Effects of lovastatin and gemfibrozil on high-density lipoprotein subfraction density and composition in patients with familial hypercholesterolemia.

The effects of gemfibrozil and lovastatin treatment on composition and hydrated density distribution of high-density lipoprotein (HDL) were studied in 21 patients with heterozygous familial hypercholesterolemia with the use of HDL density gradient ultracentrifugation. At baseline the patients with familial hypercholesterolemia had a markedly reduced or missing HDL2 subfraction and their HDL3 was more dense with reduced content of cholesteryl ester and increased content of triglyceride compared with HDL of control subjects with normal lipid values. Gemfibrozil and lovastatin caused primarily similar alterations in HDL components in HDL2 and HDL3 subfractions. Both agents increased apolipoprotein AI and apolipoprotein AII concentrations significantly in HDL2, whereas the apolipoprotein changes in HDL3 were relatively smaller. The difference between the effects of these two agents was related to the HDL lipid composition. Gemfibrozil increased the cholesterol concentrations of HDL2 and HDL3 (p less than 0.05 for both), and lovastatin caused significant increases in HDL2 (p less than 0.05) and HDL3 phospholipids (p less than 0.01). The observed similarity of qualitative alterations in HDL subfractions produced by these two agents in patients with familial hypercholesterolemia differs from those reported in other types of hyperlipidemia and is probably a consequence of the basic abnormalities in HDL that are characteristic of familial hypercholesterolemia.     

Influence of atorvastatin versus simvastatin on fibrinogen and other hemorheological parameters in patients with severe hypercholesterolemia treated with regular low-density lipoprotein immunoadsorption apheresis.

Low-density lipoprotein (LDL) apheresis is a treatment option in patients with coronary artery disease and elevated LDL cholesterol concentrations if maximal drug therapy fails to achieve adequate LDL cholesterol reduction. This therapy is more effective when combined with strong lipid-lowering drugs, such as atorvastatin. However, conflicting data have been published concerning the effect of atorvastatin on fibrinogen concentration. Therefore, we investigated the effect of atorvastatin compared to simvastatin on fibrinogen concentration and other hemorheological parameters in patients treated by weekly LDL apheresis. Hemorheological parameters were, studied twice in 9 patients (4 female, 5 male, 54.0+/-8.9 years) with coronary artery disease treated by weekly LDL immunoadsorption, once during concomitant simvastatin therapy (40 mg daily) and once during atorvastatin therapy (40 mg daily). Fibrinogen concentration, plasma and blood viscosity at different shear rates, parameters of red cell aggregation at stasis and shear rate 3/s, and erythrocyte filterability were determined 7 days after the last LDL apheresis after each drug had been given for a minimum for 8 weeks. Fibrinogen concentration did not show any statistically significant difference during therapy with atorvastatin (3.09+/-0.36 g/L) compared to simvastatin (3.13+/-0.77 g/L). Plasma and blood viscosity as well as erythrocyte filterability were also unchanged. The increase in red cell aggregation at stasis during atorvastatin treatment (5.82+/-1.00 U versus 4.89+/-0.48 U during simvastatin; p < 0.05) was inversely correlated with a lower high-density liprotein (HDL) cholesterol concentration (1.17+/-0.21 mmol/L versus 1.31+/-0.30 mmol/L during simvastatin; p < 0.05). LDL cholesterol showed a strong trend to lower concentrations during atorvastatin (4.14+/-0.61 mmol/L versus 4.56+/-0.66 mmol/L during simvastatin; p = 0.07), despite a reduced plasma volume treated (3,547+/-1,239 ml during atorvastatin versus 3,888+/-1,206 mL during simvastatin; p < 0.05). In conclusion, fibrinogen concentration and other hemorheological parameters were unchanged during atorvastatin compared to simvastatin therapy with the exception of a higher red cell aggregation at stasis. Therefore, with respect to hemorheology, we conclude that atorvastatin should not be withheld from hypercholesterolemic patients regularly treated with LDL immunoadsorption.     

Effects of rosuvastatin versus atorvastatin, simvastatin, and pravastatin on non-high-density lipoprotein cholesterol, apolipoproteins, and lipid ratios in patients with hypercholesterolemia: additional results from the STELLAR trial

BACKGROUND: Non-high-density lipoprotein cholesterol (HDL-C), apolipoprotein (apo) B, and lipid and apolipoprotein ratios that include both atherogenic and antiatherogenic lipid components have been found to be strong predictors of coronary heart disease risk. OBJECTIVE: The goal of this study was to examine prospectively the effects of rosuvastatin, atorvastatin, simvastatin, and pravastatin across dose ranges on non-HDL-C, apo B, apo A-I, and total cholesterol (TC):HDL-C, low-density lipoprotein cholesterol (LDL-C):HDL-C, non-HDL-C:HDL-C, and apo B:apo A-I ratios in patients with hypercholesterolemia (LDL-C > or =160 mg/dL and <250 mg/dL and triglycerides <400 mg/dL) in the Statin Therapies for Elevated Lipid Levels compared Across doses to Rosuvastatin (STELLAR) trial. METHODS: In this randomized, Multicenter, parallel-group, open-label trial (4522IL/0065), patients > or =18 years of age received rosuvastatin 10, 20, 40, or 80 mg; atorvastatin 10, 20, 40, or 80 mg; simvastatin 10, 20, 40, or 80 mg; or pravastatin 10, 20, or 40 mg for 6 weeks. Pairwise comparisons were prospectively planned and performed between rosuvastatin 10, 20, and 40 mg and milligram-equivalent or higher doses of comparators. RESULTS: A total of 2268 patients were randomized to the rosuvastatin 10- to 40-mg, atorvastatin, simvastatin, and pravastatin groups. Fifty-one percent of patients were women, the mean (SD) age was 57 (12) years, and 19% had a documented history of atherosclerotic disease. Over 6 weeks, rosuvastatin significantly reduced non-HDL-C, apo B, and all lipid and apolipoprotein ratios assessed, compared with milligram-equivalent doses of atorvastatin and milligram-equivalent or higher doses of simvastatin and pravastatin (all, P < 0.002). Rosuvastatin reduced non-HDL-C by 42.0% to 50.9% compared with 34.4% to 48.1% with atorvastatin, 26.0% to 41.8% with simvastatin, and 18.6% to 27.4% with pravastatin. Rosuvastatin reduced apo B by 36.7% to 45.3% compared with 29.4% to 42.9% with atorvastatin, 22.2% to 34.7% with simvastatin, and 14.7% to 23.0% with pravastatin. The highest increase in apo A-I (8.8%) was observed in the rosuvastatin 20-mg group, and this increase was significantly greater than in the atorvastatin 40-mg and 80-mg groups (both, P < 0.002). CONCLUSION: Rosuvastatin 10 to 40 mg was more efficacious in improving the lipid profile of patients with hypercholesterolemia than milligram-equivalent doses of atorvastatin and milligram-equivalent or higher doses of simvastatin and pravastatin.     

Effects of atorvastatin on high-density lipoprotein apolipoprotein A-I metabolism in dogs

BACKGROUND: The mechanisms involved in the decline of high-density lipoprotein (HDL) levels at a higher dose of atorvastatin have not yet been elucidated. We investigated the effects of atorvastatin on HDL-apolipoprotein (apo) A-I metabolism in dogs, a species lacking cholesteryl ester transfer protein activity. MATERIALS AND METHODS: Seven ovariectomized normolipidaemic female Beagle dogs underwent a primed constant infusion of [5,5,5-(2)H(3)] leucine to determine HDL-apo A-I kinetics before and after atorvastatin treatment (5 mg kg(-1) d(-1) for 6 weeks). Plasma lipoprotein profiles, activity of HDL-modifying enzymes involved in reverse cholesterol transport and hepatic scavenger receptor class B type I (SR-BI) expression were also studied. RESULTS: Atorvastatin treatment decreased HDL-cholesterol levels (3.56 +/- 0.24 vs. 2.64 +/- 0.15 mmol L(-1), P < 0.05). HDL-triglycerides were not affected. HDL-phospholipids levels were decreased (4.28 +/- 0.13 vs. 3.29 +/- 0.13 mmol L(-1), P < 0.05), as well as phospholipids transfer protein (PLTP) activity (0.83 +/- 0.05 vs. 0.60 +/- 0.05 pmol microL(-1) min(-1), P < 0.05). Activity of lecithin: cholesterol acyl transferase (LCAT), hepatic lipase (HL) and SR-BI expression did not change. HDL-apo A-I absolute production rate (APR) was higher after treatment (twofold, P < 0.05) as well as fractional catabolic rate (FCR) (threefold, P < 0.05). This resulted in lower HDL-apo A-I levels (2.36 +/- 0.03 vs. 1.55 +/- 0.04 g l(-1), P < 0.05). Plasma lipoprotein profiles showed a decrease in large HDL(1) levels, with lower apo A-I and higher apo E levels in this subfraction. CONCLUSIONS: Although a high dose of atorvastatin up-regulated HDL-apo A-I production, this drug also increased HDL-apo A-I FCR in dogs. This effect could be explained by a higher uptake of apo E-enriched HDL(1) by hepatic lipoprotein receptors.     

Effects of treatment with a commercially available St John's Wort product (Movina) on cholesterol levels in patients with hypercholesterolemia treated with simvastatin

OBJECTIVE: To assess the effect of treatment with a St John's Wort product (Movina) on cholesterol levels (total cholesterol, LDL-cholesterol, and HDL-cholesterol) in patients with hypercholesterolemia on treatment with a stable dose of simvastatin. DESIGN: Controlled, randomized, open, crossover pharmacodynamic study. SETTING: Two primary healthcare centres. Intervention. Patients were treated with Movina one tablet (containing 300 mg of Hypericum perforatum) twice daily and control (a commercially available multivitamin tablet, Vitamineral). The trial started with a run-in period of 4 weeks. Then the treatment order between control and active treatment was decided (randomization using sealed envelopes). The duration of each treatment period was 4 weeks and simvastatin treatment was kept unchanged during the whole study period (12 weeks). SUBJECTS: Twenty-four patients with hypercholesterolemia treated with a stable dose of simvastatin (10-40 mg daily) for at least three months. MAIN OUTCOME MEASURES: Assessments of total cholesterol, HDL- cholesterol, LDL-cholesterol, and triglycerides were performed in the morning with the patients in a fasting condition. RESULTS: All patients completed the study. LDL-cholesterol was significantly increased during active treatment compared with control. Thus, the mean LDL-cholesterol after 4 weeks' active treatment was 2.72 mmol/L compared with 2.30 mmol/L after treatment with control (p <0.0001). An increase in total-cholesterol was also observed (5.08 mmol/L compared with 4.56 mmol/L, p <0.0001). CONCLUSION: Products containing St John's Wort should not be given to patients with hypercholesterolemia who are on treatment with simvastatin.     

Low-dose, time-release nicotinic acid: effects in selected patients with low concentrations of high-density lipoprotein cholesterol.

In a retrospective analysis, 63 participants in a cardiac rehabilitation-preventive cardiology program were identified as having low blood concentrations (mean, 34 mg/dl) of high-density lipoprotein cholesterol (HDL-C) and a mean total cholesterol level of 223 mg/dl after 3 months of hygienic measures (aerobic exercise, avoidance of tobacco, diet, and weight loss) designed to increase the HDL-C level. These patients (treatment group) were treated with low-dose, time-release nicotinic acid (mean, 1,297 mg/day) for a mean duration of 7.4 months. All subjects were able to take the drug without intolerable side effects. Fifty-four patients similar to those in the treatment group participated in the same program but were not treated with nicotinic acid (control group). Exercise, diet, body weight, and smoking remained stable throughout the period of observation. For the treatment group, HDL-C levels increased a mean of 18% (+6 mg/dl), total cholesterol concentrations decreased 9% (-20 mg/dl), the ratio of total cholesterol to HDL-C decreased 25% (from 6.8 to 5.1), low-density lipoprotein cholesterol levels decreased 13% (-20 mg/dl), and triglyceride levels decreased 20% (from 165 mg/dl to 132 mg/dl). Aspartate aminotransferase and uric acid concentrations were minimally increased after treatment, and the blood glucose level was unchanged. In the control group, HDL-C levels increased a mean of 8% (+3 mg/dl) and the other blood lipid variables were not improved after a mean of 8.3 additional months of diet and exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

A 52-week, randomized, open-label, parallel-group comparison of the tolerability and effects of pitavastatin and atorvastatin on high-density lipoprotein cholesterol levels and glucose metabolism in Japanese patients with elevated levels of low-density lipoprotein cholesterol and glucose intolerance

BACKGROUND: Statin therapy has been found to produce substantial reductions in low-density lipoprotein cholesterol (LDL-C) levels, resulting in a reduced risk for cardiovascular events. Recently, research interest has focused on modification of high-density lipoprotein cholesterol (HDL-C) levels for the potential prevention of cardiovascular events. The effects of pitavastatin and atorvastatin on HDL-C have not been directly compared. OBJECTIVES: This study compared the effects of pitavastatin and atorvastatin on HDL-C and other lipids and glucose metabolism in Japanese patients with elevated LDL-C levels and glucose intolerance. The tolerability of the 2 treatments was also compared. METHODS: This was a multicenter, open-label, parallel-group trial. Patients with LDL-C levels>or=140 mg/dL and glucose intolerance (defined according to Japanese criteria for borderline diabetes and World Health Organization criteria for impaired fasting glucose and impaired glucose tolerance) were randomly assigned to receive either pitavastatin 2 mg/d or atorvastatin 10 mg/d for 52 weeks. Levels of serum lipids and lipoproteins and measures of glucose metabolism (fasting insulin, fasting glucose, glycosylated hemoglobin, and homeostasis model assessment for insulin resistance) were obtained at baseline and at 8, 26, and 52 weeks of treatment. The effect of study drug on glucose metabolism was evaluated as a tolerability outcome. Tolerability was further assessed based on adverse events, either spontaneously reported or elicited by questioning; physical examination findings; and clinical laboratory test results. Study physicians rated the relationship of adverse events to study medication as unrelated, suspected, or probable. RESULTS: Two hundred seven patients were enrolled in the study, and efficacy was evaluated in 173 patients (88 pitavastatin, 85 atorvastatin). Thirty-four patients were excluded for reasons including failure to start medication or lack of >or=6 months of follow-up. Women accounted for 62% (108/173) of the evaluable population, which had a mean age of 63.3 years and a mean weight of 63.0 kg; 89% (154/173) had diabetes mellitus. The percent change in HDL-C levels was significantly greater in the pitavastatin group compared with the atorvastatin group (8.2 vs 2.9, respectively; P=0.031), as was the percent change in apolipoprotein (Apo) A-I (5.1 vs 0.6; P=0.019). The percent change in LDL-C levels was significantly lower with atorvastatin compared with pitavastatin (-40.1 vs -33.0, respectively; P=0.002), as were the percent changes in non-HDL-C (-37.4 vs -31.1; P=0.004), Apo B (-35.1 vs -28.2; P<0.001), and Apo E (-28.1 vs -17.8; P<0.001). The significant results for these parameters were unchanged when all 189 subjects who received>or=1 dose of study medication were included in the analysis, using last-value-carried-forward methodology. There were no significant differences between treatments with respect to the measures of glucose metabolism. Both statins appeared to be well tolerated. Adverse events occurred in 9% (9/96) of the pitavastatin group and 14% (13/93) of the atorvastatin group (P=NS). Two patients in the pitavastatin group and none in the atorvastatin group had an alanine aminotransferase value>3 times the upper limit of normal (P=NS). CONCLUSIONS: In these patients with elevated LDL-C levels and glucose intolerance, 52 weeks of treatment with pitavastatin 2 mg/d was associated with significantly greater increases in HDL-C and Apo A-I levels than atorvastatin 10 mg/d. Both treatments were well tolerated.     

Effects of atorvastatin and simvastatin on low-density lipoprotein subfraction profile, low-density lipoprotein oxidizability, and antibodies to oxidized low-density lipoprotein in relation to carotid intima media thickness in familial hypercholesterolemia.

BACKGROUND: Little is known about the effects of statins on the quality of circulating low-density lipoprotein (LDL) in relation to atherosclerosis progression. METHODS: In a double-blind, randomized trial of 325 patients with familial hypercholesterolemia (FH), we assessed the effects of high-dose atorvastatin (80 mg) and conventional-dose simvastatin (40 mg) on LDL subfraction profile (n = 289), LDL oxidizability (n = 121), and circulating autoantibodies to oxidized LDL (n = 220). Progression of atherosclerosis was measured by carotid intima media thickness (IMT) (n = 325). RESULTS: At baseline, the patients showed an intermediate LDL subfraction profile composed of three LDL subfractions (LDL1, LDL2, LDL3), with LDL2 as the predominant subfraction. A strong negative correlation was found between plasma triglycerides and the LDL subfraction profile (r = -.64, p = .000). Both plasma levels of triglycerides and small dense LDL3 correlated weakly with baseline IMT (r = .11, p = .04 and r = .15, p = .01, respectively; n = 289). No association was found between baseline IMT and oxidation parameters or circulating antibodies to oxidized LDL. Atorvastatin reduced triglycerides, LDL cholesterol, and all LDL subfractions to a greater extent than did simvastatin and led to regression of carotid IMT. However, LDL subfraction pattern and plasma levels of autoantibodies to oxidized LDL remained unchanged in both treatment groups, and LDL oxidizability increased minimally to a similar extent in both groups. Significant treatment differences were found for the rate of in vitro oxidation of LDL and the amount of dienes formed during in vitro oxidation of LDL, which both decreased more following atorvastatin than after simvastatin. CONCLUSION: Change of IMT after statin treatment was associated with baseline IMT (r = .41), LDL cholesterol (r = -.20), and the amount of dienes formed during in vitro oxidation of LOL (r = .28) but not with plasma levels of antibodies to oxidized LDL, in vitro LDL oxidizability, and LDL subfraction profile.     

血必净注射液对脓毒症患者高密度脂蛋白胆固醇水平的影响

目的 探讨血必净注射液对脓毒症患者高密度脂蛋白胆固醇(high-density lipoprotein cholestero,HDL-C)水平的影响.方法 将38例脓毒症合并低HDL-C血症患者随机分为两组,对照组19例予常规综合治疗,治疗组19例在对照组基础上加用血必净注射液,分别监测两组治疗前及治疗后3 d、7 d、10 d血清HDL-C、载脂蛋白A_1(apoA I)及APACHEⅡ评分的动态变化,分析血必净注射液对脓毒症患者HDL-C水平预后的影响.结果 治疗组7 d、10 d后HDL-C、apoA Ⅰ较用药前明显升高,与对照组比较差异亦有统计学意义(P<0.05),APACHEⅡ评分降低,预后改善.结论 血必净注射液能提高脓毒症患者体内HDL-C水平,在一定程度改善脓毒血症预后.     

辛伐他汀对高胆固醇血症患者RANTES表达的影响

目的 通过观察高胆固醇血症患者RANTES表达的变化及辛伐他汀对其表达变化的影响,探讨RANTES在动脉粥样硬化发生中的作用及他汀对其作用的影响.方法 2005年5月至2005年10月在我院健康查体中心随机选取健康对照60例和高胆固醇血症患者(血总胆固醇＞6.24mmol/L)80例,分别为对照组和高脂组;高脂组予以辛伐他汀20 mg·d-1,睡前口服,共12周,为他汀组.对照组、高脂组及他汀组治疗12周肘静脉取血,分离血清、血浆并提取单个核细胞.放射免疫法检测血浆的血管紧张素Ⅱ(AngⅡ)水平,实时定量RT-PCR和Western blot方法分别检测单个核细胞RANTES的mRNA和蛋白质表达水平.SPSS 12.0分析软件对试验的结果进行方差分析,Microsoft Excel对变量间的相关关系进行直线相关分析.结果 ①高脂组的血浆AngⅡ水平较对照组明显升高[(92.13±22.03) vs (50.85±12.12),P＜0.01],他汀组明显降低[(78.57±18.35) vs(92.13±22.27),P＜0.05].②高脂组单个核细胞RANTES的mRNA和蛋白质表达较对照组明显升高[(0.87±0.19) vs (0.23±0.05),P＜0.01和(1.17±0.22)对(0.38±0.09),P＜0.01],他汀组均明显降低[(0.46±0.11) vs (0.87±0.19),P＜0.01和(0.69±0.15) vs (1.17±0.22),P＜0.01].③高脂组AngⅡ与RANTES表达的相关分析显示,RANTES的表达与血浆的AngⅡ水平呈显著正相关(r=0.409,P＜0.01).结论 辛伐他汀下调高胆固醇血症患者单个核细胞RANTES表达的增高,高胆固醇血症患者单个核细胞RANTES表达的增高与血浆AngⅡ水平的增高有关.     

Total cholesterol and high-density lipoprotein cholesterol in sensorineural deafness

In order to verify an assumed hypothesis of a correlation between sensorial hearing loss and arteriosclerosis type injuries, these parameters were studied: total cholesterol and cholesterol associated to high density lipoproteins in order to evaluate the risk of developing coronary heart disease in patients with cochleopathy as compared to control patients. It proved impossible to point out any significant difference between results obtained in the two groups for any of the analytical parameters considered.     

Xanthelasma: clinical indicator of decreased levels of high-density lipoprotein cholesterol

The fasting plasma lipid and lipoprotein levels were measured prospectively in 41 consecutive patients with xanthelasma seen over a four-year period. The study group included 25 women and 16 men with mean ages of 60 and 56 years, respectively. Each patient had clinical evaluation for medications or illnesses that might affect plasma lipid levels before entry into the study. The most striking lipid abnormality was the preponderance of decreased levels of high-density lipoprotein cholesterol (HDL-C). In 94% of the study population, HDL-C values were less than the mean values of the age-matched reference population. For men the mean HDL-C level was 30.8 mg/dl (vs 45 mg/dl in the reference population, P less than .001); for women the mean HDL-C level was 33 mg/dl (vs 50 mg/dl, P less than .001). The total cholesterol, low-density lipoprotein, and triglyceride levels of those in the study were not significantly different from those of the patients in the reference population. Evaluation of cardiac risk based solely on HDL-C levels showed 80% of the study population to have three to four times the average risk. This study points out the high probability of decreased HDL-C levels in patients with xanthelasma. Since the level of HDL-C has been shown to be inversely related to the incidence of cardiovascular disease, it may be prudent to evaluate HDL-C levels and do a thorough cardiovascular evaluation in patients with xanthelasma.     

Correlation between total homocysteine, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol in the serum of patients with myocardial infarction

OBJECTIVES: Determine the Low-density lipoprotein cholesterol (LDL-C), High-density lipoprotein cholesterol (HDL-C) and serum total homocysteine in myocardial infarction patients and control subjects. DESIGN AND METHODS: The study group consisted of 126 patients 67 male, and 59 females, aged 29-73 (mean 48.65 +/- 3.81) years. The entry criteria for the patient group was typical or atypical chest pain, unequivocal changes in the electrocardiogram. The control group consisted of 135 normal volunteers, 71 male and 64 females, age 21-63 (mean 42.73 +/- 5.79) years. Measurement of serum total homocysteine was performed using gas chromatography. Measurement of Low-density lipoprotein cholesterol, and High-density lipoprotein cholesterol were performed using spectrophotometer. RESULTS: Patients with myocardial infarction were found to have higher serum total homocysteine levels than controls, (P < 0.05). Serum total homocysteine levels were significantly correlated with low-density lipoprotein cholesterol and high-density lipoprotein cholesterol. There was a negative correlation between total homocysteine and HDL-C levels (P < 0.05, r = -0.93). There was a positive correlation between total homocysteine and LDL-C levels (P < 0.05, r = 0.98). CONCLUSIONS: The above mentioned findings suggest the potential usefulness of LDL-C, HDL-C and serum total homocysteine as prognostic markers in myocardial infarction patients. These findings should influence future studies on the etiology and pathogenesis of myocardial infarction.     

正常(或低)胆固醇冠心病患者的脂蛋白谱特点

目的研究血清总胆固醇（ＴＣ）正常或低于平均水平的冠心病（ＣＨＤ）患者的脂蛋白谱特点。方法观察诊断明确的男性ＣＨＤ２２５例，以年龄配对、生活水平相似的健康男子２２５例为对照。两组中均排除与脂代谢有关的疾病及用药。对血脂作多指标［１４项，包括载脂蛋白（ａｐｏ）８项］综合分析。结果ＣＨＤ患者中ＴＣ高于５．１７ｍｍｏｌ／Ｌ者１０８例（４８％），低于此水平者１１７例（５２％）。高ＴＣ组的血脂特点以低密度脂蛋白胆固醇（ＬＤＬ－Ｃ）和ａｐｏＢ增高为主，低ＴＣ组（ＴＣ平均４．４１ｍｍｏｌ／Ｌ，相应的对照组为４．８１ｍｍｏｌ／Ｌ）的特点是高密度脂蛋白胆固醇（ＨＤＬ－Ｃ）及其亚类明显偏低，尤以ａｐｏＡＩ低下最明显。多数ＨＤＬ－Ｃ低的病例并无甘油三酯增高，部分病例以低ＨＤＬ（包括ＨＤＬ－Ｃ，ａｐｏＡＩ、ＡＩ）为单一的血脂异常。逐步回归分析优选判断ＣＨＤ的指标，在低ＴＣ组首选是ａｐｏＡＩ，其次为脂蛋白（ａ）；但高ＴＣ组以ａｐｏＢ为首选。结论低ＴＣ组在ＬＤＬ致动脉硬化作用明显减弱的情况下，低ＨＤＬ成为主要的（独立的）脂类危险因素