon during stent implantation in patients with acute myocardial infarction (AMI) using intravascular ultrasound (IVUS) with volumetric analysis. Of 70 patients with AMI who underwent IVUS-guided stent implantation within 24 hours of symptom onset, 12 developed decreased Thrombolysis In Myocardial Infarction flow grade during stent implantation and without subsequent restoration to Thrombolysis In Myocardial Infarction flow grade before stenting. External elastic membrane cross-sectional area and maximum diameter at the culprit lesion as measured by IVUS before stent implantation were significantly larger in the no-reflow group (n = 12) than in the normal reflow group (n = 58; 20.1 +/- 6.5 vs 16.4 +/- 4.3 mm2, p = 0.015 for cross-sectional area and 5.2 +/- 0.9 vs 4.8 +/- 0.6 mm, p = 0.049 for maximum diameter). Plaque volume, volumetric plaque burden (plaque volume/external elastic membrane volume), and change in plaque volume during stent implantation (plaque volume after vs before) were significantly greater in the no-reflow group than in the normal reflow group (239 +/- 142 vs 178 +/- 72 mm3, p = 0.030; 0.76 +/- 0.07 vs 0.71 +/- 0.06, p = 0.010; and -46 +/- 63 vs -11 +/- 37 mm3, p = 0.013, respectively). In conclusion, high atherothrombotic burden and decreased plaque volume as detected by IVUS may be risk factors for development of the no-reflow phenomenon during stent implantation in patients with AMI.

Aged↗
PubMed2005

Up-regulated synthesis of mature-type adrenomedullin in coronary circulation immediately after reperfusion in patients with anterior acute myocardial infarction.

OBJECTIVE: Levels of adrenomedullin (AM), a potent vasodilatory peptide, have been shown to increase in the early stage of acute myocardial infarction (AMI). The purpose of this study was to determine whether coronary sinus-aortic step-up of mature forms of AM is accelerated in patients with AMI after reperfusion. METHODS: The subjects were 29 consecutive patients with a first episode of anterior AMI and 10 normal controls. All patients with AMI underwent balloon reperfusion therapy within 24 h after symptom onset. Plasma levels of two molecular forms of AM (an active, mature form [AM-m] and an intermediate, inactive glycine-extended form [AM-Gly]) in the aorta and coronary sinus (CS) were measured by specific immunoradiometric assay after reperfusion. RESULTS: Plasma levels of AM-m and AM-Gly in the aorta and CS were higher in AMI patients than in controls. CS-aortic step-up of AM-m, which is an index of myocardial production of AM-m, was significantly greater in AMI patients than in controls (1.7 +/- 1.4 vs. 0.4 +/- 0.3 pmol/L, P < 0.01). However, there was no significant difference in CS-aortic step-up of AM-Gly (P = 0.30). AMI patients with left ventricular dysfunction (n = 10) had a significantly higher CS-aortic AM-m step-up than AMI patients without left ventricular dysfunction (n = 19). AM-m in the aorta and CS negatively correlated with the left ventricular ejection fraction (r = -0.50, r = -0.48, P < 0.01). CONCLUSIONS: Myocardial synthesis of AM-m is accelerated in patients with reperfused AMI, especially in patients with critical left ventricular dysfunction. Increased myocardial synthesis of active AM may protect against cardiac dysfunction, myocardial remodeling, or both after the onset of AMI.

Adrenomedullin↗
PubMed2005

Transient mid-ventricular ballooning cardiomyopathy: a new entity of Takotsubo cardiomyopathy.

We present a case of a 64-year-old man with transient mid-ventricular ballooning cardiomyopathy. Left ventriculography showed morphological differences with ballooning around the whole mid-portion of the left ventricle, although precipitating factors and clinical courses were similar to Takotsubo cardiomyopathy. We suspect that transient mid-ventricular ballooning cardiomyopathy is a new pathological entity in Takotsubo cardiomyopathy.

Cardiomyopathies↗
PubMed2005

Glimepiride induces nitric oxide production in human coronary artery endothelial cells via a PI3-kinase-Akt dependent pathway.

Diabetes mellitus is one of the major risk factors for coronary artery disease (CAD). A recent study reported that glimepiride, a new third-generation sulfonylurea, inhibited the formation of atheromatous plaques in high-cholesterol fed rabbits. However, the mechanism by which glimepiride induces atheroprotection remains unknown. In the present study, we tested the hypothesis that glimepiride may stimulate NO production in vascular endothelial cells. Human coronary artery endothelial cells (HCAECs) were treated with glimepiride, glibenclamide or vehicle, and NO release was measured. Akt phosphorylation was evaluated by Western blot. The effects of LY294002, a specific PI3-kinase inhibitor, and antisense oligonucleotides directed to Akt, on glimepiride-induced NO production were examined. Glimepiride (0.1-10 microM), but not glibenclamide, induced NO production, significantly increasing it by 1.8-fold (n=6, p<0.05). LY294002 inhibited glimepiride-induced NO production by 68%. Akt was rapidly phosphorylated by glimepiride and antisense oligonucleotides directed to Akt completely inhibited glimepiride-induced NO production. These data demonstrate that glimepiride induces NO production in HCAECs by activating PI3-kinase and Akt, and also suggest that use of glimepiride in type 2 diabetes may show promise for preventing CAD in addition to lowering glucose levels.

Cells, Cultured↗
PubMed2005

Activated leukocytes and endothelial cells enhance retention of ultrasound contrast microspheres containing perfluoropropane in inflamed venules.

PURPOSE: To characterize the flow dynamics of albumin ultrasound contrast microspheres containing perfluoropropane (PFP) in normal and inflamed microvasculature. MATERIALS AND METHODS: Mesenteric microvessels of rats were examined after an intravenous injection of fluorocein-labeled erythrocytes or PFP microspheres by fluorescence intravital microscopy with and without local application of 10(-8) M platelet activating factor (PAF) as an experimental form of inflammation. RESULTS: All the microspheres passed freely through arterioles and capillaries. Mean velocities of the microspheres in each vessel were closely correlated with those of erythrocytes. Only a minor fraction of the microspheres was retained in the venules (> or =0.1 s stoppage) by attachment to endothelial cells. The frequency of microsphere retention in venules was significantly enhanced by PAF (2.6+/-2.1%, P<0.01 vs. control), especially in regions with leukocyte adhesion. Treatment with a monoclonal antibody to intercellular adhesion molecule-1, P-selectin or the common leukocyte antigen inhibited PAF-induced microsphere retention in venules (P<0.05). In the inflamed microcirculation, a small subgroup of microspheres becomes attached to venular endothelial cells in regions with leukocyte adhesion via interaction among microspheres, activated leukocytes and endothelial cells via adhesion molecules. CONCLUSION: In inflamed microcirculation, a small subgroup of microspheres becomes attached to venular endothelial cells in regions with leukocyte adhesion via interaction among microspheres, activated leukocytes and endothelial cells via adhesion molecules. These results suggest that ultrasonography with microspheres has the potential to evaluate inflammatory site distribution as well as tissue perfusion.

Animals↗
PubMed2005

Close association of hypoadiponectinemia with arteriosclerosis obliterans and ischemic heart disease.

Adiponectin is an adipose-derived cytokine, and it is suggested that hypoadiponectinemia increases the prevalence of ischemic heart disease (IHD). The present study was undertaken to determine serum adiponectin levels in patients with arteriosclerosis obliterans (ASO) and IHD. Forty-nine patients with ASO and 49 age-, sex-, and body mass index-matched control subjects were examined. The diagnosis of ASO was derived from an ankle brachial index of less than 0.90 and stenotic or obstructive change in angiogram. Ischemic heart disease was diagnosed by ischemic or stenotic change in ECG, treadmill, or coronary angiogram. Serum adiponectin level was 8.6 +/- 0.9 microg/mL in the patients with ASO, a value significantly less than that of 12.4 +/- 1.0 microg/mL in the control subjects ( P < .01). Next, we subgrouped the subjects into 4 groups according to the presence of ASO and IHD. Serum adiponectin levels were 9.4 +/- 1.5 and 10.2 +/- 1.6 microg/mL in the subjects with ASO (n =23) and those with IHD (n = 13), respectively. It was further reduced to 7.9 +/- 1.2 microg/mL in the subjects having both ASO and IHD (n = 26), a value significantly less than that of 13.2 +/- 1.4 microg/mL in the control subjects (n = 36; P < .05). Serum high-density lipoprotein cholesterol was significantly less in the subjects with ASO than in the control subjects (42.1 +/- 1.7 vs 48.5 +/- 2.0 mg/dL; P < .05), but there were no differences in blood pressure, total cholesterol, low-density lipoprotein cholesterol, triglyceride, and uric acid levels. The present results indicate that a reduction in serum adiponectin level is associated with the prevalence and magnitude of systemic atherosclerosis including IHD and ASO.

Adiponectin↗
PubMed2005

Evaluation of transmural myocardial perfusion by ultra-harmonic myocardial contrast echocardiography in reperfused acute myocardial infarction.

BACKGROUND: The transmural distribution of myocardial perfusion is important for predicting the contractile reverse of an infarcted wall in reperfused acute myocardial infarction (AMI). Evaluating transmural myocardial perfusion by myocardial contrast echocardiography (MCE) could predict the long-term recovery of left ventricular (LV) function. METHODS AND RESULTS: The study group comprised 20 consecutive patients with a first-episode anterior AMI with total occlusion of the proximal left anterior descending artery, who underwent successful percutaneous coronary intervention within 24 h of onset. MCE was performed on the 15th day after the onset, using ultraharmonic gray-scale imaging with intermittent end-systolic triggering every 4 beats or every 6 beats. Regions of interest were placed over both the endocardial and epicardial region at the mid-septal level. Regional wall motion (RWM) of the infarcted anterior wall and global LV function were assessed by 2-dimensional echocardiography and left ventriculography in both the acute and chronic phase. The transmural distribution of myocardial perfusion by MCE demonstrated a significant relation with RWM score index (r = 0.75, p = 0.0004). Recovery of RWM and LV ejection fraction (LVEF) at 6 months after reperfusion was significantly greater in the group with good perfusion of the epicardium according to MCE than in the poor perfusion group [RWM (SD/cord); -1.23+/-0.91 vs -3.51+/-0.84, p = 0.001, LVEF (%); 63.8+/-10.4 vs 47.0+/-3.4, p = 0.04]. CONCLUSIONS: Assessing the transmural distribution of myocardial perfusion by MCE can predict the long-term recovery of LV function after a reperfused AMI.

Acute Disease↗
PubMed2005

Exercise after heparin administration: new therapeutic program for patients with-option arteriosclerosis oblitrans.

BACKGROUND: A prospective study examined whether a combination of an exercise program and heparin administration improves the clinical symptoms of patients with arteriosclerosis obliterans (ASO) without an indication for surgical revascularization because of the lack of distal target vessels or other reasons such as high surgical risk or lack of a vein conduit from previous coronary artery bypass surgery. METHODS AND RESULTS: A total of 19 consecutive patients with symptomatic non-option ASO diagnosed by angiography were randomly assigned to 3 groups: heparin + exercise (walking for 60 min after heparin injection [3,000 units/day IV for 14 days], n = 6), heparin administration only (n = 6), and exercise only (n = 7). Plasma levels of hepatocyte growth factor (HGF) were serially measured before and after intravenous administration of heparin. Ankle brachial pressure index was measured and treadmill exercise test (2.5 km/h, 12% slope) was performed before the 2-week treatment, just after finishing treatment, and 12 weeks after beginning the treatment. Ophthalmic examinations, including visual acuity test, ocular fundoscopy and fluorescein angiographic fundus photography, were performed before and 12 weeks after the treatment program. In all patients, HGF levels increased more than 4-fold of the basal level at 30 min after heparin injection. Maximum walking time was significantly higher in the heparin + exercise group than in the other 2 groups (p < 0.05). There were no patients who showed pathological retinal angiogenesis. CONCLUSION: The combination of an exercise program and heparin administration improves the clinical symptoms of patients with non-option ASO.

Aged↗
PubMed2005

Repair of infarcted myocardium mediated by transplanted bone marrow-derived CD34+ stem cells in a nonhuman primate model.

Rodent and human clinical studies have shown that transplantation of bone marrow stem cells to the ischemic myocardium results in improved cardiac function. In this study, cynomolgus monkey acute myocardial infarction was generated by ligating the left anterior descending artery, and autologous CD34(+) cells were transplanted to the peri-ischemic zone. To track the in vivo fate of transplanted cells, CD34(+) cells were genetically marked with green fluorescent protein (GFP) using a lentivirus vector before transplantation (marking efficiency, 41% on average). The group receiving cells (n = 4) demonstrated improved regional blood flow and cardiac function compared with the saline-treated group (n =4) at 2 weeks after transplant. However, very few transplanted cell-derived, GFP-positive cells were found incorporated into the vascular structure, and GFP-positive cardiomyocytes were not detected in the repaired tissue. On the other hand, cultured CD34(+) cells were found to secrete vascular endothelial growth factor (VEGF), and the in vivo regional VEGF levels showed a significant increase after the transplantation. These results suggest that the improvement is not the result of generation of transplanted cell-derived endothelial cells or cardiomyocytes; and raise the possibility that angiogenic cytokines secreted from transplanted cells potentiate angiogenic activity of endogenous cells.

Animals↗
PubMed2005

Three episodes of inferior acute myocardial infarction due to thrombotic occlusion of the right coronary artery: a case report.

A 77-year-old female with two previous inferior myocardial infarctions was transferred to our medical center with a third inferior acute myocardial infarction. Coronary angiography revealed 99% stenosis with rich thrombus in the distal right coronary artery [Thrombolysis in Myocardial Infarction (TIMI) grade 2 flow]. The angiographic appearance of the right coronary artery was similar to the two previous myocardial infarctions. Coronary aspiration was performed and TIMI grade 3 flow was established. To confirm the presence of thrombus, intravascular ultrasound (IVUS) and coronary angioscopy were performed at pre-discharge. IVUS showed a thrombus-like low-density area at the mid right coronary artery. Red thrombi were observed in the same area using coronary angioscopy. Although warfarin had been prescribed for secondary prevention since the first acute myocardial infarction, both the second and third acute myocardial infarction occurred after cessation of warfarin. Patients with acute myocardial infarction due to thrombotic occlusion, confirmed by IVUS or angioscopy, might be good candidates for permanent warfarin therapy.

Aged↗
PubMed2005

Recurrent cardiogenic shock caused by dynamic mitral regurgitation in a patient with hypertrophic obstructive cardiomyopathy: a case report.

A 68-year-old man with hypertrophic obstructive cardiomyopathy developed recurrent cardiogenic shock due to dynamic mitral regurgitation. The pressure gradient in the left ventricular outflow tract under medication was 30 mmHg, and he complained of no symptom. He developed shock with dyspnea suddenly after bathing and defecation. Echocardiography and left ventriculography revealed massive mitral regurgitation and mild increment of pressure gradient in the left ventricular outflow tract (50 mmHg). He underwent successful mitral valve replacement following treatment with beta-blocker under intraaortic balloon pumping support. This case illustrates that exacerbation of the systolic anterior motion of the mitral anterior leaflet can cause dynamic severe mitral regurgitation with 'mild' increment of pressure gradient in the left ventricular outflow tract, resulting in cardiogenic shock with severe lung edema.

Adrenergic beta-Antagonists↗
PubMed2005

Successfully treated triple valve infective endocarditis: a case report.

A 45-year-old woman presented with triple valve infective endocarditis and ventricular septal defect. There were vegetations on the tricuspid valve, pulmonary valve, and aortic valve. She had multiple complications such as nephrotic syndrome, severe anemia, congestive heart failure, and convulsion. Her general condition was extremely poor. Intensive medical therapy, such as blood transfusion, mechanical ventilation, and continuous venovenous hemofiltration, allowed her to tolerate surgery. Triple valve replacement and ventricular septal defect closure was successfully performed without major complication. She was ambulatory at the time of discharge.

Anemia↗
PubMed2004

Contribution of fluid shear response in leukocytes to hemodynamic resistance in the spontaneously hypertensive rat.

The mechanisms for elevation of peripheral vascular resistance in spontaneously hypertensive rats (SHR), a glucocorticoid-dependent form of hypertension, are unresolved. An increase in hemodynamic resistance caused by circulating blood may be a factor. Physiological fluid shear stress induces a variety of responses in circulating leukocytes, including pseudopod retraction. Due to high rigidity, leukocytes with pseudopods have greater difficulty to pass through capillaries. Because SHR have more circulating leukocytes with pseudopods, we hypothesize that inhibition of the leukocyte shear response by glucocorticoids in SHR impairs normal leukocyte passage through capillaries and causes enhanced resistance in capillary channels. Fluid shear leads to retraction of pseudopods in normal leukocytes, whereas shear induces pseudopod projection in SHR and dexamethasone-treated Wistar rats. The high incidence of circulating leukocytes with pseudopods results in slower cell passage through capillaries under normal blood flow and during reduced flow enhanced capillary plugging both in vivo and in vitro. SHR blood requires higher pressure (90.0+/-8.2 mm Hg) than Wistar Kyoto rat (WKY, 69.6+/-6.5 mm Hg; P<0.0001) or adrenalectomized SHR (73.5+/-2.1 mm Hg; P=0.0009) at the same flow rate in the resting hemodynamically isolated skeletal muscle microcirculation. Intravenous injection of blood from SHR, but not WKY, causes blood pressure increase in normal rats, which depends on pseudopod formation. We conclude that in addition to enhanced vascular tone, pseudopod formation with lack of normal fluid shear response may serve as mechanisms for an elevated hemodynamic resistance in SHR.

Animals↗