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Muneyasu Saito

Publications and source records attributed to Muneyasu Saito.

At least 19 recordsLinked to original sources
PubMed2004

Exercise at ventilatory threshold aggravates left ventricular remodeling in patients with extensive anterior acute myocardial infarction.

BACKGROUND: The effects of physical training on ventricular remodeling after extensive anterior acute myocardial infarction (AMI) have not yet been defined. This randomized controlled study examines whether exercise aggravates left ventricular (LV) remodeling in patients with extensive anterior AMI. METHODS: Forty-eight consecutive patients with a first extensive anterior AMI and an LV ejection fraction (EF) of <45% assessed with left ventriculography (LVG) within 3 days of onset were randomly allocated to a training group (n = 24) or a control group (n = 24). Exercise intensity was determined by the heart rate of each patient at ventilatory threshold (VT). Three weeks after onset, a second LVG was performed, followed by a supervised exercise program at VT for 12 weeks. The LVG was reassessed after the exercise program. We then calculated the global LV volume (end-diastolic volume index [EDVI], end-systolic volume index [ESVI]) and systolic expansion volume index (SEVI), a new parameter for measuring the infarction site expansion at the end-systolic phase. RESULTS: Both EDVI and ESVI significantly decreased in the control group from 1 to 4 months after onset (91.2 +/- 26.1 to 83.3 +/- 24.0 mL/m2, P <.05; 52.4 +/- 22.5 to 45.7 +/- 18.8 mL/m2, P <.01, respectively), but not in the exercise group. The SEVI also significantly decreased in the control group from 1 to 4 months (33.1 +/- 16.9 to 25.7 +/- 13.9 mL/m2, P <.05), but not in the training group (34.2 +/- 12.9 to 36.5 +/- 15.5 mL/m2, P = not significant). CONCLUSION: Exercise while healing in patients with extensive anterior AMI, even at the VT level, induces LV enlargement and thus might aggravate LV remodeling. Therefore, in these patients, clinicians should consider withholding exercise training for at least 8 weeks, versus the 3-week period used in this trial.

Aged↗
PubMed2004

Effect of atrial septal aneurysm on risk of cerebrovascular events in Japanese patients.

BACKGROUND: The aim of the present study was to determine whether atrial septal aneurysm (ASA) detected by transthoracic echocardiography (TTE) is an independent risk factor of cerebrovascular events for Japanese people. METHODS: A control study was conducted with 178 patients with ASA (follow-up rate, 96.7%; median follow-up period, 5.6 years) and 176 control patients (follow-up rate, 97.8%; median follow-up period, 5.4 years), selected from 42,528 consecutive patients who underwent TTE in the Omiya Medical Center, Jichi Medical School, from April 1991 to March 2001. Data were collected by structured review of patient charts and a subsequent telephone survey. Long-term cerebrovascular risk factors were evaluated by logistic regression analysis. RESULTS: A previous episode of cerebral infarction had occurred in nine ASA patients (5.1%) and 11 control patients (6.3%). During the follow-up period, new cerebral infarction occurred in 12 ASA patients (6.7%) and six control patients (3.4%). Only atrial fibrillation was found to be an independent risk factor of new cerebral infarction (OR, 5.06; 95% CI, 1.32-19.46; P=0.04). CONCLUSIONS: ASA is not an independent risk factor of cerebrovascular events for Japanese patients. Thus, aggressive strategies such as anticoagulation are not essential for ASA patients without embolic episodes.

Aged↗
PubMed2004

Urinary excretion of aquaporin-2 water channel exaggerated dependent upon vasopressin in congestive heart failure.

BACKGROUND: Impaired water excretion occurs in patients with congestive heart failure. The present study was undertaken to determine whether urinary excretion of aquaporin-2 (AQP-2) water channel is exaggerated in patients with congestive heart failure dependent upon arginine vasopressin (AVP). METHODS: Sixty-five patients with congestive heart failure and eight age- and gender-matched control subjects were examined. The patients were divided into four groups according to the criteria of New York Heart Association (NYHA). Plasma AVP levels, urinary excretion of AQP-2, and cardiac index were determined. RESULTS: Plasma AVP levels were progressively increased following the severity of NYHA class in the patients with congestive heart failure. Cardiac index was inversely decreased, and there was a negative correlation between plasma AVP levels and cardiac index (r=-0.430, P < 0.02). Urinary excretion of AQP-2 was 187.3 +/- 50.2 fmol/mg creatinine in the control subjects. It was markedly increased in the patients. Urinary excretion of AQP-2 was elevated to 1144.4 +/- 257.5 and 990.5 +/- 176.0 fmol/mg creatinine in the patients with NYHA class III and class IV, respectively, values significantly greater than the control subjects (P < 0.05). Urinary excretion of AQP-2 had a positive correlation with plasma AVP levels (r= 0.280, P < 0.02). CONCLUSION: The present study indicates that exaggerated urinary excretion of AQP-2 is dependent on baroreceptor-mediated release of AVP in patients with congestive heart failure.

Adult↗
PubMed2004

Effect of reperfusion therapy on cardiac rupture after myocardial infarction in Japanese.

BACKGROUND: Cardiac rupture after acute myocardial infarction (AMI) is unpredictable and almost always fatal, so the present study reviewed all the clinical characteristics of patients with cardiac rupture to determine if its occurrence can be predicted. METHODS AND RESULTS: The clinical characteristics of 1,296 consecutive AMI patients from January 1992 to February 2002 were retrospectively evaluated using multi-logistic analysis. Cardiac rupture occurred in 45 patients (3.5%), comprising left ventricular free wall rupture (n=23), ventricular septal perforation (n=20) and papillary muscle rupture (n=2). Early-phase rupture (within 72 h after AMI onset) was associated with anterior infarction. Of the 45 patients who experienced ruptures, 24 (53.3%) survived to discharge; 21 (46.6%) of the 45 ruptures occurred after admission. Successful reperfusion therapy was performed within 24 h for 840 patients. The incidence of rupture was significantly lower for reperfused patients than for non-reperfused patients (0.6% vs 3.5%, respectively; p<0.01). Peak C-reactive protein concentration was a reliable predictor of late-phase rupture (p=0.01), but not of early-phase rupture. CONCLUSIONS: Reperfusion therapy appears to aid in the prevention of cardiac rupture, especially late-phase rupture.

Aged↗
PubMed2004

Increases in interleukin-6 and matrix metalloproteinase-9 in the infarct-related coronary artery of acute myocardial infarction.

BACKGROUND: To elucidate the involvement of inflammation in coronary artery occlusion, the regional changes in cytokines and matrix metalloproteinases (MMPs) in the infarct-related coronary artery were determined in patients with acute myocardial infarction. METHODS AND RESULTS: Cardiac catheterization was carried out within 24 h of the onset of infarction in 36 patients. Blood samples were collected from the infarct-related coronary artery, the ascending aorta and the peripheral vein. Plasma interleukin (IL)-6 concentrations were elevated in all 3 samples. Particularly, the plasma IL-6 concentrations were 14.4 pg/ml in the infarct-related coronary artery, a value significantly greater than the respective 8.0 pg/ml and 6.5 pg/ml in the ascending aorta and peripheral vein. Plasma IL-6 concentrations in the infarct-related coronary artery had positive correlation with all of the following references measured by intravascular ultrasound: external elastic membrane cross-sectional area (EEM-CSA) (r=0.47, p<0.01), lesion EEM-CSA (r=0.51, p<0.01) and plaque area (r=0.48, p<0.01). MMP-9 was increased regionally in the infarct-related coronary artery, at 11.8 ng/ml vs 8.2 ng/ml in the ascending aorta (p<0.001). CONCLUSIONS: The present findings suggest that IL-6 at least is released from the ruptured vulnerable atherosclerotic plaque and that regional activation of macrophages is involved in the occlusive process of coronary artery in acute myocardial infarction.

Adult↗
PubMed2004

Multi-detector computed tomography for imaging of subendocardial infarction: prediction of wall motion recovery after reperfused anterior myocardial infarction.

BACKGROUND: After reperfusion therapy for acute myocardial infarction (AMI), evaluation of transmural myocardial microcirculation can indicate prognosis. The aim of the present study was to determine whether the evaluation of transmural myocardial microcirculation by newly developed 4-slice computed tomography (CT) can estimate the recovery of left ventricular function. METHODS AND RESULTS: Seventeen consecutive patients who had anterior AMI with a total occlusion in the proximal left anterior descending artery (LAD) and who had undergone successful balloon reperfusion therapy within 24 h of the onset of AMI were examined. Four-slice CT was performed 10-14 days after AMI onset. The median of the epicardial perfusion ratio (infarcted anterior epicardial CT number/intact lateral epicardial CT number ratio = 92%) was used to categorize the cases into 2 groups: the transmural infarction group (n=8) and the subendocardial infarction group (n=9). Although no significant difference was observed between myocardial enhancement by CT in the acute phase and anterior wall motion or ejection fraction in the acute phase, the transmural infarction group showed poor recovery of anterior wall motion at 6 months after AMI onset, whereas the subendocardial infarction group exhibited good recovery of regional and global left ventricular function. CONCLUSIONS: Transmural myocardial microcirculation imaged by 4-slice CT can predict wall motion recovery after AMI.

Angioplasty, Balloon↗
PubMed2004

Effects of a distal protection device during primary stenting in patients with acute anterior myocardial infarction.

BACKGROUND: The angiographic no-reflow phenomenon is an adverse prognostic factor in patients with acute myocardial infarction (AMI). The aim of the present study was to evaluate the effects of an occlusive balloon type distal protection device (PercuSurge GuardWire: GW) during primary stenting in patients with anterior AMI. METHODS AND RESULTS: The GW group included 42 patients treated by primary stenting with GW protection and the control group included 30 patients treated by primary stenting after thrombectomy without distal protection. Left ventricular (LV) function was measured and compared by left ventriculography obtained soon after percutaneous coronary intervention (PCI) and 3 weeks after onset. The corrected TIMI frame count values were lower in the GW group than in the control group (27.5+/-2.3 vs 35.1 +/-2.5, p=0.030). The number of patients with myocardial blush grade 3 after PCI was higher in the GW group than in the control group (45.7 vs 20.0%, p=0.029). Peak concentration of creatine kinase myocardial fraction was lower in the GW group than in the control group (326.6+/-41.5 vs 454.9+/-46.2 mg/dl, p=0.043). GW patients showed greater improvement at 3 weeks after PCI in terms of LV ejection fraction (+4.6+/-1.2 vs -1.1+/-1.5, p=0.004), LV end-systolic volume index (+0.5+/-2.4 vs +9.0+/-2.7, p=0.023), and regional wall motion abnormalities (-2.03+/-0.14 vs -2.51+/-0.14, p=0.018). CONCLUSION: Primary stenting with GW protection can restore epicardial coronary flow and myocardial perfusion, and also preserve LV function in anterior AMI.

Blood Flow Velocity↗
PubMed2004

Long-term prognosis of fulminant myocarditis rescued by percutaneous cardiopulmonary support device.

BACKGROUND: The long-term prognosis and cardiac function of fulminant myocarditis treated with percutaneous cardiopulmonary support (PCPS) was compared with the outcome of those not treated with PCPS. METHODS AND RESULTS: From 1991 to 2000, 14 patients with fulminant myocarditis (left ventricle ejection fraction (LVEF) < or =40%) were admitted to hospital. PCPS was necessary for treatment of shock in 8 (PCPS group), but not for the remaining 6 patients (non-PCPS group). In the PCPS group, 6 patients (75%) survived the critical phase and did not have any cardiac problems after discharge (range of follow-up period, 1.4-6.0 years). All patients in the non-PCPS group survived the acute phase; 1 patient had congestive heart failure 1.5 years after discharge, and another died from malignancy (follow-up period range, 2.2-9.4 years). Although the left ventricular ejection fraction (LVEF) of the PCPS group was significantly lower than that of the non-PCPS group in the acute phase, there was no significant difference in LVEF between the 2 groups in the chronic phase. CONCLUSION: Patients who survive the acute phase crisis of acute myocarditis have a favorable long-term survival rate, whether or not mechanical support is used.

Adult↗
PubMed2004

[Prospective randomized study of argatroban versus heparin anticoagulation therapy after percutaneous coronary intervention for acute myocardial infarction].

OBJECTIVES: Argatroban, a selective thrombin inhibitor, is expected to decrease acute coronary re-occlusion and restenosis via direct suppression of thrombin generation after percutaneous coronary intervention (PCI) in patients with acute myocardial infarction. This study evaluated the effect of argatroban compared with heparin as an adjunctive anticoagulation therapy after PCI in patients with acute myocardial infarction. METHODS: Fifty-four consecutive patients with acute myocardial infarction underwent PCI within 6 hr from the onset and were randomly allocated to receive argatroban (argatroban group: n = 27) or heparin (heparin group: n = 27) after PCI. Each drug was administered intravenously for 72 hr. Coronary angiography was repeated at 1 and 6 months after the onset of acute myocardial infarction. In-hospital cardiac events, bleeding complications, and long-term outcome were surveyed. RESULTS: Baseline clinical and angiographic variables were similar in the two groups. Acute coronary re-occlusion and major hemorrhagic complications did not occur in either group. Minor bleeding complications, such as hematoma of the puncture sites, occurred significantly less frequently in the argatroban group than in the heparin group (4% vs 30%, p < 0.05). After 6 months, there were no significant differences in restenosis rate and target vessel recanalization rate between the two groups. Subgroup analyses revealed no significant differences in restenosis rate between patients treated with only balloon angioplasty and stent implantation. CONCLUSIONS: Argatroban provides similar prevention of acute thrombotic events and restenosis compared with heparin. However, argatroban might reduce bleeding complications in patients with acute myocardial infarction after PCI.

Angioplasty, Balloon, Coronary↗
PubMed2003

Src family kinases and nitric oxide production are required for hepatocyte growth factor-stimulated endothelial cell growth.

Hepatocyte growth factor (HGF) is a potent mitogen for vascular endothelial cells (EC); however, signal transduction pathways for HGF-stimulated EC growth remain unclear. In the present study we investigated the role of Src family kinases and nitric oxide (NO) in HGF-stimulated EC growth. Human umbilical vein endothelial cells (HUVEC) were stimulated with HGF and NO was measured by an NOx analyzing HPLC system. Activation of ERK1/2 and p38 MAPK was assessed by Western blot. NO production in HUVEC increased 1.8-fold by HGF. A Src family kinases inhibitor PP1 inhibited HGF-stimulated NO production by 71%. HUVEC growth increased 1.9-fold in cell number by HGF. PP1 and Nitro-L-arginine methylester (L-NAME) inhibited HGF-stimulated HUVEC growth by 51 and by 71%. ERK1/2 and p38 MAPK were phosphorylated by HGF and a MEK inhibitor PD98059 and a p38 MAPK inhibitor SB203580 inhibited HGF-stimulated HUVEC growth by 66% and by 58%; however, HGF-induced phosphorylation of ERK1/2 and p38 MAPK was not inhibited by L-NAME, indicating that NO is not an upstream activator of ERK1/2 and p38 MAPK. These findings demonstrated that Src family kinases regulate HGF-stimulated NO production in HUVEC and that HGF stimulates HUVEC growth through NO-dependent and NO-independent pathways.

Analysis of Variance↗
PubMed2003

Exercise training in patients with chronic heart failure improves endothelial function predominantly in the trained extremities.

The present study investigates whether lower-limb dominant exercise training in patients with chronic heart failure (CHF) improves endothelial function primarily in the trained lower extremities or equally in the upper and lower extremities. Twenty-eight patients with CHF were randomized to the exercise or control group. The exercise group underwent cycle ergometer training for 3 months while controls continued an inactive sedentary lifestyle. Exercise capacity (6-min walk test) and flow-mediated vasodilation in the brachial and posterior tibial arteries were evaluated. After 3 months, walking performance increased only in the exercise group (488+/-16 to 501+/-14 m [control]; 497+/-23 to 567+/-39 m [exercise, p<0.05]). The flow-mediated vasodilation in the brachial arteries did not change in either group (4.2+/-0.5 to 4.5+/-0.4% [control]; 4.3+/-0.5 to 4.6+/-0.4% [exercise]), but that in the posterior tibial arteries increased only in the exercise group (4.1+/-0.5 to 4.1+/-0.3% [control]; 3.6+/-0.3 to 6.4+/-0.6% [exercise, p<0.01]). Cycle ergometer training improved flow-mediated vasodilation in the trained lower limbs, but not in the untrained upper limbs. Exercise training appears to correct endothelial dysfunction predominantly by a local effect in the trained extremities.

Arm↗
PubMed2003

Influence of contrast ultrasonography with perflutren lipid microspheres on microvessel injury.

Microbubbles have been reported to enhance ultrasound (US)-related side effects in animal systems. The present study investigated the influence of contrast ultrasonography (US) with perflutren lipid microspheres, a recently developed second-generation contrast agent, on microvessels. Rat mesentery was exposed to 1.8-MHz pulsed US with intravenous injection of perflutren (0.1 or 1.0 ml/kg) or Levovist (300 mg/kg), and the microvessel bleeding and endothelial cell injury was examined. Impaired endothelial cells were identified by the fluorescence of propidium iodide. Microvessel bleeding was examined also in the rat myocardium. The interaction between 0.1 ml/kg of perflutren and US exposure did not cause microvessel bleeding, and did not increase endothelial cell injury compared with the sham operation, unless frequent, strong US exposure occurred. When the dose was increased to 1.0 ml/kg, the combination of perflutren and US exposure resulted in capillary bleeding and increased endothelial cell injury in capillaries and venules (p<0.01). However, the incidence of microvessel bleeding and endothelial cell injury did not exceed that with Levovist microbubbles. In the myocardium, microvessel bleeding was not observed under any conditions. In conclusion, perflutren lipid microspheres enhanced US-related microvessel injury as with other contrast agents at the dose of 1.0 ml/kg, but not with 0.1 ml/kg and the appropriate US setting.

Animals↗
PubMed2003

[Exercise testing].

Explore the source record for details and available documents.

Electrocardiography↗
PubMed2003

[Transient retinopathy after acute myocardial infarction treated by reperfusion therapy: clinical background and manifestation].

OBJECTIVES: The severe inflammatory reaction caused by acute myocardial infarction and reperfusion affects both the heart and other remote organs. The occurrence of retinopathy was evaluated in patients with acute myocardial infarction who underwent reperfusion therapy. METHODS: We investigated 29 patients with first acute myocardial infarction who underwent successful reperfusion therapy within 24 hr of the onset. Ophthalmic examinations including visual acuity test and ocular fundoscopy were performed within 3 days, 2 weeks, and then monthly up to 3 months after the onset of acute myocardial infarction. Plasma levels of intercellular adhesion molecule-1(ICAM-1), interleukin-6 and high sensitivity C-reactive protein were measured on admission. RESULTS: Soft exudates around the optic disc appeared in 17(58.6%) of the 29 patients, among whom 5 also developed superficial hemorrhages(17.2%). The retinopathy became most remarkable between 1 to 2 months after the onset of acute myocardial infarction and then faded away without any specific treatment. None of the patients had impairment of visual acuity, although 4 of the 17 patients with retinopathy complained of either blurred vision or metamorphopsia. Hypertension and/or diabetes mellitus tended to be more common in the retinopathy group than in the non-retinopathy group(59% vs 33%, p = 0.096). Plasma ICAM-1 levels were significantly higher than in the non-retinopathy group than in the retinopathy group(p = 0.017). There was no significant difference in plasma levels of interleukin-6 and high sensitivity C-reactive protein between the two groups. CONCLUSIONS: Retinopathy may occur after reperfusion for acute myocardial infarction. The dominant manifestation is transient soft exudates reflecting spotty retinal ischemia, probably due to microvascular obstruction.

Adult↗
PubMed2002

Endothelial cell injury in venule and capillary induced by contrast ultrasonography.

The aim of the present study was to test the hypothesis that microvascular endothelial cells (EC) are subject to the bioeffects induced by contrast ultrasound (US) because of their proximity to the circulating microbubbles. We examined EC injury in each microvessel section (arteriole, capillary or venule) in rat mesenteries among the following five groups: three controls (sham operation, microbubble injection alone, US exposure with saline injection), and two contrast-US groups (US exposure at a 1-Hz or 30-Hz frame rate with microbubble injection). Propidium iodide (PI), a fluorescent indicator of cell injury, was employed to visualize impaired EC. PI-positive nuclei were equally few among the three controls. Contrast-US increased PI-positive cells in capillaries (1-Hz frame rate, 2.4 +/- 2.2 cells per 0.1-mm vessel length, p = 0.09; 30-Hz frame rate, 4.3 +/- 1.8 cells, p < 0.01) and in venules (1-Hz frame rate, 4.1 +/- 2.5 cells, p < 0.05; 30-Hz frame rate, 13.8 +/- 3.6 cells, p < 0.01) compared with sham operation (0.10 +/- 0.22 cells). The finding indicates that diagnostic contrast US potentially causes EC injury, particularly in venules and capillaries.

Analysis of Variance↗