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Biomedical subjects

R Ceska

Publications and source records attributed to R Ceska.

At least 37 records · Page 2Linked to original sources
PubMed2001

Major apolipoprotein B-100 mutations in lipoprotein metabolism and atherosclerosis.

Apolipoprotein (apo) B-100 is a key protein compound of plasma lipid metabolism. This protein, as a sole component of LDL particles, to a great extent controls the homeostasis of LDL cholesterol in the plasma. Therefore, this protein and its structural variants play an important role in development of hyperlipidemia and atherosclerosis. Intensive research into the structure and biological functions of apoB-100 has led to identification of its complete structure as well as the responsible binding sites. With the development of the methods of molecular biology, some structural variants of the apoB-100 protein that directly affect its binding properties have been described. These are mutations leading to amino acid substitution at positions 3500 (R3500Q and R3500W) and 3531 (R3531C) that have been shown to decrease the binding affinity of apoB-100 in vitro. However, only the former mutations have been unequivocally demonstrated to cause hyperlipidemia in vivo. This minireview is aimed to discuss the impact of apoB-100 and its structural variants on plasma lipid metabolism and development of hyperlipidemia.

Apolipoprotein B-100↗
PubMed2001

Cholesterol lowering and the vessel wall: new insights and future perspectives.

The basis for most acute coronary events is either rupture or fissuring of unstable atherosclerotic plaques with subsequent thrombosis leading to coronary artery occlusion. The development of atherosclerotic plaques takes several decades, but the mechanical features determining its stability and the risk of rupture can change very rapidly depending on a number of internal factors. Unstable plaques have a large lipid core, a thin overlying fibrous cap and an abundance of inflammatory cells. The most important factor determining the plaque stability is the plasma level of atherogenic LDL particles. Increased levels of these particles cause endothelial dysfunction with impaired vasodilatation capacity and prevalence of vasoconstriction, maintain inflammatory infiltration of the plaque, impair the strength of the fibrous cap and facilitate aggregation and coagulation. Effective lowering of plasma cholesterol by pharmacological and non-pharmacological means can revert most of these processes and increase the plaque's mechanical stability within several hours to days. Lipid lowering therapy can therefore decrease the risk of acute coronary events within a very short space of time. Thus a radical decrease in lipid levels, along with modification of other risk factors, may become the cornerstone for treatment of acute coronary syndromes, in addition to being an effective treatment in primary and secondary prevention of coronary heart disease (CHD).

Anticholesteremic Agents↗
PubMed2001

Increasing plasma levels of soluble cell adhesion molecules (sE-Selectin, sP-Selectin and sICAM-1) in overweight adults with combined hyperlipidemia.

Combined hyperlipidemia (coincident present hypercholesterolemia and hypertriglyceridemia) may contribute to the development of atherosclerosis and coronary artery disease by increasing of cell adhesion molecules (CAMs). Although the cellular expression of CAMs is difficult to assess clinically, soluble forms of CAMs (sCAMs) are present in the circulation and may serve as marker of CAMs. The aim of this study was to determine whether combined hyperlipidemia in overweight adults without clinical evidence of cardiovascular disease, diabetes mellitus or hypertension is associated with increased expression of CAMs. We examined the levels of soluble cell adhesion molecules (sICAM-1, sE-Selectin and sP-Selectin) in blood plasma of overweight adults (n = 36), mean of BMI 27.08 +/- 4.12 kg/m2 with combined hyperlipidemia, with total cholesterol (TC) 7.27 +/- 1.50 mmol/l, LDL cholesterol 4.89 +/- 1.35 mmol/l, HDL cholesterol 1.27 +/- 0.51 mmol/l and triglycerides (TG) 4.08 +/- 2.22 mmol/l before lipid-lowering therapies, and in equal numbers of age, sex and BMI matched controls. Patients with combined hyperlipidemia had significantly higher plasma levels of soluble intercellular adhesion molecule-1 (sICAM-1) (298.13 +/- 41.24 ng/ml versus 241.35 +/- 37.48 ng/ml; P < 0.001), sE-Selectin (63.31 +/- 9.48 ng/ml versus 42.16 +/- 14.18 ng/ml; P < 0.001) and sP-Selectin (161.18 +/- 20.85 ng/ml versus 111.54 +/- 26.12 ng/ml; P < 0.001) compared with overweight, non-hyperlipidemic control subjects. Combined hyperlipidemia in adults with overweight is associated with elevated soluble plasma levels of CAMs. We suppose that levels of CAMs in these patients may be determined as a marker for appreciation of their potential atherosclerotic burden.

Arteriosclerosis↗
PubMed2000

[Fenofibrate 250 SR Pharmavit in patients with mixed hyperlipoproteinemia. Results of a study of 189 patients from 13 centers in the Czech Republic].

BACKGROUND: Hyperlipoproteinemia represents one of the major risk factors in the early atherosclerosis manifestation, namely in the ischaemic heart disease. In patients after the myocardial infarction, mixed hyperlipoproteinemia becomes the most frequently diagnosed impairment of the lipid metabolism. In the therapy, fibrates begin to play an important role. A new remedy containing micronised fenofibrate (Fenofibrate 250 SR Pharmavit) was recently registered for the Czech market. The aim of our study was to test its effects in almost 200 patients with mixed hyperlipoproteinemia. METHODS AND RESULTS: Into statistical analysis of the treatment effectiveness 187 persons (115 males, 72 females) were included. Other characteristics of the studied group (mean +/- SD): age 54.0 +/- 10.7 years, stature 172.0 +/- 8.7 cm, weight, BMI 28.0 +/- 3.1. Prevalence of risk factors and clinical manifestations of the atherosclerosis: ICHS 18.2%, myocardial infarction 7.5%, ICHDK 4.3%, CMP 5.3%, smoking 27.8%, arterial hypertension 63.6%, diabetes mellitus 17.6%, positive family history in ICHS 50.3%. 44.9% persons had been treated with hypolipidemics. Basic parameters of the lipid metabolism, cholesterol, LDL and HDL cholesterol and triglycerides were studied. Plasma levels of uric acid, fibrinogen, glucose and other biochemical parameters were also used to monitor the safeness of the treatment. Cholesterol concentration (7.05 +/- 0.91 mmol/l) decreased (6.14 +/- 0.89 mmol/l) almost by 15%. Triglyceride concentration decrease (from 4.43 +/- 1.84 mmol/l to 2.64 +/- 1.34 mmol/l) was more intensive (41%). HDL-cholesterol increased by almost 15%, while LDL-cholesterol decreased by 12%. Statistically significantly decreased level of the uric acid (12%), fibrinogene decrease (8.4%) reached only marginal significance. Treatment was well tolerated, only in one patient it was necessary to cut it prematurely. CONCLUSIONS: According clinical tests which included almost 200 patients with mixed hyperlipoproteinemia, Fenofibrate 250 SR Pharmavit stands for an effective and well tolerated hypolipidemics.

Female↗
PubMed2000

[Hyperlipoproteinemia, the Apo-E genotype and bone density].

BACKGROUND: Both atherosclerosis and osteoporosis often appear together, especially in the elderly; usually they are regarded as independent entities. Only recently epidemiological evidence occurred suggesting possible associations between these diseases. Several groups of factors (genetic, hormonal and biochemical) have been studied to account for this association. Among the genetic factors, apolipoprotein E has been studied most extensively; some results indicate that carriers of E4 allele are at increased risk of osteoporosis. A possible influence of plasma lipoproteins and of tissue ischaemia on bone metabolism has also been studied. AIM OF THE STUDY: To test the hypothesis that there is an association between apolipoprotein E, plasma lipid concentrations and bone mineral density. METHODS: We examined 18 apolipoprotein E2/2 and E4/4 homozygotes and 130 postmenopausal women. Bone mineral density and plasma triglycerides, total and HDL cholesterol were determined in both groups; in apolipoprotein E homozygotes biochemical markers of bone turnover were also measured. RESULTS: No significant differences in bone mineral density and bone remodelling were found between the E2/2 and E4/4 homozygotes. A negative correlation between lumbar spine bone mineral density and cholesterol and triglyceride concentrations (r = 0.20-0.39) was observed both in postmenopausal women and apolipoprotein E homozygotes. CONCLUSION: We didn't observe any association of apolipoprotein E genotype with bone mineral density and biochemical markers of bone metabolism. A negative association between plasma lipid concentrations and bone mineral density supports the hypothesis of harmful effect of hyperlipidaemia on bone metabolism.

Alleles↗
PubMed2000

Serum leptin levels in patients with hyperlipidemias.

Leptin is a protein hormone produced by adipocytes that reflects the body fat content. The aim of our study was to compare serum leptin levels in randomly selected untreated males and females with hypercholesterolemia and combined hyperlipidemia and in healthy control subjects matched for age and body mass index and to study the relations between leptin and serum lipids and lipoproteins. No statistically significant differences in serum leptin levels were found between the male control group (5.26 +/- 2.81 ng/mL(-1)) and the male group with hypercholesterolemia (8.16 +/- 3.85 ng/mL(-1)) or combined hyperlipidemia (7.51 +/- 4.83 ng/mL(-1)) and between the female control group (13.0 +/- 8.12 ng/mL(-1)) and the female group with hypercholesterolemia (15.36 +/- 8.89 ng/mL(-1)) or combined hyperlipidemia (18.63 +/- 10.15 ng/mL(-1)). Leptin concentration in male group with hypercholesterolemia did not differ significantly from the female control group; in the other male groups, leptin levels were significantly lower than those of the other female groups. Serum leptin levels in all studied groups except for the male group with hypercholesterolemia positively correlated with body mass index. Serum leptin levels correlated negatively with high-density lipoprotein cholesterol in the female group with hypercholesterolemia (r = -0.67, P < 0.01) and the male group with combined hyperlipidemia (r = -0.56, P < 0.01). A positive correlation between serum leptin and high-density lipoprotein cholesterol (r = 0.67, P < 0.01) and between leptin and lipoprotein (a) (r = 0.71, P < 005) was found in female group with combined hyperlipidemia. No other significant relationships between leptin and serum lipids or lipoproteins were found. We conclude that serum leptin levels in patients with hyperlipidemias do not significantly differ from those healthy control subjects matched by age and body mass index.

Adult↗
PubMed2000

Age and residual cholesterol efflux affect HDL cholesterol levels and coronary artery disease in ABCA1 heterozygotes.

We and others have recently identified mutations in the ABCA1 gene as the underlying cause of Tangier disease (TD) and of a dominantly inherited form of familial hypoalphalipoproteinemia (FHA) associated with reduced cholesterol efflux. We have now identified 13 ABCA1 mutations in 11 families (five TD, six FHA) and have examined the phenotypes of 77 individuals heterozygous for mutations in the ABCA1 gene. ABCA1 heterozygotes have decreased HDL cholesterol (HDL-C) and increased triglycerides. Age is an important modifier of the phenotype in heterozygotes, with a higher proportion of heterozygotes aged 30-70 years having HDL-C greater than the fifth percentile for age and sex compared with carriers less than 30 years of age. Levels of cholesterol efflux are highly correlated with HDL-C levels, accounting for 82% of its variation. Each 8% change in ABCA1-mediated efflux is predicted to be associated with a 0.1 mmol/l change in HDL-C. ABCA1 heterozygotes display a greater than threefold increase in the frequency of coronary artery disease (CAD), with earlier onset than unaffected family members. CAD is more frequent in those heterozygotes with lower cholesterol efflux values. These data provide direct evidence that impairment of cholesterol efflux and consequently reverse cholesterol transport is associated with reduced plasma HDL-C levels and increased risk of CAD.

ATP Binding Cassette Transporter 1↗
PubMed2000

[The spectrum of lipids in the intrauterine growth retarded fetus and in the parents].

OBJECTIVE: The aim of this study was to determine the relationship between the parameters of individual serum lipids and the degree of intrauterine growth retardation (IUGR) of the fetus. The lipid levels were compared in fetuses with IUGR and in eutrophic fetuses and it was determined in which studied variable IUGR newborns differ from healthy newborns. METHODS: The group under study consisted of 53 pregnant women in whom IUGR of the fetus was diagnosed by ultrasound during pregnancy. The control group consisted of 26 women who gave birth to eutrophic newborns. The cases in the control group were chosen by the method of matched control so that the results could be statistically evaluated in both groups at the same gestational age and at the same maternal age. In both groups blood samples from the umbilical cord were taken after delivery and the whole spectrum of lipid levels were evaluated (cholesterol-CH, triglycerides-TGA, high-density lipoprotein--HDL, low-density lipoprotein--LDL, Lp(a) lipoprotein, and apolipoproteins-ApoB, ApoAI, ApoE). The same parameters were evaluated in maternal and paternal blood samples. In several cases, intrauterine lipid levels of the fetus were determined by cordocentesis. The incidence of hyperlipoproteinemia in the families of both groups was surveyed. SETTING: Department of Obstetrics and Gynaecology, 1st medical Faculty, Charles University, Prague. RESULTS: There was a significant incidence of hyperlipoproteinemia in the families of the mothers in the group studied (chi-square test: p < 0.001). In the mothers of the groups studied, there were statistically significant higher levels of HDL, LDL, and Lp(a) in comparison to the mothers in the control group. A significant dependence was determined between the levels of ApoAI and Lp(a) of the mothers and newborns. In the regression analysis of the dependence of lipid levels on the birth weight of the newborns, a statistical correlation was determined for the values of ApoB and Lp(a). CONCLUSION: The more increased the intrauterine growth retardation of the fetus and the lower its birth weight in relation to its gestational age, the higher its lipid levels, specifically apolipoproteins. Apolipoproteins are under genetic control and present a genetic risk for changes in the metabolism of cholesterol, hemocoagulation, and cardiovascular disease in adulthood.

Adult↗
PubMed2000

Apolipoproteins and atherosclerosis. Apolipoprotein E and apolipoprotein(a) as candidate genes of premature development of atherosclerosis.

Apolipoprotein E (apoE) is a plasma lipoprotein which plays a basic role in the degradation of particles rich in cholesterol and triglycerides. It is able to bind to LDL receptors, but also to receptors for chylomicron remnants. There are three major apoE isoforms, E2, E3, and E4. Their role in lipoprotein metabolism is related to their affinity for receptors. Allele E3 is predominant and apoE3 affects metabolism of lipoproteins in a standard way. When compared to allele E3, allele E2 is associated with lower LDL levels, whereas allele E4 with higher LDL levels. This has an impact on the progression of atherosclerosis. Allele E2 exhibits a protective role, whereas allele E4 is associated with a high risk factor. Lipoprotein(a) [Lp(a)] is a plasma lipoprotein, consisting of apolipoprotein(a), linked by a covalent bond with the LDL particle. Increased Lp(a) levels are associated with an increased incidence of diseases based on atherosclerosis, namely the ischemic heart disease. Another effect of Lp(a) is its competition with plasminogen, resulting in a decrease of fibrinolysis and thrombogenic activity. ApoE and Lp(a) are independent risk factors for premature development of atherosclerosis and therefore can be considered as candidate genes of premature atherosclerosis.

Age of Onset↗
PubMed2000

Familial defective apolipoprotein B-100: a lesson from homozygous and heterozygous patients.

Familial defective apolipoprotein B-100 (FDB) is a genetic disorder caused by a substitution of glutamine for arginine at residue 3500 of the apolipoprotein B-100 molecule. We have identified 23 heterozygotes and one homozygote for FDB (frequency 1:20) in a group of 510 patients with hypercholesterolemia. Mean age of the patients (18 females and 6 males) was 46 years. The diagnosis of FDB was based on point mutation PCR analysis of exon 26 of the apo B gene. Plasma lipids in heterozygous patients were: total cholesterol 8.76+/-1.2 mmol/l, triglycerides 1.42+/-0.5 mmol/l, HDL-cholesterol 1.43+/-0.3 mmol/l, LDL-cholesterol 6.69+/-1.2 mmol/l, apoB 1.69+/-0.4 g/l, Lp(a) 0.26+/-0.2 g/l. The most frequent apoE genotype was 3/3 (19 patients), apoE 3/4 genotype was found in 3 patients and one person had apoE 2/3. Xanthelasma palpebrarum was present in 4 patients and tendon xanthomas in 3 patients including the homozygote. Premature manifestation of coronary heart disease was revealed in 3 patients. Sixteen patients were treated with statins, a combination of statin and resin was used in 2 patients (including the homozygote), whereas six patients were treated with the diet only. We conclude that although the plasma lipid levels of total and LDL cholesterol in FDB patients are lower than in patients with familial hypercholesterolemia, the patients with FDB suffer from premature atherosclerosis. The therapeutic approach to FDB individuals and patients with familial hypercholesterolemia is very similar.

Abetalipoproteinemia↗
PubMed2000

[Ciprofibrate in the treatment of combined hyperlipoproteinemia. Results in more than 600 patients from 23 centers in the Czech Republic].

A total of 633 patients with combined hyperlipoproteinaemia from 23 centres in the Czech Republic met the criteria for assessment of the effectiveness of 3-month administration of 100 mg ciprofibrate (Lipanor) per day. The cholesterol concentration declined from the original values of 6.94 mmol/l by 13%. The drop of triglycerides was even more significant from 3.03 mmol/l by more than 41%. The relatively low HDL cholesterol at the beginning, 1.14 mmol/l, increased by 15%, while LDL-cholesterol dropped significantly by almost 12%. The classical atherogenic index expressed by the ratio of total/HDL cholesterol declined by 25%. Treatment was very well tolerated by the patients and was associated with a minimum of undesirable side-effects. Treatment with ciprofibrate is effective and safe treatment in patients with combined hyperlipoproteinaemia.

Clofibric Acid↗
PubMed2000

Bone mineral density in patients with apolipoprotein E type 2/2 and 4/4 genotype.

The peak bone mass and the rate of bone loss are in part genetically determined. It has been suggested that bone mineral density (BMD) may be related to allelic variation in the apolipoprotein E (ApoE) gene locus. ApoE is important in the receptor-mediated clearance of chylomicron particles from the plasma, Apo E4 having the highest and Apo E2 the lowest receptor affinity. Chylomicrons are the main carrier of vitamin K in the plasma; vitamin K plays an important role in the carboxylation of osteocalcin. We have tested the hypothesis that persons with E4 variant would have lower BMD and increased bone turnover than those with E2 variant. A total of 18 ApoE 2/2 and ApoE 4/4 homozygotes were selected from 873 patients who were examined for the ApoE genotype. BMD in lumbar vertebral, femoral neck and distal forearm was measured and plasma concentrations of osteocalcin and C-terminal fragments of collagen (CTx) were determined. BMD values (expressed as T-score) at the three specified sites were -0.12+/-1.72, -0.52+/-1.32 and -0.52+/-0.81 in ApoE 2/2 group and -0.24+/-1.22, 0.00+/-0.84 and -0.17+/-1.07 in the ApoE 4/4 group. Plasma osteocalcin and CTx were within normal limits in both groups. In conclusion, we did not observe any association of ApoE genotype with BMD and biochemical markers of bone metabolism in ApoE 2/2 and ApoE 4/4 homozygotes.

Adult↗
PubMed2000

Effects of transdermal application of DHEA on the levels of steroids, gonadotropins and lipids in men.

In order to ascertain the kinetics of absorption and metabolism of transdermally administered dehydroepiandrosterone (DHEA), 10 men 29-72 years old (mean 52.4+/-14.5) received 50 mg DHEA/day in a gel applied onto the skin of the abdomen for 5 consecutive days. The objective was to establish the extent to which DHEA influences the levels of gonadotropins, sex hormone-binding globulin and lipids. It was found that DHEA is well absorbed and rapidly metabolized to its sulfate (DHEAS), androstenedione, and consequently to testosterone and estradiol. The DHEA levels that markedly increased after the first doses gradually declined already during the application, and this decline proceeded even after it was discontinued, reaching levels significantly lower than the original ones. On the other hand, the levels of DHEA metabolites (with the exception of DHEAS) rose during the application and reached values significantly higher than the basal ones within 5 weeks. This effect was accompanied by significantly decreased levels of LH. The serum levels of lipids, namely of cholesterol (both HDL and LDL cholesterol), triglycerides, apolipoproteins A-I and B and lipoprotein(a) after DHEA application were not changed significantly, and the atherogenic index (AI) remained unaltered. However, some correlations between hormones and lipids were found. Negative correlations concerned the following indices: DHEA/Lp(a); DHEAS/cholesterol; DHEA, DHEAS, testosterone/TG; testosterone/AI. On the other hand, LH, FSH/cholesterol, FSH, SHBG/LDL cholesterol, FSH/Apo B, Lp(a) correlated positively. It can be concluded that transdermal short-time application of DHEA results in a decrease of endogenous DHEA after finishing the treatment, with a parallel marked increase in the levels of sex hormones. Using this application protocol, exogenous DHEA neither altered the lipid spectrum, nor did it influence the atherogenic index.

Administration, Cutaneous↗
PubMed2000

[Familial hyperlipoproteinemias--correlations between phenotypes and genotypes].

Within the grant project patients with familial hyperlipoproteinaemias have been examined. The examination was performed in the oldest lipid clinic and research laboratory in the world. The classification of lipid metabolism disorders was based upon a detailed biochemical analysis of plasma lipids including electrophoresis and assessment of apolipoprotein levels. Then optimal treatment regimen could be established. The project was aimed to evaluate the efficacy of different treatment regimens in different types of hyperlipoproteinaemias. Biochemical parameters and mainly the impact of treatment of hyperlipoproteinaemia on morphology and function of the vessel wall was monitored. The non-invasive ultrasound measurement of the intima thickness of carotid arteries was used. For more precise diagnosis of genetically determined disorders of lipid metabolism a large scale of methods of molecular biology was introduced. These methods enable confirmation of familial hypercholesterolaemia, familial defective apolipoprotein B-100 or studying polymorphism of apolipoprotein E. The effort of the authors of the project was to maximally utilise the results of basic and applied research in formulating recommendations for everyday practice of physicians.

Humans↗
PubMed2000

The independent correlation of the impact of lipoprotein(a) levels and apolipoprotein E polymorphism on carotid artery intima thickness.

BACKGROUND: Apolipoprotein E (apoE) plays a key role in lipoprotein metabolism. It occurs in three isoforms E2, E3 and E4. These isoforms have different impacts on plasma lipoprotein levels. The allele, or gene, coding apoE4 is considered a candidate for premature atherosclerosis development while the apoE2 gene is assumed to be protective. Lipoprotein(a) is also atherogenic and its increased plasma concentration is presumed to be an independent risk factor for premature atherosclerosis. Lipoprotein(a) is a protein depositing directly into the atheromatous plaques, enhancing cholesterol oxidation, competitively inhibiting plasminogen formation and thus having a prothrombogenic effect. The aim of our study was to establish a relationship between common carotid artery intima thickness and two independent risk factors, apoE polymorphism and elevation of plasma lipoprotein(a) levels. METHODS: A cross-sectional study was performed on 114 patients who were referred to the lipid clinic for primary hyperlipoproteinaemia. The patients received no treatment prior to examination. Plasma levels of total cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, apoA, apoB, lipoprotein(a) and the apoE genotype were determined and the carotid artery intima thickness was measured using ultrasonography. RESULTS: The relative frequencies of apoE2, E3 and E4 were 0.049, 0.830 and 0.121. The equality of carotid intima thickness was tested using the Kruskal-Wallis test. Medians of intima thickness in a subgroup with the allele E2 were 0.72 mm, in a subgroup with the E3/E3 genotype 0.70 mm and in a subgroup with the E4 allele 0.80 mm. The relationship between carotid intima thickness and lipoprotein(a) levels was tested using Spearman's correlation coefficient. CONCLUSIONS: No statistically significant differences of carotid intima thickness among subgroups divided according to their apoE genotype were found. No relationship between carotid intima thickness and lipoprotein(a) levels was found. On the contrary a close relationship between carotid intima thickness and age and also some of the plasma lipid variables was recorded using the method of multivariate linear regression.

Apolipoprotein E2↗
PubMed2000

[Therapeutic goals in hyperlipoproteinemia].

In the treatment of hyperlipoproteinaemias (HLP) our main effort should be treatment of the patient and not achievement of defined biochemical values. The basic goals of HLP treatment can be defined on the basis of results of intervention studies as follows: reduction of general mortality, reduction of morbidity from IHD, reduction of the incidence of CMP, improved course of ischaemia of the lower extremities, better quality of life of patients with cardiovascular disease and reduced necessity of revascularization surgery. Even if we shall assume that the positive effect of treatment with HLP are in the first place optimization of the lipid spectrum, in particular a drop of total and LDL cholesterol, we cannot overlook so-called "non-lipid" effects of hypolipidaemic agents, in particular statins. In the treatment of patients with HLP it is important in the first place to evaluate the comprehensive risk of the patient, nevertheless it is possible to define "target values" e.g. according to recommendations of "European societies". Even these target values may be the subject of further discussions. It may be however stated that the objective is that total cholesterol should be less than 5 mmol/l, LDL cholesterol less than 3 mmol/l and triglycerides less than 2 mmol/l, HDL cholesterol higher than 1 mmol/l. Attention should be however drawn to the fact that evidence is increasing that in particular patients with already manifest IHD will benefit from even more aggressive treatment and attempts to achieve minimal lipid and lipoprotein values. LDL cholesterol should be reduced to 2.5 mmol/l and triglycerides should be below 2 mmol/l. It is a problem how to achieve these values. The strongest evidence is in favour of statin administration. On the other hand it is important to mention that optimation of the lipid and lipoprotein spectrum may be more important than prescription of a drug from a certain group.

Cardiovascular Diseases↗