Intermediate-density lipoprotein and cholesterol-rich very low density lipoprotein in angiographically determined coronary artery disease.

Tatami, Ryozo; Mabuchi, Hiroshi; Ueda, Kosei; Ueda, Ryosei; Haba, Toshihiro; Kametani, Tomio; Itô, Seigo; Koizumi, Junji; Ohta, Masayuki; Miyamoto, Susumu; Nakayama, Akira; Kanaya, Honin; Oiwake, Hisanori; Genda, Akira; Takeda, Ryoyu

doi:10.1161/01.cir.64.6.1174

Cited by 228 publications

(84 citation statements)

References 46 publications

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“…However, the interest has been, in general, limited to plasma VLDL concentrations without paying too much attention to the lipoprotein composition. The latter has become increasingly important once the evidence has been forwarded that abnormalities of VLDL composition might be related to the process of atherogenesis [5][6][7].…”

Section: Discussionmentioning

confidence: 99%

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Presence of very low density lipoprotein compositional abnormalities in Type 1 (insulin-dependent) diabetic patients; effects of blood glucose optimisation

et al. 1988

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Summary. Plasma lipoprotein compositional abnormalities were investigated in eight normolipidaemic (plasma cholesterol < 5.70 mmol/1; triglyceride < 2.03 mmol/1) young male Type 1 (insulin-dependent) diabetic patients (before and after a short period of optimised blood glucose control) and in nine healthy control subjects, matched for sex, age and body mass index. Free and esterified cholesterol, triglyceride, phospholipids were assayed in all lipoprotein classes (VLDL, IDL, LDL) and in HDL subclasses (HDL2 and HDL3); apoB was measured only in very low density lipoproteins (VLDL). All VLDL constituents were increased in the diabetic group, the differences being more striking for apoB (6.0_+ 1.1 mg/dl vs 2.0 _+ 0.1 mg/dl, p< 0.02), free cholesterol (0.27 _+ 0.04 mmol/1 vs 0.13+0.02mmol/1, p<0.02) and esterified cholesterol (0.32___0.08 retool/1 vs 0.13+0.01 mmol/1, p<0.05). Also HDL subfractions showed differences between the two groups: all HDL2 constituents were increased, while in HDL3 only triglyceride was significantly increased (0.11 + 0.01 mmol/1 vs 0.08+0.004mmol/1, p<0.02). After two weeks of optimised blood glucose control all VLDL constituents were reduced and particularly: esterified cholesterol (-39%, p<0.02), free cholesterol (-37%, p<0.05), apoB (-35%, p< 0.05). Expressing each VLDL constituent as percent of the total lipoprotein mass, it was evident that the diabetic VLDL was rich in cholesterol both esterified (8.4+1.0% vs 5.4+0.5%, p<0.02) and free (8.5+0.7% vs 5.5_+0.3%, p<0.001), apoB (5.1_+0.6% vs 2.6_+0.3%, p<0.001) and depleted in triglyceride (57.0+1.7% vs 64.1 _+ 1.7%, p< 0.001). Two weeks of optimised blood glucose control were not able to correct the abnormal composition of VLDL. In conclusion, Type 1 (insulin-dependent) diabetic patients, although normolipidaemic, show an abnormal VLDL composition suggesting an increased prevalence of smaller and, possibly, more atherogenic VLDL particles. This abnormality is not corrected by a short period of blood glucose optimisation.

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Section: Discussionmentioning

confidence: 99%

“…In particular, cholesterol rich VLDL lipoproteins have been shown to contribute to the process of atherosclerosis [6,7]. Therefore, we have undertaken this study in order to evaluate the plasma lipoprotein composition in a group of normolipidaemic young male Type 1 diabetic patients.…”

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confidence: 99%

Presence of very low density lipoprotein compositional abnormalities in Type 1 (insulin-dependent) diabetic patients; effects of blood glucose optimisation

et al. 1988

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“…On univariate analysis the strongest correlations were found between IDL and LDL triglyceride (IDL cholesterol and apolipoprotein B were also significantly related), suggesting that IDL and triglyceride-rich LDL may have the highest "atherogenic potential," as reported in the previously mentioned Japanese study. 8 Nevertheless, in terms of predictive power, plasma triglyceride was found to account for more variability in the score for severity of atherosclerosis than did concentrations of IDL or LDL triglyceride.…”

Section: ±11mentioning

confidence: 95%

“…Similar findings have been reported from Japan where, in one study, increased concentrations of triglyceride (and reduced HDL cholesterol) were found to be stronger predictors of CAD than the plasma cholesterol concentration.30 Another study from Japan demonstrated the significance of IDL and VLDL cholesterol as indicators of severity of coronary atherosclerosis. 8 The severity of coronary atherosclerosis determined at autopsy has also been shown to correlate better with the antemortem plasma concentration of triglyceride than of cholesterol. '1 Atherosclerosis in the large arteries of the legs is generally associated with hypertriglyceridemia.32 In our previous study,5 conducted in a manner similar to the present investigation, LDL triglyceride was one of the three independent predictors of severity score.…”

Section: ±11mentioning

confidence: 99%

Lipoprotein predictors of the severity of coronary artery disease in men and women.

Reardon¹,

Nestel²,

Craig³

et al. 1985

Circulation

246

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In this study we examined the relationships between levels of several components of plasma lipoproteins and severity of coronary artery disease in 65 men and 42 women who underwent coronary arteriography for suspected coronary disease. Severity of coronary atherosclerosis was scored as the extent of disease seen at arteriography. Univariate analyses of the relationships between the plasma lipoprotein parameters and score for severity of atherosclerosis revealed a marked difference between men and women. In men, the score for severity of atherosclerosis was strongly related to the low-density lipoprotein (LDL) cholesterol and apolipoprotein B concentrations, whereas in women it was related to the triglyceride concentrations in plasma intermediate-density lipoprotein (IDL) and LDL and to the cholesterol and apolipoprotein B concentrations in IDL. The significance of these correlations was not negated by possible confounding factors such as alcohol intake, diabetes, and treatment with thiazides and ,-adrenergic blockers. Stepwise regression analyses of data adjusted for weight and age indicated that 22% of the variation in the score for severity of atherosclerosis could be accounted for by levels of LDL cholesterol in men. No other lipoprotein parameter could account for any further variation. In contrast, cholesterol did not account for any variation in the score for severity of atherosclerosis in women, whereas plasma triglyceride accounted for 16% of the observed variation in this group. No relationships were found between score for severity of atherosclerosis and highdensity lipoprotein cholesterol or plasma apolipoprotein A-I concentrations in either group. This study indicates the importance of the triglyceride-rich lipoproteins in the development of coronary atherosclerosis in women. Circulation 71, No. 5, 881-888, 1985. EPIDEMIOLOGIC STUDIES have clearly established that a high plasma cholesterol level is associated with an increased risk of coronary artery disease (CAD). This risk is associated primarily with the cholesterol level of the low-density lipoprotein (LDL) fraction." 2 In -contrast, the cholesterol level in the high-density lipoprotein (HDL) fraction is an important determinant of reduced risk.3 Of the lipid-related indexes, the ratio of plasma cholesterol to HDL cholesterol has been suggested to be the most powerful predictor of premature development of CAD.4 In 1978, a report from this laboratory was among the first to relate lipoprotein lipid concentrations to the severity of CAD, as determined from the extent of disease in eight major segments of the coronary circu-

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“…IDL levels have also been found to be strong predictors of atherosclerosis in genetically hyperlipidaemic [33] and cholesterol-or casein-fed rabbits [34]. In humans without major genetic or secondary forms of hyperlipidaemia, IDL and small VLDL have been shown to be independent predictors of the presence, severity, or progression of atherosclerosis [35][36][37][38][39]. Patients with type III hyperlipoproteinaemia [8], chronic renal failure [40] or NIDDM [41] have elevated levels of remnant lipoproteins as well as accelerated development of atherosclerosis.…”

Section: U Rmentioning

confidence: 98%

Effect of exogenous hyperinsulinaemia on atherogenesis in cholesterol-fed rabbits

1997

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Coronary heart disease and thus atherosclerosis is the leading cause of death among patients suffering from diabetes mellitus; men and women with diabetes have a three to fivefold higher coronary heart disease mortality or incidence rate compared with non-diabetic subjects [1]. Although a number of factors such as hyperglycaemia, dyslipidaemia, a procoagulant state, hyperinsulinaemia, glycation of proteins, oxidation or glycation of lipoproteins, as well as enhanced smooth muscle cell proliferation and foam cell formation, have all been suggested as possible links between diabetes and atherosclerosis [1], the increased risk of coronary heart disease among diabetic patients still remains largely unexplained.Hyperinsulinaemia could be directly involved in atherogenesis [2], although this possibility is fiercely debated [3][4][5][6]. In patients with insulin-dependent diabetes (IDDM) exogenous hyperinsulinaemia exists due to intermittent injections of large amounts of insulin [1], and in patients with non-insulin dependent diabetes (NIDDM) endogenous hyperinsulinaemia Diabetologia (1997) 40: 512-520 Effect of exogenous hyperinsulinaemia on atherogenesis in cholesterol-fed rabbits Summary To examine the hypothesis that hyperinsulinaemia promotes atherosclerosis, cholesterol-fed rabbits were injected subcutaneously with 6 IU of human insulin (n = 16) or placebo (n = 20) daily for 24 weeks; injection of insulin resulted in hyperinsulinaemia for up to 16 h after injection. Compared to placebo rabbits, insulin-treated rabbits had higher levels of insulin antibodies in plasma, similar levels of intermediate density, low density and high density lipoprotein cholesterol and similar activities of hepatic and lipoprotein lipase in post-heparin plasma, but lower levels of plasma C-peptide, blood glucose, postprandial plasma triglycerides, plasma cholesterol and very low density lipoprotein cholesterol. On univariate analysis, with and without adjustment for differences in plasma cholesterol levels between the two groups, there were no significant differences in extent or severity of atherosclerosis between insulin and placebo rabbits. Furthermore, after combining the results from all the rabbits to examine plasma insulin levels and the other variables mentioned above as predictors of atherosclerosis severity, plasma insulin level was not a predictor, on univariate or multiple linear regression analysis; the first ranked independent predictors were postprandial intermediate density lipoprotein cholesterol in the arch, and postprandial plasma triglyceride in both the thoracic and abdominal aorta. These results suggest that exogenous hyperinsulinaemia does not promote atherogenesis in cholesterol-fed rabbits, but that postprandial levels of intermediate density lipoprotein cholesterol or plasma triglycerides may be involved in atherogenesis. [Diabetologia (1997)

show abstract

Intermediate-density lipoprotein and cholesterol-rich very low density lipoprotein in angiographically determined coronary artery disease.

Cited by 228 publications

References 46 publications

Presence of very low density lipoprotein compositional abnormalities in Type 1 (insulin-dependent) diabetic patients; effects of blood glucose optimisation

Presence of very low density lipoprotein compositional abnormalities in Type 1 (insulin-dependent) diabetic patients; effects of blood glucose optimisation

Lipoprotein predictors of the severity of coronary artery disease in men and women.

Effect of exogenous hyperinsulinaemia on atherogenesis in cholesterol-fed rabbits

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