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At least 19 recordsLinked to original sources
PubMed1973

Hyperlipidemia in coronary heart disease. II. Genetic analysis of lipid levels in 176 families and delineation of a new inherited disorder, combined hyperlipidemia.

To assess the genetics of hyperlipidemia in coronary heart disease, family studies were carried out in 2520 relatives and spouses of 176 survivors of myocardial infarction, including 149 hyperlipidemic and 27 normolipidemic individuals. The distribution of fasting plasma cholesterol and triglyceride values in relatives, together with segregation analyses, suggested the presence of five distinct lipid disorders. Three of these-familial hypercholesterolemia, familial hypertriglyceridemia, and familial combined hyperlipidemia-appeared to represent dominant expression of three different autosomal genes, occurring in about 20% of survivors below 60 yr of age and 7% of all older survivors. Two other disorders-polygenic hypercholesterolemia and sporadic hypertriglyceridemia-each affected about 6% of survivors in both age groups. The most common genetic form of hyperlipidemia identified in this study has hitherto been poorly defined and has been designated as familial combined hyperlipidemia. Affected family members characteristically had elevated levels of both cholesterol and triglyceride. However, increased cholesterol or increased triglyceride levels alone were also frequently observed. The combined disorder was shown to be genetically distinct from familial hypercholesterolemia and familial hypertriglyceridemia for the following reasons: (a) the distribution pattern of cholesterol and triglyceride levels in relatives of probands was unique; (b) children of individuals with combined hyperlipidemia did not express hypercholesterolemia in contrast to the finding of hypercholesterolemic children from families with familial hypercholesterolemia; and (c) analysis of informative matings suggested that the different lipid phenotypes owed their origin to variable expression of a single autosomal dominant gene and not to segregation of two separate genes, such as one elevating the level of cholesterol and the other elevating the level of triglyceride. Heterozygosity for one of the three lipid-elevating genes identified in this study may have a frequency in the general population of about 1%, constituting a major problem in early diagnosis and preventive therapy.

Adolescent↗
PubMed1976

[Studies on the heredity and pathogenesis of familial combined hyperlipidemia ("multiple lipoprotein type" hyperlipidemia)].

A family with familial combined hyperlipidemia (multiple-lipoprotein type hyperlipidemia) was investigated with regard to mode of inheritance, phenotypic expression, presence of genetic markers, and biochemical parameters related to lipid metabolism. The family of 22 subjects (13 males, 9 females) was composed of 5 type IIa, 8 type IIb, 1 type IV hyperlipoproteinemias and 5 normolipidemics. The distribution of serum cholesterol and serum triglyceride concentration was bimodal. No relationship was observed between hyperlipidemia and blood groups or histocompatibility antigens. Subjects with high HLA 8 or W 15 had, on the average, higher lipid levels than others. However, these antigens were observed in normolipidemics too. The response to therapy with alufibrate (2g/day) was not uniform. Subjects with marked triglyceride lowering exhibited only moderate cholesterol lowering, and marked cholesterol lowering was associated with poor triglyceride lowering. The reduction in serum lipids was observed in unaffected family members as well. It is therefore concluded that alufibrate does not exert an effect on the defect in familial combined hyperlipidemia but on some unspecific sites probably on lipoprotein lipase. The familial combined hyperlipidemia appears to be transmitted in an autosomal dominant mode and very probably determined by more than one gene.

Adolescent↗
PubMed2000

[The effect of hyperlipidemia on metabolism, distribution and secretion of lidocaine in patients with primary hyperlipidemia].

High prevalence and coexistence of lipid disturbances and ischaemic heart disease (IHD) presents a new challenge to safe and effective pharmacotherapy in this group of patients. Ventricular arrhythmias are common in patients with IHD and lidocaine is the principal drug for their management. The aim of this study was to analyze the pharmacokinetics and pharmacodynamics of lidocaine in primary hyperlipidemia, depending on the type of hyperlipidemia, and to draw conclusions concerning therapeutic safety. The study was performed in 31 subjects, aged 25-58 years (mean 43.5 years), divided into four groups. The control group included 8 subjects aged 28-52 years. Group 2 included 8 patients aged 29-54 years with hypercholesterolemia. Group 3 included 8 patients aged 25-58 years with hypertriglyceridemia, and group 4 included 7 patients aged 38-58 years with mixed hyperlipidemia. The concentration of lidocaine and its main metabolite, monoethylglycinexylidide (MEGX), was measured. A single dose of lidocaine was administered intravenously during 2 minutes. Blood was sampled from the cubital vein before (0) and 5', 15', 30', 60', 120', 240', 360' and 600' after injection. The concentrations of lidocaine and MEGX were established using high-pressure liquid chromatography (HPLC)--Tab. 1-5. It was found that hyperlipidemia influences the pharmacokinetics and pharmacodynamics of lidocaine. The pattern depends on the type of hyperlipidemia. The main difference in the pharmacokinetics of lidocaine in patients with hypercholesterolemia is a greater volume of distribution and longer terminal half-life of the drug. In conclusion, dosage modification is necessary in hypercholesterolemia.

Adult↗
PubMed1998

Cerivastatin in the treatment of mixed hyperlipidemia: the RIGHT study. The Cerivastatin Study Group. Cerivastatin Gemfibrozil Hyperlipidemia Treatment.

The Cerivastatin Gemfibrozil Hyperlipidemia Treatment (RIGHT) study--a multicenter, randomized, double-blind, placebo-controlled study--compared the lipid-lowering effects of cerivastatin, once daily at doses of 0.1, 0.2, and 0.3 mg with those of twice-daily gemfibrozil 600 mg in 751 patients with primary mixed hyperlipidemia. Randomization to the first 16 weeks of treatment followed an initial 4-week washout period and subsequent 6-week diet-controlled, placebo run-in phase. Patients continued to receive study medication for a further 36 weeks, with those previously on placebo switched to 0.1 mg/day cerivastatin at the end of week 16. Additional cholestyramine therapy was permitted at week 36 in patients with uncontrolled low-density lipoprotein (LDL) cholesterol levels. Cerivastatin achieved significant dose-dependent reductions in LDL cholesterol of 15-24% after 16 weeks of treatment, compared with reductions of 7.5% with gemfibrozil. Over this period both cerivastatin (0.3 mg) and gemfibrozil (1,200 mg) significantly decreased levels of triglycerides (20.3% vs 50.3%, respectively) and very low-density lipoprotein (VLDL) cholesterol (30.8% vs 47.1%, respectively), as well as increasing high-density lipoprotein (HDL) cholesterol (11.3% vs 13.3%, respectively). The reductions in LDL cholesterol and other atherogenic lipids and lipoproteins at 16 weeks were sustained in the subsequent 36-week double-blind continuation phase, during which time <10% of patients received additional cholestyramine therapy. Both study drugs were well tolerated, with the incidence of adverse events similar to that of placebo treatment. Clinically significant increases in hepatic transaminases and creatine phosphokinase occurred at a similar low frequency of around 1%. This study demonstrated that cerivastatin is a safe, well-tolerated, and effective treatment for lowering elevated LDL cholesterol and triglycerides in patients with mixed hyperlipidemia.

Adolescent↗
PubMedDate not supplied

Use of simvastatin treatment in patients with combined hyperlipidemia in clinical practice. For the Simvastatin Combined Hyperlipidemia Registry Group.

OBJECTIVE: To describe and understand current care of simvastatin-treated patients with combined hyperlipidemia in routine clinical practice. DESIGN: A 6-month prospective observational study. Demographics, simvastatin dosage, cardiac risk factors, and lipid profile were collected from August 1997 to December 1998 at 20 sites (230 patients) across the United States. RESULTS: Overall mean percentage of reduction in total cholesterol levels was 27% (P<.001), low-density lipoprotein cholesterol (LDL-C) was 35% (P<.001), and triglyceride values was 28% (P<.001). Among those patients with low baseline high-density lipoprotein cholesterol (HDL-C) values (<0.91 mmol/L [<35 mg/dL]) (N = 49), there was a 17% increase in HDL-C (P< or =.001); 35% of these patients achieved National Cholesterol Education Program HDL-C goal (ie, < or =0.91 mmol/L [> or =35 mg/dL]). Coronary heart disease (CHD) patients were given significantly higher initial doses (mean, 15.1 mg) compared with non-CHD patients (mean, 11.5 mg) (P< or =.001). Overall, 74% of patients achieved LDL-C goal (52% on starting dose, 22% after 1 titration). Among those patients who were not at goal and had a follow-up lipid profile result available, only 1 patient (2%) was at the maximum dose (80 mg); 69% were receiving 20 mg or less. Approximately 63% of patients with CHD, 80% of patients with 2 or more risk factors, and 91% of patients with fewer than 2 risk factors achieved LDL-C goal. CONCLUSIONS: Multiple factors contribute to LDL-C goal achievement in a usual care setting. A significant opportunity exists to increase the number of patients who achieve LDL-C goal by appropriate dose titration and/or give patients a higher initial dose of simvastatin.

Adult↗
PubMed2002

Lack of agreement between the plasma lipid-based criteria and apoprotein B for the diagnosis of familial combined hyperlipidemia in members of familial combined hyperlipidemia kindreds.

Our objective was to analyze the concordance between abnormally high-cholesterol and triglyceride concentrations and increased apoliprotein B (apoB) concentrations for considering subjects as affected in familial combined hyperlipidemia (FCHL) kindreds. Twenty-two FCHL families (n = 217) were included. There was a lack of agreement in the identification of the abnormal subjects when several cholesterol- and triglyceride-based criteria were compared against various apoprotein B-based criteria. The agreement, measured as kappa coefficients, between 14 lipid-based criteria and 8 apoB concentrations is reported. For the most frequently used criterion (> or = 90th percentile for cholesterol or triglyceride concentrations), the agreement was low for all apoB levels (kappa, 0.42 to 0.49). A concentration of triglycerides > or = 150 mg/dL and cholesterol > or = 200 mg/dL was the only criterion with a kappa value above 0.6; the acceptable agreement was found with an apoB concentration > or = 120 mg/dL (kappa = 0.604). In conclusion, the data reported here clearly show that a large degree of diagnostic uncertainty exists in the categorization as normal or abnormal of members of FCHL kindred. Different diagnostic criteria would result in conflicting results. This is a critical issue, depending on the diagnostic criteria used, completely different conclusions could result from the linkage analysis in the FCHL studies.

Adult↗
PubMed2002

Chlamydia pneumoniae and hyperlipidemia are co-risk factors for atherosclerosis: infection prior to induction of hyperlipidemia does not accelerate development of atherosclerotic lesions in C57BL/6J mice.

Chlamydia pneumoniae has been shown to accelerate atherosclerotic lesion development in hyperlipidemic animals. This study showed that C. pneumoniae did not accelerate lesion development in mice if a high-fat/high-cholesterol diet was started after infection, indicating that C. pneumoniae is a co-risk factor with hyperlipidemia for cardiovascular disease.

Animals↗
PubMed1976

Hyperlipidemia, hypercoagulability, and accelerated thrombosis: studies in congenitally hyperlipidemic rats and in rats and monkeys with induced hyperlipidemia.

Inbred Carworth Farms Nelson (CFN) congenitally hyperlipidemic rats had significantly shorter coagulation and prothrombin times and higher levels of coagulation factors, II, V, VII, VIII, and X than did controls. Conversely, congenitally hypolipidemic rats of the same strain had significantly longer coagulation and prothrombin times and lower levels of factors II, V, VII, X and XII and of blood platelets than did controls. A loop-shaped polyethylene cannula was inserted into the aorta to assess the potential for thrombosis. The hyperlipidemic group obstructed this significantly faster and the hypolipidemic group slower than did the controls. Normal CFN rats made hypertensive by unilateral renal artery clip developed hypertension together with significantly elevated serum cholesterol and factor VII and X levels. Rhesus monkeys with diet-induced hyperlipidemia showed shorter prothrombin times and higher factor X levels than did controls on normal diet. By selective breeding, two groups of squirrel monkeys were obtained. Both groups had similar serum cholesterol levels on a normal diet but one group (hyperresponders) showed higher serum cholesterol levels on a cholesterol-containing diet than did the other (hyporesponder) group. Both groups showed significantly elevated levels of factors II, V, VII, IX and X on a cholesterol-containing diet. There was good correlation between the levels of many coagulation factors and serum cholesterol in both rats and monkeys. If thrombosis is important in the genesis of atherosclerosis, these findings could indicate that elevation of plasma lipids may play a role, via the coagulation pathway, in the production of human vascular disease.

Animals↗
PubMed1993

[The Navarra study (PECNA). Hyperlipidemia IV. Prevalence of hyperlipidemia in the infant- and juvenile population of Navarra. Variations based on age, gender and health care accessibility].

As part of an epidemiological study on cardiovascular risk factors among children and adolescents in Navarra, lipids and lipoproteins were analyzed in 5,829 children of both sexes. These children were between 4 and 17 years of age and were randomly selected from the school population of our community. In this article, we analyze the prevalence of lipid risk, according to its different definitions, among children and adolescents in Navarra, and its variations related to age, sex and sanitary area. The prevalence of hypercholesterolemia (C > 200 mg/dl) among children and adolescents, aged 4 to 17 years, is very high: 21.07% +/- 0.54%. In spite of having high serum levels of HDL, the lipid risk measured by the risk quotient LDL/HDL > 2.2 is still very high: 15-70% +/- 0.49%. If we define the lipid risk during childhood and adolescence by the quotient LDL/HDL > 2.2, male adolescents turn out to be the group with the highest risk. This phenomenon coincides with the results of the epidemiological studies made among adults. Nevertheless, they do not coincide with these results if the lipid risk is defined by C > 200 mg/dl. In our opinion, during infancy and adolescence, the lipid risk is better defined by the quotient LDL/HDL > 2.2.

Adolescent↗
PubMed1995

[Treatment of hyperlipidemia. Guidelines for treatment of hyperlipidemia for secondary prevention of ischemic heart disease].

The new programme and guidelines have been developed for secondary prevention of coronary heart disease in patients with hyperlipaemia. All patients who have suffered myocardial infarction, have angina pectoris, have had a coronary by-pass, or have undergone angioplastic surgery, should have the following serum lipid profile established within one to two months: total cholesterol < 5 mmol/l, ratio total cholesterol/HDL-cholesterol < 4, LDL-cholesterol < 3 mmol/l, triglycerides < 2 mmol/l and HDL-cholesterol > 1 mmol/l in men and 1.3 mmol/l in women.

Coronary Disease↗