Biomedical subjects

Shigemasa Hashimoto

Publications and source records attributed to Shigemasa Hashimoto.

6 recordsLinked to original sources

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

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↗

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

[Exercise testing].

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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↗