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T Miida

Publications and source records attributed to T Miida.

At least 55 records · Page 3Linked to original sources
PubMed1996

[Postural change and within-day variation in total cholesterol and high-density lipoprotein-cholesterol levels].

To clarify whether the effect of the postural change on lipid levels can be corrected after the adjustment of albumin levels, and if so, whether there is within-day variation in corrected lipid levels, we measured total cholesterol (TC), high-density lipoprotein-cholesterol (HDL-C), and albumin levels before and after 60 min of the supine posture in 6 volunteers. We also measured the same variables before and after meals and at midnight in 30 inpatients with diabetes mellitus. We found that TC levels decreased by -7.7 +/- 2.7% (p < 0.005), and HDL-C by -5.8 +/- 5.3% (p < 0.05) after 60 min of the supine posture. The decreases disappeared after the adjustment of albumin to the baseline levels (TC; -0.2 +/- 1.0%, HDL-C; -1.7 +/- 4.2%, not significant). The within-day variation decreased from 10.9 +/- 4.9% to 5.8 +/- 2.2% in TC, and from 13.8 +/- 4.7% to 9.5 +/- 3.9% in HDL-C after the albumin adjustment. Corrected TC levels were, however, significantly lower after breakfast through at midnight than those before breakfast. This study indicates that the postural changes in lipid levels can be corrected after the adjustment of albumin levels, and that there is within-day variation in corrected TC levels. These findings suggest that the timing of sampling should be standardized for TC measurement in the management of diabetes mellitus with hypercholesterolemia.

Adult↗
PubMed1996

[Abnormality of HDL subfractions in cholesteryl ester transfer protein deficiency].

High-density lipoprotein (HDL) in cholesteryl ester transfer protein (CETP) deficiency is deficient in reverse cholesterol transport although HDL-cholesterol levels markedly increase in such patients. This may be responsible for the abnormal metabolism of pre beta 1-HDL, the initial acceptor of cell-derived cholesterol. To answer this question, we determined HDL subfraction levels in 8 CETP deficiency and 21 normolipidemic subjects. We also measured the rate of decrease in pre beta 1-HDL level by LCAT activity during the incubation at 37 degrees C for 90 min. We found that HDL2b was 2.4 times higher in CETP deficiency than in control [52.2 +/- 14.3, vs. 21.5 +/- 9.8% of plasma apoA-I(%AI), p < 0.005] while HDL2a and HDL3 were significantly lower in the former than in the latter (HDL2a; 25.5 +/- 8.0 vs. 40.4 +/- 6.5% AI, p < 0.005) (HDL3; 10.0 +/- 6.8 vs. 28.3 +/- 5.9% AI, p < 0.005). There were no significant differences in pre beta 1-HDL level between 2 groups (4.9 +/- 3.0 vs. 4.5 +/- 2.3% AI, NS). However, the rate of decrease in pre beta 1-HDL was significantly less in CETP deficiency than in control (-33.2 +/- 22.9 vs. -73.7 +/- 12.2%, p < 0.005). In conclusion, the metabolism of pre beta 1-HDL is delayed in CETP deficiency. It is suggested that the esterification of cell-derived cholesterol removed by pre beta 1-HDL may be deficient in CETP deficiency.

Apolipoproteins↗
PubMed1996

Pre beta 1-high-density lipoprotein increases in coronary artery disease.

Pre beta 1-HDL promotes cholesterol efflux from cell membranes. Its plasma concentration is regulated by lecithin: cholesterol acyltransferase (LCAT). To clarify whether the concentration of pre beta 1-HDL changes in coronary artery disease (CAD), we determined the distribution of apolipoprotein A-I (apoA-I) among HDL subfractions in 20 CAD patients and 20 healthy controls, using nondenaturing two-dimensional gel electrophoresis. We found that CAD patients had significantly higher concentrations of pre beta 1-HDL than the controls [7.6% +/- 3.4% vs 4.6% +/- 2.3% of apoA-I (P < 0.01)]. Even after correcting for apoA-I concentrations, this increase remained significant [87 +/- 37 vs 63 +/- 28 mg/L apoA-I (P < 0.05)]. The mean LCAT concentration was significantly lower (P < 0.05) in CAD patients than in controls. These findings, that pre beta 1-HDL concentrations increase in CAD, strongly suggest that the process of reverse cholesterol transport could be altered in CAD.

Aged↗
PubMed1995

Effects of modified low density lipoprotein and hypoxia on the expression of endothelial leukocyte adhesion molecule-1.

OBJECTIVES: Expression of endothelial leukocyte adhesion molecule (ELAM-1 or CD62E) plays a role as an early event of atherogenesis. It is well known that interleukin-1 (IL-1) expresses ELAM-1 on vascular endothelial cells. We have examined pathological factors that induce ELAM-1 expression on cultured endothelial cells. METHODS: Examined factors were native low density lipoprotein (LDL), oxidized LDL, glycated LDL, hypoxia, and IL-1. Peroxidation of LDL was performed by ultraviolet radiation. Hypoxia was reproduced by adding a hypoxic cell-culture medium that was deoxygenated by use of a vacuum pump and nitrogen gas. Endothelial cells were harvested from a porcine aorta and were allowed to proliferate to be subconfluent in slide chambers. Expression of ELAM-1 was evaluated by counting the number of cells that were characterized by positive staining with the immunohistochemical technique. RESULTS: Without any stimulants, about 6.9% of the endothelial cells expressed ELAM-1. Weakly oxidized LDL (12 pmol/micrograms protein) significantly expressed ELAM-1 (14.8%) after an incubation period of 1 hour. Glycated LDL induced significant expressions (12.6%) in a fructosamine concentration of 65 pmol/micrograms protein. A one-hour incubation with a hypoxic culture medium expressed ELAM-1 in 16.3% of the cells. Native LDL did not cause any significant increases in the percentage. IL-1 expressed ELAM-1 in 30% of the cells even with as low a concentration as 3.1 U/ml. CONCLUSIONS: The present study shows that not only IL-1 but also weakly oxidized LDL, glycated LDL, and hypoxia may be possible factors that cause the expression of ELAM-1.

Animals↗
PubMed1995

A case of unprotected left main coronary stenosis rescued by directional coronary atherectomy as a last resort.

The prognosis of left main coronary stenosis complicating cardiogenic shock is very poor. Unprotected left main coronary stenosis usually preclude percutaneous transluminal coronary angioplasty because of the appearance of elastic recoil and the risk of hemodynamic collapse after acute closure of the artery. An 85-year-old woman with no history of heart disease developed cardiogenic shock. Coronary arteriography showed an unprotected left main coronary stenosis. Due to her advanced age, her family opposed coronary artery bypass surgery. We report here the successful treatment of this case of unprotected left main coronary stenosis by directional coronary atherectomy as a last resort.

Aged↗
PubMed1994

Additional ST-segment elevation immediately after reperfusion and its effect on myocardial salvage in anterior wall acute myocardial infarction.

Rapid resolution of ST-segment elevation is a reperfusion-associated electrocardiographic change in acute myocardial infarction. However, some patients have additional ST-segment elevation immediately after reperfusion before such resolution. The clinical significance and the effect on myocardial salvage of this electrocardiographic change are unknown. To examine this electrocardiographic feature and determine its clinical basis for occurrence and influence on left ventricular function, 58 consecutive patients with a first anterior wall acute myocardial infarction who had intracoronary thrombolysis or coronary angioplasty, or both, were assessed. With the use of frequent electrocardiographic procedures during reperfusion therapy, patients were divided in 2 groups: those with additional ST-segment elevation (n = 35; group A, > or = 0.5 mV increase in summed ST-segment elevation in lead V1-V6 within 15 minutes after reperfusion), and those without this phenomenon (n = 23; group B). Baseline characteristics, creatine kinase kinetics and left ventricular function were compared between both groups. Before reperfusion, group A had a greater summed ST-segment elevation (2.44 +/- 1.07 vs 1.57 +/- 0.98 mV; p = 0.003) and poorer collaterals (p = 0.001) than did group B. Peak creatine kinase was significantly higher in group A than in B (6,550 +/- 3,477 vs 4,310 +/- 1,880 IU/liter; p = 0.003). Group A had less improvement in ejection fraction (-4.2 +/- 9.9% vs 1.7 +/- 9.6%; p = 0.04) and regional wall motion (0.28 +/- 0.74 vs 0.76 +/- 0.79 SD/chord; p = 0.03) than did group B. It is thought that additional ST-segment elevation immediately after reperfusion occurred in myocardium with severe ischemic damage before reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Acute occlusion due to coronary dissection as a PTCA complication resolved by reentry achieved by pulling an inflated balloon in the true lumen.

We experienced 2 patients in whom conventional percutaneous methods were not useful for acute occlusions sequel to coronary angioplasty. Acute occlusions seemed to be caused by large dissections. Pulling an inflated balloon at the dissected lesions achieved reentry from the false lumen to the true lumen, thus resolving collapse of the true lumen and recanalizing the occluded coronary artery.

Angioplasty, Balloon, Coronary↗
PubMed1993

Quantitation of pre beta-HDL-dependent and nonspecific components of the total efflux of cellular cholesterol and phospholipid.

Both receptor-mediated and diffusional processes have been proposed as mechanisms for the efflux of cellular cholesterol to plasma. The depletion of a minor high-density lipoprotein subfraction (pre beta-1-HDL) from plasma by incubation was associated with a proportional reduction in up to 58% of cholesterol and lecithin efflux from cultured fibroblasts. Pre beta-HDL-dependent efflux was blocked by protease pretreatment of the cells, while residual ("nonspecific") efflux was protease-insensitive. The whole of cholesterol efflux from blood erythrocytes was both pre beta-1-HDL-and protease-independent. These data suggest that two distinct pathways contribute to total efflux from fibroblast monolayers; one of these is directly proportional to plasma pre beta-1-HDL concentration and may involve a cell-surface protein.

Cells, Cultured↗
PubMed1993

Coronary perforation to the left ventricular cavity by a guide wire during coronary angioplasty.

We describe a case in which the guide wire penetrated through the left anterior descending artery into the left ventricular cavity during percutaneous transluminal coronary angioplasty. This complication of coronary angioplasty which had not been previously reported was suspected because of the characteristic motion of the guide wire on the X-ray image and was confirmed by echocardiography.

Angioplasty, Balloon, Coronary↗
PubMed1993

High-output heart failure in mitochondrial myopathy: a fulminant form with severe lactic acidosis and rhabdomyolysis.

A 17-year-old male with mitochondrial myopathy was transferred to our hospital because of respiratory distress and a rapidly deteriorating level of consciousness. He had a markedly increased cardiac output with low systemic vascular resistance and decreased arteriovenous oxygen difference. Severe lactic acidosis, rhabdomyolysis and acute renal failure were also present. He was treated in the intensive care unit with continuous hemofiltration and hemodialysis. This case demonstrates that cardiac failure in mitochondrial encephalomyopathy may be caused by myocardial abnormalities as well as by reduced systemic vascular resistance secondary to disturbed oxidative metabolism.

Acidosis, Lactic↗
PubMed1992

Regulation of the concentration of pre beta high-density lipoprotein in normal plasma by cell membranes and lecithin-cholesterol acyltransferase activity.

A minor fraction of plasma high-density lipoprotein (pre beta-1 HDL) has been shown to promote cholesterol efflux from peripheral cell membranes [Castro, G. R., & Fielding, C. J. (1988) Biochemistry 27, 25-29]. When isolated native plasma is incubated at 37 degrees C, this fraction is specifically decreased. On the other hand, the level of plasma pre beta-1 HDL is fully protected in the presence of even very low levels of fibroblasts, vascular smooth muscle cells, or macrophages. Blood cells were completely inactive in maintaining plasma pre beta-1 HDL levels in the absence of peripheral cells, even at the relatively high levels present in whole blood. The loss of pre beta-1 observed in isolated plasma was dependent upon lecithin-cholesterol acyltransferase (LCAT) activity. These data suggest that reverse cholesterol transport catalyzed by pre beta-1 HDL, and subsequent LCAT-mediated cholesterol esterification, is directly dependent upon the interaction between this HDL species and competent peripheral cells.

Cell Membrane↗
PubMed1992

Precordial ST segment elevation in acute ischemia caused by right coronary artery occlusion.

The purpose of this study is to determine why precordial ST elevation (V1 lead) occurs during acute occlusion of the right coronary artery (RCA). Nineteen patients with vasospastic angina, in whom ergonovine administration into RCA provoked spasms, were divided into 2 groups by precordial ST change during spasms. Group I (n = 6) had precordial ST elevation; group II (n = 13) had no precordial ST elevation. A subgroup, IIA was comprised 6 patients in group II with spasms in the RCA proximal segment (segment number less than 2 of AHA coronary classification). None had left coronary dominancy. There was no difference in collateral flow during spasms. Location of spasms in group I was in the RCA proximal segment, and was significantly more proximal compared to group II. There was no difference in sigma ST in II, III, aVF between group I and II or IIA. Max ST elevation time by which duration of ischemia was estimated was significantly longer in group I than in group IIA. Three patients in group I displayed precordial ST depression before elevation, in all of whom in sigma ST in II, III, aVF was higher during precordial ST elevation than during depression. During acute occlusion in the RCA proximal segment, precordial ST elevation is caused by ischemia of the right ventricular anterior wall. Furthermore, precordial ST elevation can occur in a patient with RCA dominance, even if ischemic injury in the left ventricular infero-posterior wall increases progressively.

Acute Disease↗
PubMed1991

Metabolism of low-density lipoprotein free cholesterol by human plasma lecithin-cholesterol acyltransferase.

The metabolism of cholesterol derived from [3H]cholesterol-labeled low-density lipoprotein (LDL) was determined in human blood plasma. LDL-derived free cholesterol first appeared in large alpha-migrating HDL (HDL2) and was then transferred to small alpha-HDL (HDL3) for esterification. The major part of such esters was retained within HDL of increasing size in the course of lecithin-cholesterol acyltransferase (LCAT) activity; the balance was recovered in LDL. Transfer of preformed cholesteryl esters within HDL contributed little to the labeled cholesteryl ester accumulating in HDL2. When cholesterol for esterification was derived instead from cell membranes, a significantly smaller proportion of this cholesteryl ester was subsequently recovered in LDL. These data suggest compartmentation of cholesteryl esters within plasma that have been formed from cell membrane or LDL free cholesterol, and the role for HDL2 as a relatively unreactive sink for LCAT-derived cholesteryl esters.

Carrier Proteins↗
PubMed1991

[Transient increase in ST-segment elevation immediately after reperfusion in acute myocardial infarction].

The significance of transient increase in ST-segment elevation immediately after reperfusion in acute myocardial infarction (AMI) was assessed by 12-lead electrocardiography. The study population consisted of 18 patients with initial anterior AMI, whose totally-occluded left anterior descending arteries were reperfused within 6 hours after the onset of symptoms. The ST-segment elevation was defined as that of more than 0.2 mV in the V3 lead immediately after reperfusion. Collateral circulation, timing of reperfusion, CPK release, left ventricular ejection fraction and mean % 201Tl uptake in the infarct regions were compared between patients with and without ST elevation. Eleven patients (61%) had ST-segment elevation (0.61 +/- 0.29 mV). Well-developed collaterals were observed in 43% of patients without ST-segment elevation (p < 0.05) but not in those with ST elevation. ST-segment elevations were accompanied by delays in timing of reperfusion (3.7 +/- 1.2 hrs vs 2.5 +/- 0.9 hrs, p < 0.05), higher peak CPK values (6,190 +/- 3,156 IU/l vs 3,222 +/- 2,053 IU/l, p < 0.05) and lower mean % 201Tl uptake (54.2 +/- 11.4% vs 73.9 +/- 11.3%, p < 0.01). We concluded that transient increase in ST-segment elevation immediately after reperfusion may relate to poorly-developed collaterals and prolongation of ischemia; i.e., severe ischemia before reperfusion, and therefore may reflect myocardial reperfusion injuries.

Collateral Circulation↗
PubMed1990

Mechanism of transfer of LDL-derived free cholesterol to HDL subfractions in human plasma.

The transfer of [3H]cholesterol in low-density lipoprotein (LDL) to different high-density lipoprotein (HDL) species in native human plasma was determined by using nondenaturing two-dimensional electrophoresis. Transfer from LDL had a t1/2 at 37 degrees C of 51 +/- 8 min and an activation energy of 18.0 kCal mol-1. There was unexpected specificity among HDL species as acceptors of LDL-derived labeled cholesterol. The largest fraction of the major alpha-migrating class (HDL2b) was the major initial acceptor of LDL-derived cholesterol. Kinetic analysis indicated a rapid secondary transfer from HDL2b to smaller alpha HDL (particularly HDL3) driven enzymatically by the lecithin-cholesterol acyltransferase reaction. Rates of transfer among alpha HDL were most rapid from the largest alpha HDL fraction (HDL2b), suggesting possible protein-mediated facilitation. Simultaneous measurements of the transport of LDL-derived and cell-derived isotopic cholesterol indicated that the former preferably utilized the alpha HDL pathway, with little label in pre-beta HDL. The same experiments confirmed earlier data [Castro, G.R., & Fielding, C.J. (1988) Biochemistry 27, 25-29] that cell-derived cholesterol is preferentially channeled through pre-beta HDL. We suggest that the functional heterogeneity of HDL demonstrated here includes the ability to independently process cell- and LDL-derived free cholesterol.

Cholesterol↗
PubMed1990

Treatment of unstable angina with cholesterol embolization as a complication of left heart catheterization.

We describe 3 patients with cholesterol embolization after left heart catheterization via the femoral route. The left catheterizations were performed via the femoral route in all reported cases in which cholesterol embolization occurred as a complication of left catheterization. Postmortem examinations reveal that PTCA, using the right brachial approach, is the safest method for treatment of intractable angina in patients with evidence of cholesterol embolization.

Aged↗