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Biomedical subjects

T Iwasaka

Publications and source records attributed to T Iwasaka.

At least 109 records · Page 6Linked to original sources
PubMed1998

Adjuvant chemotherapy after radical hysterectomy for cervical carcinoma: a comparison with effects of adjuvant radiotherapy.

OBJECTIVE: To compare the efficacy of adjuvant chemotherapy after radical hysterectomy with that of adjuvant radiotherapy. METHODS: One hundred one women with invasive cervical carcinoma (stage IB through early stage IIB) underwent radical hysterectomy at Saga Medical School Hospital. Of these patients, 53 with squamous or adenosquamous carcinoma were classified as high risk, based on the presence of one or more of the following high-risk factors for recurrence: 1) lymph node metastasis, 2) deep cervical stromal invasion (greater than 3/4 thickness), and 3) parametrial invasion. Adjuvant chemotherapy with a combination of cis-diamminedichloroplatinum (CDDP), vincristine, mitomycin C, and peplomycin (POMP), was prescribed. The outcome was compared with that for 127 patients who were classified as high risk under the same criteria and who received adjuvant radiotherapy at Kyushu University Hospital. RESULTS: The 5-year survival rates were much the same: 83.0% for adjuvant chemotherapy and 81.7% for adjuvant radiotherapy. In the chemotherapy group, intra- and extrapelvic recurrences accounted for 85 and 23% of all recurrences, respectively, whereas recurrences were noted for 38 and 71% in the radiotherapy group, respectively (P < .01). CONCLUSION: The use of adjuvant chemotherapy reduces extrapelvic recurrences. The combination of both adjuvant therapies may improve the prognosis for high-risk patients.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1998

Determinants of heart rate variability in chronic hemodialysis patients.

To clarify determinants of heart rate variability in hemodialysis patients, we evaluated 187 patients receiving chronic hemodialysis. Ambulatory electrocardiogram was recorded for 24 hours from the beginning of hemodialysis. Standard deviation of the normal RR interval (SDNN) was used as a marker of heart rate variability. Multiple regression analysis was performed to select independent variables associated with SDNN from the following 14 variables: age, sex, body mass index before hemodialysis, presence of ischemic heart disease, diabetic nephropathy as primary renal disease, smoking, duration of hemodialysis, mean blood pressure before hemodialysis, left ventricular mass index and fraction shortening in echocardiography, use of beta blockers, use of angiotensin-converting enzyme inhibitors, hematocrit, and blood urea nitrogen. Older age (P < 0.0001), presence of diabetic nephropathy as primary renal disease (P < 0.0001), lower hematocrit (P = 0.0121), larger body mass index before hemodialysis (P = 0.0133), longer duration of hemodialysis (P = 0.0200), and smoking (P = 0.0350) were associated with reduced SDNN. In hemodialysis patients, SDNN as a marker of cardiac autonomic modulation was associated with hematocrit, body mass index, and duration of hemodialysis, in addition to previously reported variables.

Adult↗
PubMed1998

The role of infarction-associated pericarditis on the occurrence of atrial fibrillation.

AIMS: Transient atrial fibrillation is a relatively common arrhythmia in the early phase of acute Q-wave myocardial infarction. However, the role of infarction-associated pericarditis on the genesis of atrial fibrillation is controversial. This study was designed to examine the relative importance of infarction-associated pericarditis among other clinical variables on the genesis of transient atrial fibrillation in patients with acute myocardial infarction. METHODS AND RESULTS: Three hundred and ninety-eight patients with acute Q-wave myocardial infarction were examined carefully by means of auscultation, ECG, two-dimensional echocardiography and haemodynamic measurements. The diagnosis of pericarditis was made on the basis of pericardial rub detected during the first 3 days after admission. At least 0.5 mm of PQ-segment depression from a TP segment lasting more than 24 h in both limb and precordial leads was considered diagnostic of PQ-segment depression. Atrial fibrillation was present in 76 patients (19%). Sixteen (42%) of 38 patients with PQ-segment depression had atrial fibrillation, whereas 23 (30%) of 77 patients with pericardial rub had atrial fibrillation. Based on ten clinical variables, multivariate analysis was performed to determine the important variables related to the occurrence of atrial fibrillation. PQ-segment depression (chi-square = 4.10, P < 0.05) was selected with age (chi-square = 10.52, P < 0.005), the number of left ventricular segments with advanced asynergy (chi-square = 7.73, P < 0.01) and pericardial effusion (chi-square = 7.95, P < 0.005) as important factors related to atrial fibrillation. Patients with PQ-segment depression had a significantly higher pulmonary capillary wedge pressure than those without it. CONCLUSION: Among patients with infarction-associated pericarditis, those with PQ-segment depression represent atrial involvement associated with extensive myocardial damage and hence, PQ-segment depression is one of the clinical signs related to the occurrence of atrial fibrillation in acute Q-wave myocardial infarction.

Aged↗
PubMed1998

Diastolic time during weight carrying exercise in patients with myocardial infarction.

Cardiovascular responses to static-dynamic exercises were studied in 27 patients with recent myocardial infarction. Patients with ischemic electrocardiographic changes at peak weight carrying exercise (group 1 = 8 patients) had a significantly larger left ventricular end-diastolic volume than those without (group 2 = 19 patients). A higher tension time index and shortening of diastolic time/min was observed in group 1 compared to group 2 during weight carrying. Thus, in addition to the increased myocardial oxygen demand, shortening of the diastolic perfusion time was observed during static-dynamic exercise in patients with dilated heart after myocardial infarction.

Diastole↗
PubMed1998

Determinants of ventricular arrhythmias in hemodialysis patients. Evaluation of the effect of arrhythmogenic substrate and autonomic imbalance.

BACKGROUND/AIMS: In chronic hemodialysis patients, we evaluated determinants of repetitive ventricular tachyarrhythmias which included late potentials and heart rate variability. METHODS: We compared the presence of late potentials and heart rate variability obtained by ambulatory electrocardiogram (ECG), findings of echocardiography, and laboratory data between patients with and those without ventricular arrhythmias of Lown class 4A or 4B. Ambulatory ECG was recorded for 24 h from the beginning of hemodialysis. Heart rate variability was evaluated by the standard deviation of the normal RR interval (SDNN). RESULTS: Thirty patients (17%) had ventricular arrhythmias of Lown class 4A or 4B. They were older than patients without such arrhythmias (p=0.0021). Left-ventricular wall motion score (2.0+/-3.9 and 0.3+/-1.2, respectively, p < 0.0001) and left-ventricular mass index (167 +/-59 and 140+/-44 g/m2, respectively, p=0.0053) were larger in patients with ventricular arrhythmias of Lown class 4A or 4B than in those without. Stepwise logistic regression analysis was performed to select variables related to ventricular arrhythmias of Lown class 4A or 4B from the following 8 candidate variables; age, sex, presence of ischemic heart disease, diabetic nephropathy as the primary renal disease, presence of late potentials, SDNN, left-ventricular wall motion score and left-ventricular mass index. Higher left-ventricular wall motion score (p < 0.0001), older age (p=0.0022) and male sex (p=0.0235) were the variables associated with ventricular arrhythmias of Lown class 4A or 4B. CONCLUSION: In patients receiving hemodialysis, predominantly with chronic glomerulonephritis, ventricular arrhythmias of Lown class 4A or 4B were not associated with arrhythmogenic substrate revealed by late potentials or autonomic dysfunction assessed by heart rate variability. Left-ventricular wall motion abnormalities, age and sex were significant factors.

Autonomic Nervous System Diseases↗
PubMed1998

Tissue-specific expression of human angiotensin II AT1 and AT2 receptors and cellular localization of subtype mRNAs in adult human renal cortex using in situ hybridization.

All studies analyzing the localization of angiotensin II (Ang II) receptors in the human kidney have been performed at the protein level using 125I-Ang II as a probe. In this study, cellular localizations of Ang II type l (AT1-R) and type 2 (AT2-R) receptor mRNAs in the adult human renal cortex were examined for the first time using in situ hybridization, and their expression patterns determined by RNase protection assay were compared with those in other human tissues. In the human renal cortex obtained from tumor-free portions in renal cell carcinoma, AT1-R mRNA levels were about 8- to 10-fold higher than AT2-R mRNA levels. Human liver and aorta predominantly expressed AT1-R mRNA, while human right atrium contained both AT1-R and AT2-R mRNAs. Ligand-binding assays revealed that the total Ang II receptor number in the human renal cortex was 16.0 +/- 3.3 fmol/mg protein, similar to that in liver (17.7 +/- 5. 8) but significantly higher than in right atrium (11.6 +/- 3.2) and aorta (5.6 +/- 2.7). Relative distribution ratios of AT1-R and AT2-R numbers in the renal cortex and right atrium were 82/17 and 56/42%, respectively. In situ hybridization study indicated that strongest AT1-R mRNA signals were located in interlobular arteries and tubulointerstitial fibrous regions surrounding interlobular arteries and glomeruli, followed in decreasing order by glomeruli and cortical tubules. Expression of AT2-R mRNA was highly localized in interlobular arteries. Cells present in tubulointerstitial regions were positive for vimentin and collagen type 1, indicating that the majority of the cells present in the regions are fibroblasts. Presence of strong AT1-R mRNA signals in the tubulointerstitial fibrous regions surrounding arteries and glomeruli and the expression of AT2-R mRNA in the interlobular artery were the first evidence, suggesting a pharmacological framework for the differential effects of Ang II receptor subtype mediated renal function in the adult human kidney.

Adult↗
PubMed1998

Coronary artery diameter and left ventricular function in patients on maintenance hemodialysis treatment: comparison between diabetic and nondiabetic patients.

BACKGROUND/AIMS: This study examined the role of diabetes mellitus on determining left ventricular function by evaluating coronary artery diameter in patients with end-stage renal disease on maintenance hemodialysis treatment. METHODS: We studied 12 diabetic and 12 nondiabetic patients on maintenance hemodialysis treatment without significant stenoses of the major epicardial coronary arteries. Patients were matched for age, sex distribution, duration of dialysis and incidence of major coronary risk factors. Left ventricular wall thickness (septal and posterior walls) and left ventricular diameter (end-diastolic and systolic phases), were measured by echocardiography. Hemodynamic measurements and coronary angiography were performed on the day of hemodialysis and coronary artery diameter at the proximal and mid portion of three major coronary arteries were measured using the computed densitometry method. RESULTS: Right and left anterior descending and circumflex coronary artery diameters were all significantly smaller and the frequency of coronary artery calcification was higher in diabetic (58%) compared to nondiabetic (8%) patients. Although there were no significant differences in left ventricular wall thickness, left ventricular diameter, mean right atrial pressure and cardiac index between the two groups, left ventricular end-diastolic pressure was significantly higher in diabetic (22 +/- 9 mm Hg) compared to nondiabetic patients (14 +/- 5 mm Hg). CONCLUSION: Despite that there were no significant stenoses of the major epicardial coronary arteries, diffuse luminal narrowing of the epicardial coronary arteries in diabetic patients on maintenance hemodialysis treatment was associated with increased left ventricular end-diastolic pressure.

Aged↗
PubMed1998

Role of calcium-sensitive tyrosine kinase Pyk2/CAKbeta/RAFTK in angiotensin II induced Ras/ERK signaling.

In cardiac fibroblasts, angiotensin II (Ang II) induced a rapid increase in extracellular signal regulated kinase (ERK) activity in a pertussis toxin insensitive manner. This ERK activation was abolished by the Gq-associated phospholipase C inhibitor U73122 but was insensitive to protein kinase C (PKC) inhibitors or PKC downregulation by phorbol ester. Intracellular Ca2+ chelation by BAPTA-AM or TMB-8 abolished Ang II induced ERK activation, whereas treatment with EGTA or nifedipine did not affect it. Ca2+ ionophore A23187 also induced a rapid increase in ERK activity to an extent similar to that of Ang II stimulation. Calmodulin inhibitors (W7 and calmidazolium) and tyrosine kinase inhibitors (genistein and ST638) completely blocked ERK activation by Ang II and A23187. Both Ang II and A23187 caused a rapid increase in the binding of GTP to p21(Ras), which was nearly abolished by genistein and calmidazolium. Transfection with the dominant negative mutant of Ras and the Ras inhibitor manumycin completely inhibited Ang II induced ERK activation. It was also found for the first time that cardiac fibroblasts abundantly expressed Ca2+-sensitive tyrosine kinase Pyk2/CAKbeta/RAFTK and that Ang II markedly induced its activation in a Ca2+/calmodulin-sensitive manner. Overexpression of the dominant negative mutant of Pyk2 significantly attenuated Ang II or A23187-induced ERK activities (36% and 38% inhibition compared with that in mock-transfected cells, respectively) and ERK tyrosine phosphorylation levels, as well as an increase in the binding of GTP to p21(Ras). These findings demonstrate that in cardiac fibroblasts, Ang II induced Ras/ERK activation is dominantly regulated by Gq-coupled Ca2+/calmodulin signaling and that Pyk2 plays an important role in the signal transmission for efficient activation of the Ang II induced Ras/ERK pathway.

Angiotensin II↗
PubMed1998

Variant angina in isolated adrenocorticotropin deficiency, inappropriate vasopressin secretion and Hashimoto's thyroiditis.

We report a 62-year-old male patient who had variant angina and isolated adrenocorticotropic hormone (ACTH) deficiency. His serum sodium concentration was low and vasopressin was inappropriately high for the low plasma osmolality. Serum free thyroxine (FT4) was low and thyroid stimulating hormone (TSH) was high with positive anti-thyroperoxidase antibodies, compatible with Hashimoto's thyroiditis. Treatment with Amrodipine and hydrocortisone relieved chest symptoms and hyponatremia, and hypothyroidism was also normalized. It is suggested that coronary artery spasm may be related to cortisol deficiency and/or inappropriately high vasopressin secretion and that hypothyroidism was ameliorated because the reduced responsiveness to TSH returned to normal due to hydrocortisone supplement.

Adrenocorticotropic Hormone↗
PubMed1998

Role of platelet-activating factor on extravascular lung water after coronary reperfusion in dogs.

Platelet-activating factor (PAF), one of the harmful substances released after coronary reperfusion, has been reported to increase pulmonary vascular permeability and induce pulmonary edema. In this study, we sought to examine the possible role of PAF in the genesis of pulmonary edema after coronary reperfusion. Extravascular lung water (EVLW) was measured by the thermal-dye double indicator dilution method during coronary ligation and after reperfusion in situ in dogs. The proximal left anterior descending coronary artery was occluded for 15 min and reperfused in 5 dogs (group 1), while five other dogs (group 2) were treated with PAF-antagonist (TCV-309, 1 mg/kg) before coronary artery occlusion. EVLW and hemodynamic indices were measured at baseline, 15 min of coronary occlusion, and 15 and 30 min after coronary reperfusion. EVLW increased at 15 min of coronary occlusion in both groups, but there was no significant difference between the two groups (6.4 to 10.3 ml/kg and 5.4 to 7.1 ml/kg in groups 1 and 2, respectively). After coronary reperfusion, EVLW increased further in group 1 (6.4 to 16.5 ml/kg, p < 0.01), but no further increase was observed in group 2 at 30 min after coronary reperfusion. There were no significant differences in hemodynamic indices between the two groups throughout the test. Thus, PAF-antagonist attenuated the increase in EVLW after coronary reperfusion independent of hemodynamic indices, and hence, PAF may play an important role in the genesis of pulmonary edema caused by coronary reperfusion.

Animals↗
PubMed1998

[Immune complex-mediated glomerulonephritis associated with infective endocarditis with aortic valve vegetation].

A 61-year-old male was referred to our hospital for rapidly progressive azotemia. He was also found to have huge vegetation at the aortic valve causing regurgitation. Biochemical examinations revealed the presence of an immunocomplex associated with decreased circulating complements. In biopsy samples from the kidney, we found the presence of fibrillar crescents, proliferation of mesangial cells, increase in extracellular matrix proteins, atrophy of tubules, infiltration of mononuclear cells in the interstitial regions, high density deposits in the mesangial area and mesangial interposition. Since the patient strongly rejected operative treatment by valvular replacement, we continued non-invasive treatment such as hemodialysis and treatment with penicillin G. This transiently improved the condition of the patient, including biochemical data and cardiac function, but there was no reduction in the size of vegetation at the aortic valve and the bacteria responsible for infective endocarditis were not identified. About three months after admission, overt signs of congestive heart failure emerged and the patients was subjected to intensive care with a respirator and hemodynamic monitoring. Although the cardiac function was improved, concomitant severe pneumonia occurred and the patient died of septic shock. Thus, we report a rare case in whom immune complex-mediated glomerulonephritis was associated with infective endocarditis with aortic valve vegetation.

Antigen-Antibody Complex↗
PubMed1998

[Aortic valvular vegetation in annuloaortic ectasia due to idiopathic cystic medial necrosis: a case report].

Annuloaortic ectasia is often accompanied by Marfan syndrome and associated with infective endocarditis usually involving the mitral valves. We treated a patient with annuloaortic ectasia due to idiopathic cystic medial necrosis who developed congestive heart failure with aortic valvular vegetation. A 56-year-old man had dyspnea on effort since the beginning of January, 1997 and was admitted to our hospital on April 6, 1997 because of orthopnea. The diagnosis was congestive heart failure due to severe aortic regurgitation with annuloaortic ectasia detected by echocardiography. Medication and rest after hospitalization relieved his symptoms but congestive heart failure deteriorated after he had a high fever. At this time, a vegetation attached to the noncoronary cusp of the aortic valve was found which had not been detected on admission. Blood culture yielded Streptococcus sanguis. The diagnosis was infective endocarditis involving the aortic valve. Surgical correction (Bentall method) improved congestive heart failure and he was discharged on August 4, 1997 without recurrence of endocarditis. Infective endocarditis involving the aortic valves is a possible cause of development or deterioration of congestive heart failure in patients with annuloaortic ectasia.

Aortic Diseases↗
PubMed1997

Angiotensin type 2 receptors are reexpressed by cardiac fibroblasts from failing myopathic hamster hearts and inhibit cell growth and fibrillar collagen metabolism.

BACKGROUND: Angiotensin (Ang) II type 1 receptor (AT1-R) induces cardiomyocyte hypertrophy and fibroblast proliferation, whereas the physiological role of AT2-R in cardiac remodeling remains poorly defined. METHODS AND RESULTS: Using Bio14.6 cardiomyopathic (CM) hamsters, we found that AT2-R sites were increased by 153% during heart failure compared with F1B controls. AT1-R numbers were increased by 72% in the hypertrophy stage and then decreased to the control level during heart failure. Such differential regulation of AT2-R and AT1-R during heart failure was consistent with changes in the respective mRNA levels. Autoradiography and immunocytochemistry revealed that both AT2-R and AT1-R are localized at higher densities in fibroblasts present in fibrous regions. Surrounding myocardium predominantly expressed AT1-R, but the level of expression was less than that in fibrous regions. Cardiac fibroblasts isolated from CM hearts during heart failure but not from control hamsters expressed AT2-R (30 fmol/mg protein). Using the cardiac fibroblasts expressing AT2-R, we found that Ang II stimulated net collagenous protein production by 48% and pretreatment with an AT2-R antagonist, PD123319, evoked a further elevation (83%). Ang II-induced synthesis of fibronectin and collagen type I were enhanced by 40% and 53%, respectively, by pretreatment with PD123319. Ang II-induced DNA synthesis (assessed by [3H]thymidine uptake) was significantly increased by PD123319, and the AT2-R agonist CGP42112A reduced the serum-stimulated increase in cell numbers by 23%. Treatment with an AT1-R antagonist, TCV116, for 20 weeks inhibited progression of interstitial fibrosis by 28%, whereas with 44-week PD123319 treatment but not 20-week treatment, the extent of the fibrous region was increased significantly, by 29%. CONCLUSIONS: These findings demonstrate that AT2-R is re-expressed by cardiac fibroblasts present in fibrous regions in failing CM hearts and that the increased AT2-R exerts an anti-AT1-R action on the progression of interstitial fibrosis during cardiac remodeling by inhibiting both fibrillar collagen metabolism and growth of cardiac fibroblasts.

Angiotensin Receptor Antagonists↗
PubMed1997

Effect of cilostazol in preventing restenosis after percutaneous transluminal coronary angioplasty.

This study sought to evaluate the effect of cilostazol in preventing restenosis after successful percutaneous transluminal coronary angioplasty (PTCA) in 68 patients: 35 patients received cilostazol immediately after PTCA and 33 patients received aspirin or ticlopidine. Repeat coronary angiography was performed 4 to 6 months after PTCA and the incidence of restenosis was significantly lower (17%) in the cilostazol group than in the non-cilostazol group (40%) (p < 0.05), which indicates that cilostazol has the potential to prevent restenosis after PTCA.

Aged↗
PubMed1997

Resolution of late potentials with improvement in left ventricular systolic function in patients with first acute myocardial infarction.

BACKGROUND: Ventricular late potentials predict subsequent arrhythmic events and sudden death in postinfarction patients. Late potentials are recorded in the infarcted area, but it should be pointed out that they probably represent micropotentials in the area of delayed conduction found among isolated areas of scar tissue and normal myocardium. HYPOTHESIS: The study was undertaken to investigate the relationship between chronic reversible myocardial ischemia, such as stunned or hibernating myocardium, and late potentials in 38 patients with a first myocardial infarction. METHODS: The patients were divided into two groups, one with (Group 1) and one without (Group 2) resolution of late potentials recorded by signal-averaged electrocardiogram at 6 months after onset of myocardial infarction. We investigated the clinical, echocardiographic, and signal-averaged electrocardiographic characteristics of Groups 1 and 2. RESULTS: In the chronic phase of myocardial infarction, a higher incidence of patency of the infarct-related artery and an improvement of wall motion score were found in Group 1, and left ventricular ejection fraction was better preserved in Group 1 than in Group 2. CONCLUSIONS: These results suggest that the resolution of late potentials was influenced by the improvement of left ventricular systolic function and patency of the infarct-related artery. We concluded that chronic reversible myocardial ischemia, such as stunned or hibernating myocardium, might be the substrate that generated late potentials.

Action Potentials↗