Increased Serum High-density Lipoprotein Cholesterol Research Articles

Serum Lipid and Lipoprotein Levels in Postmenopausal Women: Short-Course Effect of Caigua

The present study was designed to determine lipid profiles in postmenopausal women, as well as the effect of short-term increasing oral doses of dehydrated natural caigua (Cycladin®) on serum cholesterol levels, low-density lipoprotein (LDL) cholesterol levels, high-density lipoprotein (HDL) cholesterol levels, and triglycerides levels during 12 weeks of treatment. Eighteen premenopausal and twenty-four postmenopausal women were studied. The family and personal histories of dyslipidemia. hypertension, and obesity were similar in pre- and postmenopausal women, as were body weight, body mass index (BMI). waist/hip ratios, and blood pressure. The postmenopausal women were shorter. Postmenopausal women had higher plasma cholesterol levels, higher LDL cholesterol levels, higher triglyceride levels, and lower HDL cholesterol levels than did the premenopausal women. In postmenopausal women, six capsules daily of dehydrated caigua was the study's only dose that effectively reduced total serum cholesterol levels and LDL cholesterol levels and also significantly increased serum HDL cholesterol levels. At the end of 12 weeks of treatment, serum cholesterol levels were 22% below pretreatment values and serum LDL cholesterol was 33% below initial values, whereas serum HDL cholesterol levels increased to >33% of initial values. Daily treatment with four capsules, two capsules, or placebo failed to modify lipid profiles effectively in postmenopausal women. Treatment with six capsules of caigua daily during 12 weeks reduced the rate of hypercholesterolemia from 75% at the beginning of the study to 12.5% at the end of treatment: similarly, it reduced the rate of hyper-LDL cholesterolemia from 75 to 12.5% and hypo-HDL cholesterolemia from 62.5 to 12.5%. Treatment with caigua had no effect on the prevalence of hypertriglyceridemia. We conclude that our patients with menopause had different lipid profiles from those of the premenopausal women. Menopause alters the lipid profile, and treatment with caigua. a natural plant that is administered dehydrated and capsulated, can reverse dyslipidemia in the postmenopausal woman.

Effect of propranolol versus no antiarrhythmic drug on serum lipids in patients with heart disease and complex ventricular arrhythmias

Propranolol administered to patients for 3 days to 1 year reportedly increases serum triglyceride levels and decreases serum high-density lipoprotein (HDL) cholesterol levels. We investigated the effects of propranolol administered for 3 to 44 months on serum lipids in a study of 245 elderly patients with complex ventricular arrhythmias, heart disease (65% with prior Q-wave myocardial infarction and 35% with hypertensive heart disease) and a left ventricular ejection fraction ≥40%. A total of 123 patients were randomized to receive propranolol 85 ± 28 mg daily and 122 patients to no antiarrhythmic drug. Serum lipids were determined before randomization; at 3, 6, 12, 18, 24, 30, 36, and 42 months after randomization; and at the end of the study. Five patients stopped taking propranolol before follow-up serum lipid measurements were recorded at 3 months. Ninety-nine patients were alive at the end of the study. The mean follow-up time was 29 ± 15 months, in the group receiving propranolol; no significant differences were found in serum total cholesterol, low-density lipoprotein (LDL) cholesterol, HDL cholesterol, total cholesterol:HDL cholesterol ratio, or triglyceride levels before or after treatment. The mean follow-up time was 27 ± 15 months in patients who received no antiarrhythmic drug; there was a significant reduction in serum total cholesterol (2%, P = 0.0001), in LDL cholesterol (3%, P = 0.0001), and in the total cholesterol:HDL cholesterol ratio (4%, P = 0.0001); a marginally significant decrease in serum triglycerides (3%, P = 0.052); and a marginally significant increase in serum HDL cholesterol (3%, P = 0.054) in these patients.

Rationale and design of a secondary prevention trial of increasing serum high-density lipoprotein cholesterol and reducing triglycerides in patients with clinically manifest atherosclerotic heart disease (the bezafibrate infarction prevention trial)

Controlled clinical trials have demonstrated the efficacy of reducing the Mood levels of tow-density lipoprotein cholesterol in reducing the incidence of coronary artery disease in hypercholesterolemic middle-aged men. However, a similar reversibility of the risk of coronary artery disease has not been demonstrated for high-density lipoprotein cholesterol elevation and triglyceride reduction. Therefore, the effect of administering 400 mg of bezafibrate retard daily versus placebo (double Mind) to patients with myocardial infarction preceding randomization by 6 months to 5 years, or a clinically manifest anginal syndrome documented by objective evidence of dynamic myocardial ischemia, or both, is being investigated. Three thousand subjects (aged 45 to 74 years) are being enrolled from 19 cardiac departments in Israel, with total serum cholesterol between 180 and 250 mg/dl, high-density lipoprotein cholesterol ≤45 mg/dl and triglycerides ≤300 mg/dl. In addition, tow-density lipoprotein cholesterol concentrations are required to be ≤180 mg/dl (≤160 mg/dl for patients aged <50 years). Patients needing lipid-modifying therapy, exhibiting ≥1 prespecified exclusion criterion or not giving informed consent, or a combination, are not randomized. The primary end points for evaluating efficacy are the incidence of fatal and nonfatal myocardial infarction, and sudden death. The hypothesized effect of bezafibrate administration under the aforementioned protocol is to reduce an estimated cumulative end point event incidence of ≥15% by 20 to 25% over an average follow-up period of 6.25 years, through early 1998, when the last patient recruited will have completed 5 years. The sample size was determined on the basis of previous studies of the natural history of myocardial infarction in Israel, a plan for 2 interim analyses, an experiment-wise, 2-sided significance level of 0.05, and a power of 0.8 to detect an effect on end point incidence. Patient safety, and protocol and medication adherence are being monitored throughout.

Relationship between zinc intake, physical activity, and blood levels of high-density lipoprotein cholesterol in a healthy elderly population

We investigated the relationship between level of exercise, ingestion of zinc supplements, and serum high-density lipoprotein (HDL) cholesterol levels in 270 healthy men and women over age 60. After controlling for sex, alcohol intake, and body mass, there was a significant positive correlation between level of exercise and serum HDL cholesterol in the 180 subjects not taking supplemental zinc ( r = 0.26, P = .005) but not for those subjects taking supplemental zinc ( r = −0.18, P = .14). Multiple regression analysis showed a significant interaction of zinc intake and activity level on HDL cholesterol ( P = .04). In 22 subjects who were ingesting > 15 mg of supplemental, elemental zinc daily, cessation of zinc supplements for 8 weeks was associated with a significant increase in HDL cholesterol levesls (2.0 mg/dL; P = .04). The change in HDL after stopping zinc was positively correlated with the level of exercise of the subjects ( r = .41, P = .05). Thus supplemental zinc ingestion appears to block the exercise-induced increase in serum HDL cholesterol in a healthy population.

Effect of beta blockers on blood lipid profile

Several drugs used for antihypertensive therapy may interact with lipoprotein metabolism and increase associated coronary risk factors. Beta-blocker monotherapy with cardioselective or noncardioselective beta blockers without intrinsic sympathomimetic activity (ISA) usually increases serum triglyceride and decreases the concentration of high-density lipoprotein (HDL), especially HDL 2 cholesterol. With the exception of the noncardioselective beta blocker sotalol, beta-blocker therapy has little influence on the serum total cholesterol or low-density lipoprotein (LDL) cholesterol concentrations. The magnitude of these changes in serum lipids does not significantly differ between cardioselective and noncardioselective beta blockers. Two beta blockers possessing ISA, acebutolol and pindolol, did not increase serum triglycerides and serum total cholesterol or LDL cholesterol. Acebutolol produced a nonsignificant decrease in HDL cholesterol level. Pindolol, with marked ISA, exhibited the most favorable lipid profile, increasing serum HDL cholesterol and the ratio of HDL cholesterol to total cholesterol. The concentration of apolipoprotein A-I increased slightly during pindolol therapy. Beta blockers, with the exception of pindolol, decrease the concentration of serum free fatty acids. Beta-blocker therapy has little influence on the adipose tissue lipoprotein lipase activity, but lecithin cholesterol acyltransferase activity may increase during pindolol therapy. Thus beta-blocking drugs possessing ISA, such as acebutolol and pindolol, might be desirable choices as antihypertensive agents, since they do not appear to produce adverse effects on the lipid profile.

Effects of β-Blockers on Plasma Lipids During Antihypertensive Therapy

Several drugs used for antihypertensive therapy may interact with lipoprotein metabolism and may increase associated coronary risk levels. beta-Blocker monotherapy with selective or nonselective beta-blockers without intrinsic sympathomimetic activity (ISA) usually increases serum triglyceride and decreases high-density lipoprotein (HDL), especially HDL2 cholesterol concentration. With the exception of the nonselective beta-blocker sotalol, beta-blocker therapy has little influence on the serum total cholesterol or low-density lipoprotein (LDL) cholesterol concentrations. The magnitude of these changes in serum lipids did not distinctly differ between selective and nonselective beta-blockers. Two beta-blockers possessing ISA, acebutolol, and pindolol did not show the increase in serum triglycerides and in serum total cholesterol or LDL cholesterol. Acebutolol showed the nonsignificant decrease in HDL cholesterol level. Pindolol with marked ISA exhibited the most favorable lipid profile, increasing serum HDL cholesterol and the ratio of HDL cholesterol to total cholesterol. The concentration of apolipoprotein A-I increased slightly during pindolol therapy. beta-Blockers with the exception of pindolol decrease the concentration of serum free fatty acids. beta-blocker therapy has little influence on the adipose tissue lipoprotein lipase activity, but lecithin cholesterol acyltransferase activity may increase during pindolol therapy.

Increased serum high-density lipoprotein cholesterol in hypertensive men treated with the potent vasodilator carprazidil

The effects of the potent arteriolar vasodilator carprazidil on serum lipoproteins and various clinical, biochemical and endocrine parameters were assessed in 15 men with mild to moderate essential hypertension. Following a carprazidil monotherapy (average dose 50 to 60 mg/d) of 8 weeks (N = 15) or 16 weeks (N = 12) duration, blood pressure was decreased significantly ( P < 0.01), while serum high-density lipoprotein cholesterol (+ 26% and + 24%, respectively; P < 0.01) and the α-lipoprotein fraction (+ 26% and + 41%) were increased. Low- and very low-density lipoprotein cholesterol, triglycerides, as well as mean body weight, blood and plasma volume, heart rate, and plasma renin, aldosterone, norepinephrine, and epinephrine were not consistently altered. These results indicate that treatment of hypertensive men with carprazidil in modest dosage may have a favorable influence both on blood pressure and serum lipoproteins.