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Active clinical trials for "Hyperlipoproteinemia Type II"

Results 151-160 of 215

Genetic Causes of Familial Hypercholesterolemia

Familial Hypercholesterolemia

Familial hypercholesterolemia (FH) is a common disease. The genetic background to FH is not yet fully understood. In the present prospective cohort study we aim to study the association between different clinical characteristics, gene mutations and prognosis.

Active4 enrollment criteria

Study of Alirocumab (REGN727/SAR236553) in Patients With heFH (Heterozygous Familial Hypercholesterolemia)...

Heterozygous Familial Hypercholesterolemia

This is a randomized, double-blind, placebo-controlled, parallel-group, multi-national study alirocumab (REGN727/SAR236553) in patients with Heterozygous Familial Hypercholesterolemia (heFH) who are not adequately controlled with their Lipid-Modifying Therapy (LMT).

Completed22 enrollment criteria

Postprandial Response After Intake of Meals With Different Fatty Acid Composition

HealthyFamilial Hypercholesterolemia

The aim of the study is to understand more about how different fatty acids modulate postprandial lipid metabolism and inflammatory response.

Completed19 enrollment criteria

NHLBI Type II Coronary Intervention Study

Cardiovascular DiseasesCoronary Disease5 more

To determine whether lowering of cholesterol with cholestyramine in a population with Type II hyperlipidemia led to a decreased rate of progression (a regression of coronary artery disease) as demonstrated by death, myocardial infarction, or progression of disease on angiography.

Completed1 enrollment criteria

Study of AKCEA-ANGPTL3-LRX (ISIS 703802) in Patients With Homozygous Familial Hypercholesterolemia...

Homozygous Familial Hypercholesterolemia

This is a single center, open-label study to evaluate the efficacy of AKCEA-ANGPTL3- LRX for reduction of low density lipoprotein cholesterol (LDL-C) levels in patients with Homozygous Familial Hypercholesterolemia (HoFH).

Withdrawn5 enrollment criteria

Study of Coronary Calcification in Subjects With Autosomal Dominant Familial Hypercholesterolemia...

Familial Hypercholesterolemia - Heterozygous

Familial hypercholesterolemia (FH) is an autosomal dominant genetic disorder characterized by elevated plasma levels of LDL-C cholesterol. This early and significant elevation of LDL-C triggers premature atherosclerosis, particularly coronary artery disease. The initiation and management of LDL-C therapies is based on cardiovascular risk assessment. Although this is undoubtedly higher than in normocholesterolemic patients, a significant heterogeneity in heFH patients still persists that is not completely explained. Moreover, the evaluation of cardiovascular risk in patients with heFH is difficult for many reasons: non-validity of risk scores, futility of a risk calculation limited to 10 years in a young patient, late positivity of stress tests . Therefore, there is a clear need for new cardiovascular risk assessment tools to identify higher risk heFH patients who could benefit from early and aggressive treatment. The Coronary Artery Calcium (CAC) Score has been widely studied in the US and validated in European recommendations, and has shown the best reclassification index for patients at intermediate cardiovascular risk. A CAC score of zero is associated with a very low risk of event irrespective of the number of risk factors. Non-calcified plaques are by definition not detected by ACC and patients with CAC = 0 may only have soft non-calcified plaques. The prevalence of these non-calcified plaques in very high-risk patients with acute coronary syndrome is 5%. The prevalence in FH patients is unknown. It has also been shown that the extent of the atherosclerotic burden is related to cardiovascular risk. CAC score has been poorly evaluated in heFH patients. However, hypercholesterolemia and calcifications have been shown to be correlated: supra-aortic calcified masses in homozygous FH patients, early calcifications associated with chronic exposure to high LDL-C (cholesterol burden, equivalent to cigarettes) and finally, the calcifying role of statins. The early increase of LDL-C in patients with genetic forms of FH causes premature cardiovascular damage. Investigators' hypothesis is that patients with FH have earlier coronary atheroma (and thus calcifications and non-calcified plaques) due to exposure early in life to high levels of LDL-cholesterol.

Completed19 enrollment criteria

Evaluating the Efficacy of Pediatric Lipid Screening Alerts

HypercholesterolemiaHypercholesterolemia3 more

The purpose of the study is to evaluate prospectively the impact of different system alerts on the prescription of lipid panels to pediatric Geisinger patients (9-11 years old), as per the now-universal guidelines. This will help quantify the relative effectiveness of different alerts and combinations of alerts on provider prescribing behavior and patient uptake of screening.

Completed4 enrollment criteria

Evaluate the Efficacy and Safety of Lomitapide in Pediatric Patients With Homozygous Familial Hypercholesterolemia...

Homozygous Familial Hypercholesterolemia

This is a Phase 3 single-arm, open-label, international, multi-center clinical trial to evaluate the efficacy and safety of lomitapide in pediatric patients with HoFH who are receiving stable lipid-lowering therapy, including LDL apheresis. The study is comprised of a 12-week Run-in Period, a primary 24-week Efficacy Phase, followed by an 80-week Safety Phase.

Withdrawn19 enrollment criteria

A Prospective Cohort Study on Familial Hypercholesterolemia in Health Examination Population

Familial Hypercholesterolemia

To determine the prevalence and the prognosis in a corhort of patients with familial hypercholesterolemia (FH).

Not yet recruiting5 enrollment criteria

Cross-over Pilot Study of Blood Cholesterol Response to Dietary Saturated Fat in Patients With Autosomal...

Familial Hypercholesterolemia

We are performing a pilot cross-over diet study involving 5 patients with heterozygous FH and 5 patients with unexplained ADH. The patients will be randomized to a low versus high saturated fat diet for 4 weeks each. We hypothesize that patients with unexplained ADH may have an exaggerated cholesterol response to saturated fat intake. The specific aim of this study is to quantify the increase in LDL-C in unexplained ADH patients compared to FH patients. The pilot study proposed here will develop preliminary data to be used for future funding proposals of larger, randomized studies.

Withdrawn21 enrollment criteria
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