View clinical trials related to Hyperlipoproteinemias.
Filter by:The aim of the study is to identify children and families that are at risk for cardiovascular disease because of a condition known as familial hyperlipidemia. This condition may increase the risk of cardiac events such as hardening of the arteries anywhere in the body which can result in heart attacks, strokes, and death over ten fold. Children have already been assessed in the Healthy Hearts screening program and identified as having elevated cholesterol. A buccal smear will identify whether the familial hyperlipidemia condition exist in your child. If the child's test shows that they have the specific gene for familial hyperlipidemia and shows a genetic tendency towards premature heart disease, we would encourage genetic testing for as many blood family members as possible. The study plan is to determine whether the Healthy Hearts screening program is a more effective way of identifying students at risk since it is estimated that less than 10% of those individuals with the problem have been identified. If it is effective, then it will be incorporated as part of the standard screening process in the Healthy Hearts program. Aim 1: Is a school screening program a more effective method to identifying those at risk for familial hyperlipidemia? Aim 2: What percent of children with elevated cholesterol ≥ 200 mg/dl have familial hyperlipidemia?
This study will be a placebo-controlled, double-blind, randomized, phase 3 study to Evaluate the Efficacy, Safety, and Tolerability of Obicetrapib in Participants with a History of Heterozygous Familial Hypercholesterolemia (HeFH).
Phase III study to test the hypothesis that treatment with pelacarsen (TQJ230) 80 mg Q4W compared to placebo significantly reduces the rate of lipoprotein apheresis in patients with hyperlipoproteinemia (a) and established cardiovascular disease currently undergoing lipoprotein apheresis in Germany on a weekly schedule.
This a multicenter, Phase 2b, double-blind, placebo-controlled, parallel group study to provide data on efficacy and safety of LY3561774 administered subcutaneously at various doses in participants with mixed dyslipidemia and on a stable dose of a statin.
The purpose of this study is to evaluate the effectiveness, safety and health economics of precise drug use strategies based on pharmacogenomics compared with traditional drug use strategies for cardiovascular related chronic diseases.
Aim 1: To determine whether therapy with Alirocumab, compared to pre-treatment, will effectively improve carotid atherosclerotic plaque characteristics by reducing Ktrans and LRNC size. To achieve this goal, we will (a) enroll 30 subjects who are intolerant to high intensity statin therapy and only able to tolerate low potency statin or low weekly dose of high potency statin and have LDL-C ≥70 mg/dl; (b) initiate alirocumab at 150mg subcutaneously injection every 2 weeks; (c) perform carotid DCE-MRI scans at baseline, 3, 6 and 12 months; (d) perform quantitative analysis for vascular inflammation and plaque LRNC volume and other plaque characteristics; (e) compare vascular inflammation and LRNC volume between pre- and post-alirocumab at 3, 6 and 12 months. Aim 2: To examine associations between reductions in atherogenic lipids (LDL-C, Lp(a), non-HDL-C) and changes in atherosclerotic plaque characteristics. To achieve this goal, we will (a) perform laboratory assessments of lipids, lipoproteins and apo-lipoproteins at baseline and during the study; (b) compare lipids, lipoproteins and apo-lipoproteins levels between pre- and post-alirocumab; (c) correlate reductions in atherogenic lipids with changes atherosclerotic plaque characteristics.
Animal studies have found that vitamin K-dependent proteins matrix Gla protein and osteocalcin beneficially influence lipid and glucose metabolism, respectively. However, this concept has not been tested in humans at risk for dyslipidemia and diabetes risk. Vitamin K supplementation presents an opportunity to test the hypothesized link between the vitamin K-dependent proteins and markers of lipid and glucose metabolism. The investigators will conduct an 8-week vitamin K intervention (to manipulate carboxylation of matrix Gla protein and osteocalcin) and determine its effects on markers of dyslipidemia and diabetes risk. Sixty obese children will be randomly allocated to either the control group receiving placebo or the low-dose (45 mcg/d) or high-dose group (90 mcg/d) receiving vitamin K (menaquinone-7).
Front-line clinicians cannot currently test for an individual participant whether symptoms experienced are the pharmacological result of a statin or due to other phenomena. In this trial, participants who have previously ceased statins due to side effects will be offered the opportunity to undergo twelve randomly ordered 1-month periods. There will be four periods of no medication, four periods of placebo and four periods of statin. The placebo and the statin pills will be identical in appearance. Participants will record on a daily basis side-effects experienced. At the end of the study, the one-month sessions are sorted into the order shown above. The participant can then observe directly how much of the increase in symptoms seen with statin is also seen with placebo. 1. Hypothesis 1: that >30% of participants enrolling for the study will complete it. 2. Hypothesis 2: Overall >50% of symptom burden is nocebo rather than pharmacological 3. The investigators will define the Nocebo proportion of side effects. 4. Hypothesis 3: that the majority of participants, at 6 months after completion, will either be taking statins or have declined statins for reasons other than perceived side effects.
The investigators will investigate whether dapagliflozin (FORXIGA) might improve lipoprotein metabolism as well as hyperglycemia in Japanese patients with type II diabetes mellitus whose HbA1c levels are less than 7.0% (from 20 to 65 years of age). The investigators will examine changes of fasting lipoprotein profile including TG, TC, HDL-C, apoB-48 and RemL-C before and after the 8 weeks administration of dapagliflozin.