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Biomedical subjects

M Tsushima

Publications and source records attributed to M Tsushima.

At least 37 records · Page 2Linked to original sources
PubMed1997

Apheresis technology for prevention and regression of atherosclerosis: an overview.

Low density lipoprotein (LDL) apheresis is at present one method of treatment in homozygous cases of familial hypercholesterolemia (FH). It is also effective in the prevention of the development of coronary atherosclerosis in patients with heterozygous FH and other types of mild hypercholesterolemia, leading to the regression of the stenosing lesions. In this paper, an overview is presented on the development of the devices for LDL apheresis and its short- and long-term effects on FH mainly based upon experience with the Liposorber system. LDL apheresis has served to protect the lives of patients from life threatening diseases like myocardial infarction although observations for more than 10 years in some laboratories have shown that the progression of atherosclerosis has taken place in many patients, and more importantly, the involvement of the aortic valve with calcification has developed, especially in patients who had homozygous FH, making this the most obstinate complication of FH. Therefore, more aggressive treatment or the combination of LDL apheresis with other therapies is required in the future. LDL apheresis has also been approved for the treatment of glomerulosclerosis and arteriosclerosis obliterans.

Arteriosclerosis↗
PubMed1997

Insulin resistance as an independent risk factor for carotid artery wall intima media thickening in vasospastic angina.

Studies have shown the presence of insulin resistance together with compensatory hyperinsulinemia in vasospastic angina as well as obstructive coronary artery disease. There is growing evidence that the development of coronary atherosclerosis may be closely related to systemic atherosclerosis as well as coronary spasm. However, no information is available about the possible relationship between insulin resistance and the existence of carotid atherosclerosis in vasospastic angina without segmental stenosis or luminal irregularities in coronary angiograms. To evaluate the independent effect of insulin resistance on carotid intima media thickening, we performed insulin sensitivity tests (steady-state plasma glucose method) on 40 patients with vasospastic angina and 24 control subjects with angiographically intact coronary arteries. Both oral glucose tolerance tests and lipid analyses were performed. Using B-mode ultrasonography, we assessed intima media thickness and plaque formation of common carotid arteries in these subjects. The steady-state plasma glucose level in the vasospastic angina group was about twofold higher than that of the control group, confirming the presence of insulin resistance in patients with vasospastic angina. The patients with vasospastic angina showed a significant increase in the average intima media thickness of the carotid wall and frequency of plaque formation, although they were comparable to the control subjects in risk factors other than insulin resistance. The intima media thickness was correlated with age (r = .62, P < .001), 2-hour insulin area (r = .45, P < .01), and steady-state plasma glucose level (r = .68, P < .0001) in patients with vasospastic angina. Similar correlations were observed in the control subjects. Multiple regression analyses of data indicated that 67% of the variation in the intima media thickness could be accounted for by age, steady-state plasma glucose level, and cigarette-years in vasospastic angina. In addition, differences in IMT were independently related to vasospastic angina. These results suggest that insulin resistance in association with compensatory hyperinsulinemia may be an important pathogenic factor for the development of coronary artery spasms and systemic early atherosclerosis.

Adult↗
PubMed1997

[A surgical case of total anterior papillary muscle rupture after acute myocardial infarction].

Mitral regurgitation (MR) due to rupture of the papillary muscle is one of the most serious complications of acute myocardial infarction (AMI) as well as ventricular septal perforation and ventricular free wall rupture. We experienced a case of complete rupture of the anterior papillary muscle. A 68-year-old man experienced an episode of dyspnea. Electrocardiographic findings were consistent with postero-lateral infarction. Massive MR is present on color Doppler imaging. He was transferred to our hospital for urgent operative indication because of papillary muscle rupture due to AMI. Six hours after the onset, the operation was performed with intra-aortic balloon pump in place. The anterior papillary muscle was ruptured completely in the mid portion. He underwent a mitral valve replacement with a SJM prosthetic valve. There is a few cases with successful urgent surgery for a complete rupture of anterior papillary muscle.

Aged↗
PubMed1997

[Labor status of anesthesia in general hospitals in Japan Committee on Human Resources, the Japan Society of Anesthesiology].

AIMS: Investigating the labor by anesthetists in general hospitals with more than 600 beds during the month of September 1995. METHOD: Using MS/EXCEL spread sheet soft wear, we have analyzed daily OR anesthesia activities in 33 hospitals based on personal attendance of anesthesiologists. We defined anesthesia performing hours i.e. actual working hours as the time between the onset and the end of anesthesia for each anesthetist. RESULTS: An average number of monthly anesthesia cases was 961 in the first 10 hospitals we surveyed. We obtained two frequency graphs on weekly 5-day working 138 anesthetists whose anesthesia performed, and their occupied hours were as shown in fig. 1 and 2. for those who worked other less than 5 days per week, they showed the shorter hours on the frequency distribution graph as shown in fig. 3 to 7. The 5-day working anesthetists have spent more than 5 hours giving anesthesia in the 93.2% of all anesthesia times in the first 10 hospitals, while 28.1% of the times in the last 10 hospitals. There were an average of 11.6 operating tables, in the first 10 hospitals. And we have analyzed ratios of the number of 5 day working persons to the number of operating tables. The ratio was 0.86 in the first 10 hospitals, while 0.21 in the last 10 hospitals. CONCLUSIONS: There must be overwork of 5-day working anesthetists, who are working for too many hours for anesthesia. It is necessary to have better quality service in the OR.

Anesthesia↗
PubMed1996

Novel marine di-Z-carotenoids: cucumariaxanthins A, B, and C from the sea cucumber Cucumaria japonica.

The novel marine carotenoids, cucumariaxanthins A (1), B (2), and C (3), were isolated from the northern sea cucumber Cucumaria japonica. Their structures and absolute stereochemistries were determined to be (5S,6S,5'S,6'S)-(9Z,9'Z)-5,6,5',6'-tetrahydro-beta,beta- carotene-4,4'-dione for 1; (5S,6S,4'S,5'S,6'S)-(9Z,9'Z)-4'-hydroxy-5,6,5',6'-tetrahydro-beta, beta- caroten-4-one for 2; and (4S,5S,6S,4'S,5'S,6'S)-(9Z,9'Z)-5,6,5',6'-tetrahydro-beta,beta-car otene-4,4'- diol for 3 by extensive spectroscopic analysis and by the modified Mosher's method. Cucumariaxanthin C showed an inhibitory effect on Epstein-Barr virus activation in a short-term in vitro assay.

Animals↗
PubMed1996

Measurement of the free form of TFPI antigen in hyperlipidemia. Relationship between free and endothelial cell-associated forms of TFPI.

Tissue factor pathway inhibitor (TFPI), a protease with three tandem Kunitz-type (K1, K2, and K3) domains, inhibits the initial reaction of the TF-mediated coagulation pathway. TFPI occurs in a free and a lipoprotein-associated form in plasma as well as an endothelial cell-associated form on vascular walls. In a previous study we had demonstrated that free-form TFPI activity was lower in hyperlipidemic patients. In the present study we established a new enzyme immunoassay method for measuring free-form TFPI antigen; this new method uses a monoclonal antibody that recognizes the K3 domain of free-form TFPI but not lipoprotein-associated TFPI. Free-form TFPI antigen was significantly lower in hyperlipidemic patients compared with those in normolipidemic individuals. We applied this new method to measure the amount of endothelial cell-associated TFPI, which can be released by heparin injection, as "free-form TFPI." We found that free-form TFPI antigen in plasma was positively correlated with the endothelial cell-associated form. These results indicate that both of these forms of TFPI are in equilibrium in vivo and that our new method can be used for assessing changes in the levels of endothelial cell-associated TFPI antigen and, hence, for assessing thrombotic tendencies in various disease states.

Adolescent↗
PubMed1996

Insulin resistance as an independent risk factor for carotid wall thickening.

It has been reported that insulin resistance is associated with essential hypertension and that an aggregation of risk factors-hypertension, dyslipidemia, and glucose intolerance-together with insulin resistance leads to the more frequent appearance of coronary artery disease. We examined the relation between early asymptomatic atherosclerosis and these risk factors in 72 nondiabetic subjects with essential hypertension (41 men, 31 women) aged 50 to 59 years. Intima-media thickness and plaque formation of the carotid artery were assessed by B-mode ultrasonography, and insulin sensitivity was measured by the steady-state plasma glucose method. Lipoprotein profile was analyzed by ultracentrifugation. The intima-media thickness of the common carotid artery significantly correlated with systolic pressure; mean blood pressure; steady-state plasma glucose, indicating insulin resistance; fasting insulin; area under the curve of plasma insulin and glucose; body mass index; apolipoprotein B; apolipoprotein B in low-density lipoprotein; lower ratio of cholesterol to apolipoprotein B of low-density lipoprotein; and decreased high-density lipoprotein cholesterol. By multiple regression analysis, steady-state plasma glucose was the strongest risk, followed by lower high-density lipoprotein and systolic pressure. These three factors accounted for 54.9% of all the risk for increased intima-media thickness of the common carotid artery. In conclusion, insulin resistance was the strongest risk factor for carotid intima-media thickness, followed by lower high-density lipoprotein cholesterol and hypertension. An effort to maintain normal insulin sensitivity is essential for the prevention of early atheromatous lesions in essential hypertension.

Arteriosclerosis↗
PubMed1996

Clinical impact of insulin resistance syndrome in cardiovascular diseases and its therapeutic approach.

In subjects with coronary artery diseases (obstructive and vasospastic angina pectoris (AP)) who have no diabetes, hypertension, obesity and physical inactivity, insulin sensitivity was significantly reduced with compensated hyperinsulinemia on OGTT. Insulin resistance significantly correlated with coronary atherosclerosis score. In vasospastic AP (VAP), those who fulfilled more than 3 risk factors out of 5 (hyperinsulinemia, obesity, glucose intolerance, hypertension, dyslipidemia) consist of 70 and 40% for smokers and nonsmokers respectively. Insulin resistance syndrome who fulfilled all the criteria was 9-10% for VAP. In atherothrombotic brain infarction (ATTI) with the same exclusion criteria, the similar insulin resistance and hyperinsulinemia have been observed, but not in embolic (cardiac origin) or lacunar infarction. In ATTI, high TG and apo B with low HDL-chol were noted in blood. In essential hypertension without diabetes and obesity, hyperinsulinemia was noted in 25-35% and insulin resistance in 56-88%. Reduction of blood pressure with alpha blocker (bunazosin), ACE inhibitor (cilazapril), long-acting Ca++ blocker (amlodipine) significantly improved lowered insulin sensitivity. Insulin resistance rather than hyperinsulinemia is more closely associated with blood pressure. Cardiovascular diseases (vasospastic and obstructive AP, brain cortical artery diseases) are prone to develop diabetes because of insulin resistance and also promote the generation of cumulative risk factors resulting in a vicious cycle. Efforts to alleviate insulin resistance is crucial for the primary and secondary prevention of cardiovascular diseases.

Adrenergic alpha-Antagonists↗
PubMed1996

Effects of simvastatin on the number and composition of apoproteinB-containing lipoproteins in hypercholesterolemia: analysis of apoproteinB in each lipoprotein fraction by highly sensitive latex method.

We investigated the effects of simvastatin on the number and composition of apoproteinB (apoB)-containing lipoproteins in thirteen patients with hypercholesterolemia type IIa or IIb by measuring apoB by a highly sensitive latex method. Patients received simvastatin 5-10 mg (7.7 +/- 0.7 mg, mean +/- SEM) daily for 83-218 days (131 +/- 13 days). In both types of patients, treatment with simvastatin significantly reduced plasma cholesterol levels (mean +/- SEM mg/dl: in type IIa from 234.4 +/- 5.4 to 171.4 +/- 7.8, in type IIb from 242.4 +/- 11.6 to 178.8 +/- 9.6), low density lipoprotein (LDL) cholesterol levels (from 122.6 +/- 5.2 to 68.5 +/- 4.6, and from 115.6 +/- 14.0 to 70.4 +/- 11.6 in the two types, respectively) and LDL apoB levels (from 94.5 +/- 6.6 to 60.6 +/- 7.0, and from 85.0 +/- 8.4 to 56.6 +/- 6.2, respectively). There was no significant change in cholesterol, triglyceride (TG) or apoB in very low density lipoprotein (VLDL). High density lipoprotein (HDL) cholesterol did not change in this study. With respect to lipoprotein composition, the ratio of either cholesterol or TG to apoB in VLDL, intermediate density lipoprotein (IDL) and LDL did not change significantly, but that of TG to apoB in the IDL fraction increased in type IIa. Simvastatin promotes more effective reduction in cholesterol and apoB in LDL than in VLDL, probably by increasing the hepatic LDL receptor which preferentially binds LDL.

Adult↗
PubMed1996

Quantitative and qualitative derangement of apolipoprotein B-containing lipoproteins as a risk factor for diabetic macroangiopathy in nonobese NIDDM subjects.

Cholesterol, triglyceride (TG), and apolipoprotein (apo) B were determined in plasma and in lipoprotein subfractions (VLDL, intermediate-density lipoproteins [IDL], LDL, and HDL) in nonobese NIDDM subjects, who were classified into well-controlled, fairly controlled, or poorly controlled states with or without macrovascular complications (macroangiopathy [MA]). The same analyses were also performed on subjects who had coronary artery disease (CAD) with stable angina pectoris (SA) or unstable angina pectoris (UA) and acute myocardial infarction, cerebrovascular disease (CVD) with atherothrombotic or lacunar infarction, and arteriosclerosis obliterans (ASO). In nonobese NIDDM subjects, the number of apoB-containing lipoproteins (VLDL, IDL, and LDL) increased. This alteration was more prominent in subjects with poorly or fairly controlled disease as well as in subjects with MA, but not in those with well-controlled NIDDM. Cholesterol/apoB in LDL decreased in subjects with poorly or fairly controlled diabetes or with MA and was correlated with low HDL cholesterol. The disorder is characterized by hyperbetalipoproteinemia with elevated LDL cholesterol and small dense LDL. In obese NIDDM subjects, the similar disorder was more pronounced. Glycemic control had less effect and hyperinsulinemia, if present, aggravated the lipid disorder. In those with CAD, the number of IDLs increased and the LDL fraction had the properties of small dense LDL. HDL cholesterol decreased. In those with UA, the LDL number increased without elevation of LDL cholesterol, indicating typical hyperbetalipoproteinemia. The subjects with atherothrombotic brain infarction, an increased number of small-sized LDLs was noted. In those with ASO, the number of VLDL and IDL increased with small LDL. HDL cholesterol decreased in those with CAD, cerebrovascular disease, and ASO. Since similar quantitative and qualitative alterations of apoB-containing lipoprotein have been observed in NIDDM patients as well as in those with macrovascular diseases, diabetic patients are thought to be more susceptible to the initiation and progression of atheromatous lesions in coronary, brain, and peripheral arteries.

Adult↗
PubMed1996

Mechanism and clinical implication of insulin resistance syndrome.

The insulin resistance syndrome has been noted as an interesting and important new risk factor for coronary artery disease. The syndrome consists of hypertension, glucose intolerance, and dyslipidemia, all of which are likely to be derived from insulin insensitivity. In subjects with nonobese and nondiabetic essential hypertension, steady-state plasma glucose (SSPG) was higher than in normotensive subjects during an insulin sensitivity test, indicating reduced insulin sensitivity to glucose metabolism in the hypertensive group. SSPG correlated with the percentage decrease of branched chain amino acids, free fatty acids, and serum potassium during the insulin sensitivity test. With a 2-h insulin infusion, serum norepinephrine, epinephrine, plasminogen activator inhibitor 1, and intraplatelet Ca2+ decreased significantly, but 6-keto-prostaglandin (PG) F1 alpha and PGE2 did not change. Insulin resistance decreased by using antihypertensive treatments with bunazosin, cilazapril, amlodipine, and benidipine in hypertensive subjects. Diagnostic criteria for the insulin resistance syndrome, including clinical values for each risk factor, were developed. Lowered insulin sensitivity and hyperinsulinemia were demonstrated in subjects with both vasospastic and coronary artery stenotic angina. The insulin resistance syndrome together with hyperinsulinemia is likely to induce atherosclerotic changes, possibly through reduced rather than excessive action of insulin.

Angina Pectoris↗
PubMed1995

Insulin resistance associated with compensatory hyperinsulinemia as an independent risk factor for vasospastic angina.

BACKGROUND: It is generally believed that coronary artery spasm plays an important role in the progression of obstructive coronary artery disease. Since insulin resistance together with hyperinsulinemia plays an important role in the pathogenesis of coronary atherosclerosis, we investigated the association of hyperinsulinemia and insulin resistance with vasospastic angina (VAP). METHODS AND RESULTS: The study population consisted of 60 patients with VAP and 42 control subjects (62 subjects with normal glucose tolerance and 40 with impaired glucose tolerance). Insulin sensitivity was determined by the steady-state plasma glucose (SSPG) method for nondiabetic, normotensive, nonobese subjects (16 control subjects, 16 obstructive coronary artery disease patients, and 16 VAP patients). Compared with the control group, the 2-hour insulin area (area under the plasma insulin concentration-time curve) during a 75-g oral glucose tolerance test was significantly higher in both VAP groups with normal and impaired glucose tolerance. A high frequency of vasospastic angina was observed in subjects with clustered risk factors for insulin resistance syndrome, suggesting a close association of VAP with this syndrome. In stepwise discriminant analysis, the 2-hour insulin area was significantly associated with VAP independent of other risk factors. SSPG level in VAP was about twofold over control, indicating the presence of insulin resistance in patients with VAP. However, no differences were found between patients with VAP and obstructive coronary artery disease with respect to mean SSPG level. CONCLUSIONS: SSPG level was significantly elevated in patients with VAP and obstructive coronary artery disease compared with control subjects. This indicates that hyperinsulinemia is secondary to insulin resistance, both of which are thought to play important roles as risk factors for VAP in the early atheromatous lesion and in the future development of occlusive lesions when chronically present.

Angina Pectoris, Variant↗
PubMed1995

Different apheresis methods in the treatment of hypercholesterolemia in primary biliary cirrhosis: a case report.

The two different modes of low-density lipoprotein (LDL) apheresis, cascade filtration (CF) and dextran-sulfate cellulose (DSC) adsorption, were compared for efficiency of cholesterol removal in a patient with severe hypercholesterolemia due to primary biliary cirrhosis (PBC). Decrement in the total cholesterol level by the DSC method was less than that by the CF method. Apolipoprotein B was decreased to almost null by both modules whereas the decrease in albumin was much greater in the second filter of the CF method than in the DSC column. Lipoprotein X which constituted the major portion of serum cholesterol in PBC became negative by passing plasma through the second filter. The CF method was preferred to the DSC method for removal of lipoprotein X, but albumin substitution was mandatory to prevent the decrease of serum albumin in the CF method.

Adult↗