PubMed Health⌕ Search

Biomedical subjects

D B Hunninghake

Publications and source records attributed to D B Hunninghake.

At least 37 records · Page 2Linked to original sources
PubMed2000

Effective and safe modification of multiple atherosclerotic risk factors in patients with peripheral arterial disease.

BACKGROUND: Patients with peripheral arterial disease (PAD) are at an increased risk of cardiovascular mortality and morbidity and thus are an excellent group in whom to evaluate the feasibility and the effect of an aggressive multifactorial intervention on atherosclerotic vascular disease risk factors. The Arterial Disease Multiple Intervention Trial (ADMIT) was designed to determine the efficacy, safety, and compliance of an multifactorial therapy on selected atherosclerotic disease risk factors in patients with PAD. METHODS: By a 2 x 2 x 2 factorial design, eligible participants (N = 468) were randomly assigned to low-dose warfarin, antioxidant vitamins, and niacin or its corresponding placebo, and followed up for 1 year. All participants were encouraged to use aspirin. Pravastatin was added to the drug regimen for those who needed to reduce LDL cholesterol to recommended levels. RESULTS: Niacin increased HDL cholesterol levels by 30%, with the majority of effect achieved at a dosage of 500 mg twice daily. Warfarin had an anticoagulant effect. The antioxidant vitamins resulted in a significant increase in vitamin E, C, and beta-carotene plasma levels. Overall, compliance was high and few adverse effects were reported. CONCLUSIONS: ADMIT demonstrates that it is both feasible and safe to modify multiple atherosclerotic disease risk factors effectively with intensive combination therapy in patients with PAD.

Aged↗
PubMed2000

Incorporation of lean red meat into a National Cholesterol Education Program Step I diet: a long-term, randomized clinical trial in free-living persons with hypercholesterolemia.

OBJECTIVE: Clinicians often recommend that intake of all meat, particularly red meat, be reduced in conjunction with a low-fat, low-cholesterol diet to reduce low-density lipoprotein (LDL) cholesterol. This study was designed to determine the long-term effects of lean red meat (beef, veal and pork) compared to lean white meat (poultry and fish) consumption on lipoprotein concentrations in free-living hypercholesterolemic subjects consuming a National Cholesterol Education Program (NCEP) Step I diet. METHODS: A randomized, crossover design was utilized. Hypercholesterolemic men and women (LDL cholesterol between 3.37 and 4.92 mmol/L) (triglycerides <3.96 mmol/L) (n = 145) were counseled to consume > or =80% of their 170 g/d meat intake as either lean red meat or lean white meat for two 36-week phases, separated by a four-week washout period of free meat selection. Subjects were instructed to follow an NCEP Step I diet throughout the study. RESULTS: There were no significant differences in lipid concentrations between the lean red meat and lean white meat phases. LDL cholesterol was 4.02+/-0.04 (SEM) and 4.01+/-0.04 mmol/L in the white and red phases, respectively; this represented a decrease of approximately 2% from baseline concentrations (p < 0.01). Total cholesterol also declined by 1% from baseline (p < 0.05), and high-density lipoprotein (HDL) cholesterol rose over the study period by approximately 2% to approximately 3% from baseline to reach concentrations of 1.37+/-0.03 mmol/L and 1.38+/-0.03 mmol/L in the white and red phases, respectively (p < 0.001). Triglycerides were not altered by treatment. CONCLUSIONS: Consumption of lean red meat or lean white meat, as part of an NCEP Step I diet, is similarly effective for reducing LDL cholesterol and elevating HDL cholesterol concentrations in free-living persons with hypercholesterolemia.

Adolescent↗
PubMed2000

Lipid-altering efficacy and safety of simvastatin 80 mg/day: worldwide long-term experience in patients with hypercholesterolemia.

BACKGROUND AND AIM: Clinical data suggesting that larger decreases in low density lipoprotein cholesterol (LDL-C) result in greater reductions in coronary heart disease events have led to the establishment of aggressive LDL-C targets for the treatment of hypercholesterolemia. In view of this, the efficacy and safety of a new maximum dose of simvastatin, 80 mg, were evaluated in 9 studies involving 2819 hypercholesterolemic patients. This report focuses on the combined results from the 4 main or Pivotal studies in which a total of 1936 patients received simvastatin 40 or 80 mg for 36 to 48 weeks. METHODS AND RESULTS: The Pivotal studies had similar randomized, multicenter, controlled, double-blind, parallel-group designs. Their combined results demonstrated a significant advantage in the LDL-C-lowering effect for the 80 mg dose. At week 24, the mean percentage reductions (95% confidence intervals) from baseline in LDL-C for the 40 and 80 mg groups were -39.8% (-40.9, -38.7) and -45.7% (-46.5, -45.0) respectively (p < 0.001, between groups), and larger reductions in total cholesterol and triglycerides were also observed in the 80 mg group. Both doses were well tolerated. No new or unexpected adverse events were observed and the overall clinical event profiles were similar in the two groups. Clinically significant hepatic transaminase increases (> 3 times the upper limit of normal/ULN) and myopathy (muscle symptoms plus creatine kinase increase > 10 times ULN) occurred infrequently with both doses. Simvastatin 80 mg had a comparable efficacy and safety profile in women and men as well as in non-elderly and elderly patients. CONCLUSIONS: Simvastatin 80 mg provides additional LDL-C and triglyceride reductions compared to the 40 mg dose and has an excellent safety and tolerability profile.

Adolescent↗
PubMed1999

Effects of lovastatin and warfarin on early carotid atherosclerosis: sex-specific analyses. Asymptomatic Carotid Artery Progression Study (ACAPS) Research Group.

BACKGROUND: Few clinical trials have documented the efficacy of preventive treatment in asymptomatic women. METHODS AND RESULTS: Lovastatin and minidose warfarin were evaluated in a factorially designed, placebo-controlled, randomized trial. The primary outcome was 3-year change in the mean maximum intimal-medial thickness of the carotid arteries as measured by B-mode ultrasonography. Participants (n=919) were randomized to 1 of 4 treatment groups: lovastatin alone, warfarin alone, lovastatin+warfarin combination, or a double-placebo group. Eligible participants were asymptomatic for cardiovascular disease, with evidence of early carotid atherosclerosis and moderately elevated LDL cholesterol level. Almost half (n=445) of the participants were women. To avoid confounding, 117 women taking estrogen were excluded from analysis. Both sexes experienced reductions in disease progression with lovastatin; there was no evidence of an overall sex x treatment interaction (P=0.72). When estimates of the sex-specific results were examined post hoc, women experienced disease regression to the greatest extent with the lovastatin + warfarin combination (P=0.02), although the women on lovastatin alone also had a reduction in progression (P=0.09). Men experienced the greatest reduction with lovastatin alone (P=0.02), although there is a suggestion that warfarin may also reduce progression to some extent. CONCLUSIONS: Lovastatin is beneficial in reducing disease progression in women and men. Warfarin has no effect in women, although it may reduce progression in men. In men, warfarin does not add to the benefit of lovastatin and has no advantage over lovastatin alone.

Adult↗
PubMed1999

Aggressive cholesterol lowering delays saphenous vein graft atherosclerosis in women, the elderly, and patients with associated risk factors. NHLBI post coronary artery bypass graft clinical trial. Post CABG Trial Investigators.

BACKGROUND: The NHLBI Post Coronary Artery Bypass Graft trial (Post CABG) showed that aggressive compared with moderate lowering of low-density lipoprotein-cholesterol (LDL-C) decreased obstructive changes in saphenous vein grafts (SVGs) by 31%.1 Using lovastatin and cholestyramine when necessary, the annually determined mean LDL-C level ranged from 93 to 97 mg/dL in aggressively treated patients and from 132 to 136 mg/dL in the others (P<0.001). METHODS AND RESULTS: The present study evaluated the treatment effect in subgroups defined by age, gender, and selected coronary heart disease (CHD) risk factors, ie, smoking, hypertension, diabetes mellitus, high-density lipoprotein cholesterol (HDL-C) <35 mg/dL, and triglyceride serum levels >/=200 mg/dL at baseline. As evidenced by similar odds ratio estimates of progression (lumen diameter decrease >/=0.6 mm) and lack of interactions with treatment, a similar beneficial effect of aggressive lowering was observed in elderly and young patients, in women and men, in patients with and without smoking, hypertension, or diabetes mellitus, and those with and without borderline high-risk triglyceride serum levels. The change in minimum lumen diameter was in the same direction for all subgroup categories, without significant interactions with treatment. CONCLUSIONS: Aggressive LDL-C lowering delays progression of atherosclerosis in SVGs irrespective of gender, age, and certain risk factors for CHD.

Age Factors↗
PubMed1999

Rationale and design of the Arterial Disease Multiple Intervention Trial (ADMIT) pilot study.

The primary objectives of the pilot study were to: (1) evaluate the feasibility of recruiting patients with peripheral arterial disease (PAD); (2) measure the efficacy and safety of high-density lipoprotein (HDL)-raising treatment, low-density lipoprotein (LDL)-lowering therapy, antioxidant therapy, antithrombotic therapy, and their combinations; and (3) assess adherence to a complex multiple drug regimen. Secondary objectives included measurement of the effect of the interventions on prespecified biochemical markers, maintenance of therapy masking (in particular with niacin), and measurement of the intervention's impact on functional status and on quality of life. To date, no secondary prevention trial has been conducted specifically among patients with PAD. Intermittent claudication affects about 0.5% to 1.0% of persons aged >35 years. There is a striking increase in incidence of PAD with age, particularly among those aged >50 years in both sexes, although men are twice as likely as women to develop PAD. The Arterial Disease Multiple Intervention Trial was a double-blind randomized pilot trial of 468 participants with documented PAD. A 2 x 2 x 2 factorial design was used to evaluate the effect of 3 interventions. The pilot incorporated several major novel design features: first, the use of a simple noninvasive method (measurement of ankle brachial index) to identify a population with either symptomatic or asymptomatic PAD; and second, a lipid modifying strategy to increase HDL with nicotinic acid in the intervention group while lowering LDL levels equally with an hydroxymethylglutaryl-coenzyme A reductase inhibitor as needed in the intervention and control group. Two other arms, the antioxidant arm (consisting of beta-carotene and vitamins E and C) and the antithrombotic arm (using warfarin) were also added. Adherence to therapy was measured by pill count, and success in treatment was measured by the proportion of values in target range for HDL, LDL, and the international normalized ratio.

Adult↗
PubMed1999

Pharmacologic management of triglycerides.

Currently available cholesterol-lowering pharmacologic agents have been studied for their effect on reducing triglyceride levels. The fibrates increase lipoprotein lipase activity, thereby decreasing the size of triglyceride-rich particles. High doses of niacin can produce decreases in very low-density lipoprotein (VLDL) levels, triglyceride-rich particles, and low-density lipoprotein (LDL) by inhibiting hepatic lipoprotein synthesis. By increasing LDL-receptor activity, the statins increase the removal rate of triglyceride-rich particles. Each class of agents produces various degrees of triglyceride lowering, depending on the existing baseline level and other factors. Patients with elevated LDL who are also hypertriglyceridemic should receive statins as first-line therapy. Niacin may be used as an alternative first-line agent in patients with low LDL elevations. Combination therapy using other agents may be indicated depending on the patient's levels of triglycerides and LDL.

Anticholesteremic Agents↗
PubMed1999

Hemostatic effects of 1 mg daily warfarin on post CABG patients. Post CABG Studies Investigators.

Although coronary bypass graft surgery has increased the survival and quality of life of many individuals, patients remain at risk of restenosis and thrombotic occlusion of the coronary arteries and bypass grafts. In the screening period for participation in the multicenter Post Coronary Artery Bypass Graft (Post CABG) trial, the effects of 1 mg daily warfarin were evaluated using paired patient samples collected prior to and after at least 21 days of treatment. In stable patients (n = 40; 39 males 1 female; 51-74 years old) who previously had undergone coronary artery revascularization (1-10 years), no alterations in prothrombin time, international normalized ratio (INR), prothrombin fragment 1.2, or the hemostatic risk factors factor VII antigen and coagulant activity, von Willebrand's factor, fibrinogen, tPA, or PAI-1 were associated with the 1 mg daily warfarin treatment. The observations reported here supported the Post CABG Studies Steering Committee decision to treat patients with 1-4 mg warfarin daily adjusted to achieve INRs not to exceed 2. 0 consistent with low-intensity therapy.

Aged↗
PubMed1999

Effects of aggressive cholesterol lowering and low-dose anticoagulation on clinical and angiographic outcomes in patients with diabetes: the Post Coronary Artery Bypass Graft Trial.

Diabetic patients have greater risk for coronary heart disease (CHD) events after coronary artery bypass graft (CABG) surgery than nondiabetic patients. The Post CABG trial studied the effects of aggressive cholesterol lowering and low-dose anticoagulation in diabetic patients compared with nondiabetic patients. A double-blind, randomized clinical trial in 1,351 patients (1-11 years after CABG), the Post CABG trial consisted of two interventions (aggressive cholesterol-lowering versus moderate lowering and low-dose warfarin versus placebo) on angiographic end points. Angiographic changes in saphenous vein graft conduits 4.3 years after entry were compared in 116 diabetic and 1,235 nondiabetic patients. Seven clinical centers participated in the trial, as well as the National Institutes of Health project office (National Heart, Lung, and Blood Institute), the coordinating center (Maryland Medical Research Institute), and the Angiogram Reading Center (University of Minnesota). Baseline characteristics of the diabetic patients differed from the nondiabetic patients in the following ways: percentage of women participants, 15 vs. 7%, P = 0.002; mean baseline weight, 87.4 vs. 82.8 kg, P = 0.006; mean BMI, 29.5 vs. 27.6 kg/m2, P = 0.0002; mean systolic blood pressure, 141.7 vs. 133.6, P < 0.0001; mean triglyceride concentrations, 2.09 vs. 1.77 mmol/l, P < 0.0001; and mean HDL cholesterol concentrations, 0.93 vs. 1.02 mmol, P = 0.0001. The percentage of clinical events was higher in diabetic than nondiabetic patients (20.6 vs. 13.4, P = 0.033) and angiographic outcomes were not different. The benefits of aggressive cholesterol lowering were comparable in diabetic and nondiabetic patients for the angiographic end points. Warfarin use was not associated with clinical or angiographic benefit. Diabetic patients in the Post CABG trial had more CHD risk factors at study entry and higher clinical event rates during the study than nondiabetic patients. The benefits of aggressive cholesterol lowering in diabetic patients were comparable to those in nondiabetic patients for both angiographic and clinical end points. The small number of diabetic patients provided limited power to detect significant differences between diabetic and nondiabetic patients or between diabetic patients in the aggressive versus moderate cholesterol treatment strategies.

Anticholesteremic Agents↗
PubMed1998

Is aggressive cholesterol control justified? Review of the post-coronary artery bypass graft trial.

The Post-Coronary Artery Bypass Graft (CABG) trial was undertaken to compare the efficacy of aggressive low-density-lipoprotein (LDL) cholesterol lowering (<85 mg/dL) with moderate LDL-cholesterol lowering (130-140 mg/dL) in preventing atherosclerotic progression in saphenous vein grafts. In both the aggressive- and moderate-treatment groups, clinicians titrated lovastatin dosages based on individual patients' LDL-cholesterol levels. Based on angiography performed 4-5 years after enrollment, the rate of disease progression was 31% lower in aggressive-treatment patients than in those who received moderate treatment. Compliance with lovastatin therapy was 85-90%. The results confirm that LDL-cholesterol levels should be decreased to <100 mg/dL in patients with coronary artery disease. The challenge is to ensure that at-risk patients receive drug therapy in adequate, individualized doses.

Adult↗
PubMed1998

Clinical efficacy of cerivastatin: phase IIa dose-ranging and dose-scheduling studies.

Phase IIa clinical studies with cerivastatin--including 2 pilot US and European dose-ranging studies, and 1 US dose-scheduling study--were conducted to establish a dosage regimen and effective therapeutic doses of cerivastatin in the treatment of hypercholesterolemia. Both dose-ranging studies included a 10-week dietary run-in, to which placebo was added in the last 6 weeks, before patients (n = 385) were randomized to 1 of 6 4-week treatment groups: cerivastatin (0.025, 0.05, 0.1, and 0.2 mg/day), 40 mg/day lovastatin (US), 20 mg/day simvastatin (Europe), or placebo. The dose-scheduling study also included a 10-week dietary run-in and 6-week single-blind placebo run-in phase, before patients (n = 319) were randomized to 4 weeks of treatment with either 0.1 mg cerivastatin twice daily, 0.2 mg cerivastatin with the evening meal, 0.2 mg cerivastatin at bedtime, or placebo in a 2:2:2:1 ratio. The 4-week dose-ranging studies showed that all 4 doses of cerivastatin produced significantly greater reductions in low-density lipoprotein (LDL) cholesterol than placebo. Cerivastatin 0.2 mg decreased LDL cholesterol by 30.5%. Cerivastatin also significantly decreased total cholesterol, triglycerides, and apolipoprotein B, and significantly increased high-density lipoprotein (HDL) cholesterol. Similar reductions in LDL cholesterol and total cholesterol occurred with 0.2 mg/day cerivastatin in the dose-scheduling study, although the reductions were significantly greater when cerivastatin was administered once daily with either the evening meal or at bedtime compared with 2 divided doses. LDL cholesterol reductions were similar when cerivastatin was taken with the evening meal and at bedtime. Cerivastatin was well tolerated, with the incidence of adverse events comparable to that of placebo treatment. No clinically significant increases in either hepatic isoenzymes or creatine phosphokinase were observed after treatment with cerivastatin.

Apolipoproteins B↗
PubMed1998

Clinical efficacy and safety of cerivastatin: summary of pivotal phase IIb/III studies.

Cerivastatin is a new, third-generation 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor ("statin"), which is administered to hypercholesterolemic patients at doses equivalent to 1-3% of the doses of other statins. This report reviews the pivotal Phase IIb/III clinical trials in which the efficacy and safety of cerivastatin was compared with placebo and active comparator statins (lovastatin, simvastatin, and pravastatin) after both short- and long-term administration. Overall, the studies showed that at doses of 0.025-0.4 mg/day, cerivastatin produced dose-dependent reductions in low-density lipoprotein (LDL) cholesterol and total cholesterol, which were significantly greater than placebo. The greatest reductions were achieved with 0.4 mg/day cerivastatin. On this dose, >40% of patients achieved reductions in LDL cholesterol >40% and in a further 9% of patients, LDL cholesterol was decreased by >50%. At higher doses, cerivastatin also demonstrated potent triglyceride-lowering effects in a subgroup of patients with raised plasma triglycerides. Reductions in atherogenic lipids and lipoproteins were accompanied by significant increases in high-density lipoprotein (HDL) cholesterol, apolipoprotein A-I, and antiatherogenic lipoprotein A-I. Long-term administration of cerivastatin for periods of up to 2 years was associated with persistent reductions in LDL cholesterol, total cholesterol, triglycerides, and apolipoprotein B as well as increases in HDL cholesterol similar to those observed after initial administration. Long-term cerivastatin treatment was also well tolerated. There was no significant difference between the incidence of adverse effects with cerivastatin and comparator statins or between cerivastatin and other statins with respect to clinically significant increases in either hepatic enzymes or creatine phosphokinase. In conclusion, these studies indicate that cerivastatin is a safe and effective long-term treatment for patients with primary hypercholesterolemia and also suggest that higher doses should be investigated.

Adolescent↗
PubMed1998

Therapeutic efficacy of the lipid-lowering armamentarium: the clinical benefits of aggressive lipid-lowering therapy.

Hypercholesterolemia, particularly an elevated level of low-density lipoprotein (LDL) cholesterol, is an unarguably established risk factor for coronary artery disease (CAD). It is equally well established that lowering LDL cholesterol levels will decrease CAD-related morbidity and mortality in patients with established CAD. Although lipid-lowering therapy is known to retard the progression of atherosclerosis in patients with native coronary arteries, its effect in patients with coronary bypass grafts, which are particularly vulnerable to occlusion, is less well understood. Moreover, whereas several major clinical trials have documented the benefits of lowering LDL cholesterol in a variety of patient subpopulations, there has been far less clarity surrounding the question of whether aggressive lowering of LDL cholesterol is of greater benefit than moderate lowering of LDL cholesterol. The Post Coronary Artery Bypass Graft (Post-CABG) trial, a multicenter, randomized, double-blind clinical trial comprising 1,351 patients with elevated levels of LDL cholesterol and a history of bypass surgery was designed to determine whether aggressive lowering of LDL cholesterol levels with therapy based on 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors ("statins") is more effective than moderate lowering in delaying the progression of atherosclerosis in bypass grafts. Quantitative computer-assisted angiography was conducted at baseline and again at an average of 4.3 years. The primary angiographic outcome was the mean percentage per patient of grafts with a decrease of > or = 0.6 mm in lumen diameter. Patients who received aggressive therapy were significantly more likely than their moderate-treatment counterparts to achieve and maintain LDL cholesterol levels within the National Cholesterol Education Program's (NCEP's) recommended target of < or = 100 mg/dL (< or = 2.59 mmol/L). Moreover, the mean percentage of grafts with progression of atherosclerosis was 27% for aggressively treated patients, compared with 39% for those who were randomized to the moderate-treatment group (p < 0.001). This study demonstrates that aggressive lipid lowering is practical and worthwhile in at-risk patients. Aggressive treatment is far more effective than moderate treatment in lowering LDL cholesterol levels to the NCEP target level of < or = 100 mg/dL (< or = 2.59 mmol/L), and this intervention decreases the progression of atherosclerosis.

Anticholesteremic Agents↗
PubMed1998

Effect of human apolipoprotein E isoforms on plasma lipids, lipoproteins and apolipoproteins in apolipoprotein E-deficient mice.

The current study compared the acute effect of human apolipoprotein (apo) E isoforms on plasma lipids, lipoproteins and apolipoproteins 6 h after a bolus intravenous injection of individual isoforms into apo E-deficient mice. We found a large accumulation of remnant particles not only in the d<1.019 g/ml fraction but also in the d = 1.019-1.063 mg/dl fraction in the setting of absence of endogenous mouse apo E. A significant reduction in total cholesterol (49, 47 and 18%) (P<0.005), cholesterol in the d<1.019 g/ml fraction (56, 50 and 18%) and in the d = 1.019-1.063 mg/dl fraction (38, 40 and 17%) was obtained with apo E-3, E-4 and E-2, respectively. Apo E-3 and E-4 showed more pronounced total cholesterol lowering effect than E-2 (P<0.0001). In the d<1.019 g/ml fraction, apo E-3 and E-4 resulted in a marked decrease in apo B-100 (36 and 34%), B-48 (48 and 52%), A-I (48 and 44%) and A-IV (52 and 46%), respectively. The decrease caused by apo E-2 in apo B-100 (19%), B-48 (16%), A-I (18%) and A-IV (33%) was less than that of E-3 or E-4. In the d = 1.019-1.063 g/ml fraction, an apparent decline in apo B-48 (42 and 38%), A-I (39 and 40%) and an increase in apo B-100 (25 and 18%) were observed after apo E-3 and E-4 injection, respectively, while apo E-2 did not cause an appreciable change in these apolipoproteins (-4 to 6%). Compared to normal saline, liver total cholesterol content was increased by 37, 34 and 16% (P<0.05) after apo E-3, E-4 and E-2 injection, respectively. Apo E-3 and E-4 showed the same high affinity binding to mice hepatic LDL receptor, while apo E-2 was severely defective in binding. These findings indicate that apo E polymorphism is an important factor modulating remnant lipoprotein metabolism.

Animals↗
PubMed1998

Ascorbic acid supplement use and the prevalence of gallbladder disease. Heart & Estrogen-Progestin Replacement Study (HERS) Research Group.

To investigate the relation of ascorbic acid supplement use to gallbladder disease and cholecystectomy, we conducted a cross-sectional analysis of baseline from 2744 postmenopausal women, aged 44-79 years, enrolled in the Heart & Estrogen-progestin Replacement Study (HERS), a secondary coronary heart disease prevention trial. A total of 629 HERS participants (23%) reported a history of gallbladder disease. Of these, 508 (19%) also reported a history of cholecystectomy. In bivariate models, ascorbic acid supplement use was associated with a decreased prevalence of gallbladder disease [odds ratio (OR)=0.74; 95% confidence interval (CI), 0.57, 0.96] and a trend toward a decreased prevalence of cholecystectomy (OR=0.77; 95% CI, 0.58, 1.02). Because we detected significant interactions between ascorbic acid supplement use and alcohol consumption, multivariate analyses were performed stratified by drinking status. After adjustment for potential confounding variables, use of ascorbic acid supplements among drinkers was associated with a decreased prevalence of gallbladder disease (adjusted OR=0.50; 95% CI, 0.31, 0.81) and cholecystectomy (adjusted OR=0.38; 95% CI, 0.21, 0.67). Use of ascorbic acid supplements among non-drinkers was not significantly associated with either prevalence of gallbladder disease or cholecystectomy. Further study is necessary to confirm our findings and, specifically, to examine the combined effects of ascorbic acid and alcohol on cholesterol metabolism.

Adult↗
PubMed1998

Effect of the novel antiplatelet agent cilostazol on plasma lipoproteins in patients with intermittent claudication.

Cilostazol is an antiplatelet agent and vasodilator marketed in Japan for treatment of ischemic symptoms of peripheral vascular disease. It is currently being evaluated in the United States for treatment of symptomatic intermittent claudication (IC). Cilostazol has been shown to improve walking distance in patients with IC. In addition to its reported vasodilator and antiplatelet effects, cilostazol has been proposed to have beneficial effects on plasma lipoproteins. We examined the effect of cilostazol versus placebo on plasma lipoproteins in 189 patients with IC. After 12 weeks of therapy with 100 mg cilostazol BID, plasma triglycerides decreased 15% (P<0.001). Cilostazol also increased plasma high density lipoprotein cholesterol (HDL-C) (10%) and apolipoprotein (apo) A1 (5.7%) significantly (P<0.001 and P<0.01, respectively). Both HDL3 and HDL2 subfractions were increased by cilostazol; however, the greatest percentage increase was observed in HDL2. Individuals with baseline hypertriglyceridemia (>140 mg/dL) experienced the greatest changes in both HDL-C and triglycerides with cilostazol treatment. In that subset of patients, HDL-C was increased 12.2% and triglycerides were decreased 23%. With cilostazol, there was a trend (3%) toward decreased apoB as well as increased apoA1, resulting in a significant (9.8%, P<0.002) increase in the apoA1 to apoB ratio. Low density lipoprotein cholesterol and lipoprotein(a) concentrations were unaffected. Cilostazol treatment resulted in a 35% increase in treadmill walking time (P=0.0015) and a 9.03% increase in ankle-brachial index (P<0.001). These results indicate that in addition to improving the symptoms of IC, cilostazol also favorably modifies plasma lipoproteins in patients with peripheral arterial disease. The mechanism of this effect is currently unknown.

Adrenergic beta-Antagonists↗