Aim: We previously found, using a mouse model, that activation of proinflammatory cytokines after acute myocardial infarction (AMI) augments neointimal hyperplasia of a remote artery. The present study assessed the progression of luminal narrowing of non-culprit coronary arteries (NCCA) in patients following AMI.
Methods: The study group comprised 21 AMI patients successfully treated with bare-metal stents and 16 stable angina (SA) patients treated with sirolimus-eluting stents. Clinical backgrounds were similar for both groups. Quantitative coronary angiography was performed before and after stent implantation and at 6-months of follow-up.
Results: We evaluated 126 non-culprit coronary segments (73 in AMI and 53 in SA). The minimum lumen diameter (MLD) (mm) of NCCA decreased significantly from 2.61±0.79 to 2.44±0.71 in the AMI group, but changed only slightly from 2.02±0.56 to 2.02±0.50 in the SA group. The absolute change in the MLD of NCCA was significantly greater (0.17±0.53) in the AMI, than in the SA (0.0070±0.261) group.
Conclusion: luminal narrowing of non-culprit coronary segments progressed in AMI patients within 6 months of stent implantation, but progressed only slightly in SA patients.

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Aim: There is limited information on how dietary carbohydrate restriction (CR) or the combination of dietary cholesterol (chol) and CR may affect atherosclerosis development. Guinea pigs were used to evaluate the effects of chol and CR on aortic cholesterol accumulation, mechanical properties of aortas and cytokine production.
Methods: Ten male guinea pigs were fed either low (L) or high (H) chol in combination with CR or high carbohydrate (control) for 12 wk.
Results: Groups fed the high chol (control-H and CR-H) had significantly higher concentrations of cholesterol in aortas and higher activity of serum phospholipase A2 than the L groups. CR resulted in significantly lower concentrations of small LDL particles and aortic cytokines and chemokynes than the control groups. Aortas from the control-H and the CR-L were stiffer than those from the control-L and the CR-H groups. This finding could be explained by the reduction in arterial stiffness during the early stages of atherosclerotic.
Conclusion: these results demonstrate that CR has a major impact on atherogenicity.

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Aim: We established a monitoring system for the annual follow-up of blood chemistry data obtained by the National Health and Nutrition Survey in Japan.
Methods: Blood chemistry testing has been entrusted to SRL Inc. We used two external quality control assurance programs established by the Japan Medical Association (JMA) and by CDC/CRMLN during the previous 8-year period. Ten analytes were measured: total cholesterol, HDL cholesterol, triglycerides, urea nitrogen, uric acid, creatinine, AST (GOT), ALT (GPT), γ-GT (γ-GTP), and glucose. Total error (TE) was calculated from accuracy by the JMA program and precision by internal quality control of SRL. The permissible range of TE values was determined to be 50% of the evaluation limit on one side in the evaluation criteria of the College of American Pathologists (CAP). When TE fell within the permissible range, the follow-up of annual changes was considered possible.
Results: Annual follow-up of blood chemistry data was considered possible for all the analytes except urea nitrogen. Based on this study, new permissible TE ranges are proposed.
Conclusion: We confirmed the functioning of the monitoring system for the annual follow-up of blood chemistry data obtained by the National Health and Nutrition Survey in Japan.

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Aim: Recent evidence suggests that small dense low-density lipoprotein (sd-LDL) particles are more atherogenic than large-LDL in spite of their lower cholesterol content. This study aimed to determine whether sd-LDL-cholesterol (sd-LDL-C) is superior to LDL-C as a biomarker of coronary heart disease (CHD).
Methods: LDL particle size determined by gradient gel electrophoresis and sd-LDL-C concentrations quantified by heparin-magnesium precipitation were compared between 482 stable CHD patients and 389 non-diabetic subjects without CHD who were not receiving any lipid-lowering drugs.
Results: Both male and female CHD patients had significantly smaller LDL particles and lower large-LDL-C concentrations (estimated by subtracting the sd-LDL-C concentration from the LDL-C concentration), and significantly higher sd-LDL-C concentrations than the control subjects. LDL-C concentrations were modestly higher and sd-LDL-C concentrations were significantly higher in 258 patients with angiographically documented severe CHD than in the patients with mild CHD irrespective of treatment by LDL-lowering drugs and history of myocardial infarction and/or coronary revascularization. Large-LDL-C concentrations, in contrast, were similar between the two groups. Multivariate logistic regression analysis revealed that sd-LDL-C levels were significantly associated with severe CHD independently of LDL-C.
Conclusion: sd-LDL-C levels are more powerful than LDL-C levels for the determination of severe stable CHD.

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Aim: Pulse wave velocity has been used as an index of aortic stiffness. Recently, the cardio-ankle vascular index (CAVI), which reflects the stiffness of the aorta independently of blood pressure, has been developed. In this study, we analyzed the relationship between CAVI and left ventricular (LV) diastolic dysfunction.
Methods: A total of 119 patients were referred for echocardiography to evaluate ventricular function. Patients with reduced systolic function were excluded. Patients were divided on the basis of normal or reduced LV diastolic function determined by echocardiography. CAVI was measured using an automatic waveform analyzer.
Results: CAVI was significantly higher in patients with reduced LV diastolic function than those with normal LV diastolic function (9.0±1.1 and 8.5±1.1, p=0.009). Multiple linear regression analysis revealed that CAVI was independently associated with the ratio of peak early diastolic velocity to peak atrial diastolic velocity and left atrial diameter. When patients were classified on the basis of CAVI quartiles, multiple logistic regression analysis demonstrated that the highest quartile of CAVI showed an increased odds ratio for the presence of LV diastolic dysfunction.
Conclusion: The present study revealed that an increased CAVI was independently associated with LV diastolic dysfunction in patients with preserved systolic function.

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Aim: We previously reported that glycemic control deteriorated in patients receiving atorvastatin, which is useful for the treatment of hypercholesterolemia in patients with type 2 diabetes. Pitavastatin has a strong lipid-lowering effect, comparable to that of atorvastatin, but it is unknown whether pitavastatin has an adverse influence on glycemic control. The aim of this study was to examine. The effects of three different statins (pravastatin, atorvastatin, and pitavastatin) on blood glucose and HbA_1C levels in diabetic patients.
Methods: We retrospectively compared glycemic control between groups receiving atorvastatin (10 mg/day, group A, n=99), pravastatin (10 mg/day, group Pr, n=85), and pitavastatin (2 mg/day, group Pi, n=95) from the start of treatment until 3 months later. Patients were excluded if the dosage of their antidiabetic drugs was changed, if their drug therapy was altered within 3 months before starting statin therapy, or if events occurred that could affect glycemic control such as hospitalization.
Results: The subjects available for analysis were 74 patients from group A, 71 patients from group Pr, and 74 patients from group Pi. Arbitrary blood glucose levels increased from 147±51 mg/dL (mean±SD) to 176±69 mg/dL in group A, but only changed minimally from 136±31 to 134±32 mg/dL in group Pr and from 155±53 to 154±51 mg/dL in group Pi. HbA_1C increased from 7.0±1.1% to 7.4±1.2% in group A, while it was 6.9±0.9% versus 6.9±1.0% in group Pr, and 7.3±1.0% versus 7.2±1.0% in group Pi. There was no correlation between Δ LDL-C and Δ HbA_1C (the change from baseline to 3 months) in any of the groups.
Conclusion: The glycemic parameters only increased significantly in group A, suggesting that pitava-statin and pravastatin did not have an adverse influence on glycemic control in type 2 diabetic patients.

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Aim: We analyzed the lipoproteins of a patient with pancreatic cancer causing obstructive jaundice, with marked hypercholesterolemia.
Methods: The patient was a 49-year-old female. Serum total cholesterol, triglyceride, LDL-cholesterol and HDL-cholesterol levels were 1,170 mg/dL, 282 mg/dL, 1,070 mg/dL and 53 mg/dL, respectively. Cholesterol ester and lecithin:cholesterol acyltransferase decreased, and so-called remnant like particle-cholesterol increased remarkably.
Results: Fractionation of the patient's serum by polyacrylamide gel disc electrophoresis showed an abundant VLDL fraction, whereas agarose gel electrophoresis demonstrated a high level of beta-lipoprotein. Sepharose 6B gel filtration of the serum revealed that the levels of free cholesterol and apolipoprotein B were high in the VLDL- corresponding fraction.
Conclusion: The results suggested that the high cholesterol level was due to the presence of abnormally large particles rich in free cholesterol and apoB, and this abnormal fraction may correspond to lipoprotein-Y that was increased in obstructive jaundice.

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