نتایج جستجو برای: familial hypercholesterolemia fh
تعداد نتایج: 68801 فیلتر نتایج به سال:
Familial hypercholesterolemia (FH) is a genetic condition that causes high low-density lipoprotein (LDL) cholesterol (sometimes referred to as bad cholesterol) from birth. FH means high cholesterol that runs in a family. FH is caused by specific DNA changes that are passed on from parents to their children. It is not caused by lifestyle factors such as a high-fat diet or lack of exercise. There...
Ischemic stroke and coronary heart disease (CHD) share common mechanisms through blood circulation, but their relationships with cholesterol levels are different. In the case of CHD, “the lower, the better” hypothesis with regards to cholesterol has prevailed so far in clinical fields, setting upper limits of cholesterol levels and advising maintenance of the levels below the limits. However, t...
Familial hypercholesterolemia (FH) is an autosomal dominant genetic disorder that clinically leads to increased low density lipoprotein-cholesterol (LDL-C) levels. As a consequence, FH patients are at high risk for cardiovascular disease (CVD). Mutations are found in genes coding for the LDLR, apoB, and PCSK9, although FH cannot be ruled out in the absence of a mutation in one of these genes. I...
OBJECTIVE Lp(a) is an independent, causal, genetic risk factor for cardiovascular disease and aortic stenosis. Current pharmacological lipid-lowering therapies do not optimally lower Lp(a), particularly in patients with familial hypercholesterolemia (FH). APPROACH AND RESULTS In 4 phase III trials, 382 patients on maximally tolerated lipid-lowering therapy were randomized 2:1 to weekly subcut...
The present study examined the angiographic characteristics and prognosis of young males under 40 years of age with acute myocardial infarction (AMI) and familial hypercholesterolemia (FH). The study group was divided into an FH group (n=16) and a non-FH group (n=27). Lesion morphology was classified as complex or smooth. Overall 36 patients were followed up for an average of 9.4 years. The fre...
OBJECTIVE Heterozygous familial hypercholesterolemia (FH) is the most common premature atherosclerotic cardiovascular disease (ASCVD)-related monogenic disorder, and it is associated with ischemic heart disease. There is limited information whether FH increases the risk of peripheral arterial and cerebrovascular disease. Our aim was to analyze ASCVD prevalence and characteristics in different a...
The most common genetic cause of premature coronary artery disease (CAD) is familial hypercholesterolemia (FH), an autosomal dominant condition in which half the offspring of an affected individual will also be affected from birth. The causative mutations are mainly found in the LDL receptor gene (LDLR) and less frequently in the apolipoprotein B gene and the proprotein subtilisin/kexin type 9 ...
BACKGROUND Familial hypercholesterolemia (FH) is a life-threatening inherited condition. Untreated patients have the risk to develop raised plasma levels of cholesterol, atherosclerosis and cardiovascular disease (CVD). If diagnosed and treated early in life, the pathological consequences due to atherosclerosis could be avoided and patients with FH can have an anticipated normal life. Mounting ...
BACKGROUND: Familial hypercholesterolemia (FH) is an autosomal dominant disorder that affects cholesterol metabolism and is an important risk factor for heart disease. Three different genes were causally linked to this disorder: LDLR (low density lipoprotein receptor), APOB [apolipoprotein B (including Ag(x) antigen)], and PCSK9 (proprotein convertase subtilisin/kexin type 9). We evaluated a ne...
BACKGROUND Familial hypercholesterolemia (FH) is an autosomal codominant disorder caused by mutations in the low-density lipoprotein receptor (LDLR) gene. Homozygous FH patients (hoFH) have severe hypercholesterolemia leading to life threatening atherosclerosis in childhood and adolescence. Mice with germ line interruptions in the Ldlr and Apobec1 genes (Ldlr(-/-)Apobec1(-/-)) simulate metaboli...
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