Hyperlipidemias: Miura T

Shimamoto K, Miura T. · Second Department of Internal Medicine, Sapporo Medical University. · Nippon Rinsho. · Pubmed #17824086 No free full text.

This publication has no abstract.

Shimamoto K, Miura T. · Second Department of Internal Medicine, Sapporo Medical University, School of Medicine. · Nippon Rinsho. · Pubmed #16981585 No free full text.

This publication has no abstract.

Nakamura Y, Saitoh S, Takagi S, Ohnishi H, Chiba Y, Kato N, Akasaka H, Miura T, Tsuchihashi K, Shimamoto K. · Second Department of Internal Medicine, Sapporo Medical University, Japan. · Circ J. · Pubmed #17186973 links to  free full text

Abstract: BACKGROUND: The degree to which abnormal glucose tolerance contributes to the development of coronary artery disease (CAD) has not been clarified in Japanese. The relationship between abnormal glucose tolerance and severity of coronary artery stenosis, as well as the contributions of hypertension, diabetes and other risk factors for CAD to recurrence of the disease, were investigated in the present study. METHODS AND RESULTS: The subjects were 474 consecutive patients (mean age: 63.8+/-11.3 years) with suspected CAD who were admitted to Sapporo Medical University Hospital during April 1, 1997 to March 31, 2004. The coronary index and stenosis score were higher in subjects with diabetes mellitus (DM) and in subjects with impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) than in subjects with normal glucose tolerance (NGT). Ischemic episodes recurred during the observation period (mean 2.5 years) in 61 of 341 patients diagnosed as having CAD. In the follow-up subjects, systolic blood pressure (SBP) was significantly higher in the recurrence group than in the non-recurrence group, and SBP was a significant variable in logistic regression analysis after adjustment for age, gender, hemoglobin A1c, total cholesterol, body mass index, smoking history, family history and stenosis score. The relative risk of recurrence became 1.7-fold higher with a rise in SBP of 10 mmHg (95% confidence interval: 1.252-2.250). Analysis of the relationship between glucose tolerance and recurrence showed that the rate of recurrence was higher in patients with IFG+IGT+DM than in those with NGT. CONCLUSIONS: CAD progresses not only in patients with DM but also in those with IGT. The rate of recurrence of ischemic episodes increases in individuals with IGT or DM, and suggesting that hypertension is a risk factor for recurrence of ischemic episodes. Management of glucose tolerance and blood pressure is therefore important for prevention of CAD in Japanese.

Fujiwara T, Saitoh S, Takagi S, Takeuchi H, Isobe T, Chiba Y, Miura T, Shimamoto K. · Second Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan. · Hypertens Res. · Pubmed #16392771 No free full text.

Abstract: It is unclear whether the role of insulin resistance in the development of atherosclerotic cardiovascular disease is similar in populations in which the incidence of atherosclerotic diseases significantly differs from that in Western countries. The aim of this study was to determine the relationship between insulin resistance and the development of cardiovascular disease in the Japanese population. We conducted 75 g-oral glucose tolerance tests (OGTTs) on 1,928 inhabitants of two towns in Hokkaido, Japan. Subjects using antihypertensive agents and known diabetic patients were excluded from the study. Data from the remaining 1,227 subjects (540 males and 687 females; mean age 56.0 +/- 10.8 years) were used for the analysis, and 1,051 subjects were seen in a follow-up care setting for a period of 8 years. The presence of insulin resistance was defined according to the guidelines reported our previous study: insulin levels of 64.0 mU/l or higher 2 h after the 75 g-OGTT. The insulin-resistant (IR) group had several risk factors such as hypertension, diabetes, treated or untreated hypercholesterolemia, hypertriglyceridemia, low high-density-lipoprotein (HDL) cholesterol levels, and obesity. During the follow-up period of 8 years, the incidence of coronary artery disease, which was adjusted for age, body mass index, sex, systolic blood pressure, fasting plasma glucose, total cholesterol, triglyceride, and HDL cholesterol was significantly (3.2 times) higher in the IR group than in the insulin non-resistant group. The results suggested that insulin resistance is an independent risk factor for coronary artery disease in Japanese subjects, as has also been demonstrated in the case of individuals in Europe and USA.

Genda S, Miura T, Miki T, Ichikawa Y, Shimamoto K. · Second Department of Internal Medicine, Sapporo Medical University, Sapporo, Japan. · J Am Coll Cardiol. · Pubmed #12383584 No free full text.

Abstract: OBJECTIVE: This study aimed to clarify the role of adenosine triphosphate-sensitive K(+) (K(ATP)) channels in the no-reflow phenomenon and in its extension by hypercholesterolemia. BACKGROUND: The no-reflow phenomenon is an important target of therapy in patients with acute myocardial infarction, but its mechanism remains unclear. METHODS: The left circumflex coronary artery was occluded for 30 or 60 min and reperfused in rabbit hearts in situ. The no-reflow zone, area at risk, and infarct size were determined by thioflavin-S, Evans blue, and tetrazolium staining, respectively. No-reflow zone size was expressed as a percentage of infarct size (%NR/IS). Hypercholesterolemia was induced by two weeks of cholesterol-enriched diet. RESULTS: A K(ATP) channel blocker, glibenclamide (0.3 mg/kg), increased %NR/IS after 30-min ischemia/90-min reperfusion from 33.6 +/- 1.9% to 45.9 +/- 1.6% and %NR/IS after 60-min ischemia/90-min reperfusion from 32.8 +/- 3.4% to 46.1 +/- 1.7%. However, N(G)-monomethyl-L-arginine (L-NMMA), a nitric oxide (NO) synthase inhibitor, and nicorandil, a hybrid of K(ATP) channel opener and nitrate, failed to significantly modify %NR/IS. Hypercholesterolemia increased %NR/IS to 61.6 +/- 0.6%, which was not further enlarged by glibenclamide, and delayed infarct healing during the subsequent five days of reperfusion. These effects of hypercholesterolemia were significantly suppressed by nicorandil. Neither glibenclamide, L-NMMA, nicorandil, nor hypercholesterolemia modified infarct size. CONCLUSIONS: The K(ATP) channel activation, but not NO, is a major mechanism of protection against microvascular injury, causing the no-reflow phenomenon in the heart. Suppression of K(ATP) channel opening may underlie the hypercholesterolemia-induced extension of no-reflow, which delays infarct healing.