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Biomedical subjects

H Vaverková

Publications and source records attributed to H Vaverková.

At least 19 recordsLinked to original sources
PubMed2006

Brachial endothelial function in subjects with familial combined hyperlipidemia and its relationships to carotid artery intima-media thickness.

AIM: The aim of this study was to quantify the flow-mediated dilatation (FMD) of brachial artery in asymptomatic members of families with familial combined hyperlipidemia (FCH) and to determine the relation between FMD and risk factors accompanying FCH. We also investigated the association between FMD and the intima-media thickness (IMT) of the common carotid artery. METHODS: Eighty-two members of 29 FCH families were divided into two groups: probands and hyperlipidemic first-degree relatives (HL) (n=47) and normolipidemic first-degree relatives (NL) (n=35). The control (C) groups, C-HL (n=20) and C-NL (n=20), consisted of sex- and age-matched healthy individuals. FMD was assessed in the brachial artery by measuring the change in brachial artery diameter in response to reactive hyperemia. RESULTS: Both hyperlipidemic subjects and their NL had significantly lower FMD (3.4+/-3% vs 6.3+/-2.8%, P<0.001, 5.2+/-2.3% vs 7.8+/-2.8%, P<0.01, respectively) compared to controls. In multivariate backward stepwise regression analysis, FMD in members of FCH families was independently associated with sex (P<0.001), age (P<0.01), C-peptide (P<0.05) and borderline with glycemia (P=0.052). FMD correlated inversely with IMT in all subjects of FCH families and in hyperlipidemic members. In multivariate backward stepwise regression analysis this relation remained independent (P<0.001, P<0.01, respectively). CONCLUSIONS: Members of FCH families showed impaired FMD, which was independently associated with markers of insulin resistance. FMD and IMT were independently associated in hyperlipidemic, but not in normolipidemic members of FCH families.

Adult↗
PubMed2003

[Endothelial dysfunction in a family with familial combined hyperlipidemia].

Familial Combined Hyperlipidemia is the most frequent familial hyperlipidemia with a high risk a early manifestation of arteriosclerosis. Endothelial dysfunction is the first step in the development of arteriosclerosis. The aim of our investigation was to examine selected markers of endothelial dysfunction in hyperlipidemic members of families with familial combined hyperlipidemia and their normolipidemia first-line relatives and to compare them with healthy individuals. The study includes non-smoking members of the affected families (probands and first-line relatives), who have not suffered from clinical manifestations of arteriosclerosis and/or hypertension during the start of the study. The cohort was divided into hyperlipidemic individuals (N = 25) and normolipidemic individuals (N = 21). Both groups were compared with control groups of healthy individuals (two groups, N = 17 each), who were adjusted by age and sex. The following markers of endothelial dysfunction were examined: 1. ultrasound--flow mediated dilatation of brachial artery and 2. humoral--serum levels of von Willebrand factor, inhibitor of activator of plasminogen-1 and vasoadhesive molecules (vascular cell adhesion molecule-1, intercellular adhesion molecule-1). The members of families with familial combined hyperlipidemia displayed symptoms of endothelial dysfunction. In comparison with healthy controls the endothelial dysfunction was more expressed in hyperlipidemic individuals. They displayed a significantly lower flow-mediated dilatation of brachial artery (3.6 +/- 3.3% versus 6.6 +/- 2.8%, P < 0.01), higher levels of von Willebrand factor (152.8% +/- 79.1% versus 110.4% +/- 24.8%, P < 0.05), inhibitor of activator of plasminogen-1 (94.6 +/- 30.8 ng/ml versus 60.4 +/- 38.0 ng/ml, P < 0.01) and vasoadhesive molecules: vascular cell adhesion molecule-1 (927.0 +/- 167.7 ng/ml versus 814.7 +/- 171.1 ng/ml, P < 0.05), intercellular adhesion molecule-1 (601.7 +/- 89.5 ng/ml versus 544.8 +/- 59.8 ng/ml, P < 0.05). The normolipidemic individuals displayed only a significantly lower flow-mediated dilatation of brachial artery (5.6 +/- 2.6% versus 7.5 +/- 2.8%, P < 0.05) and higher levels of von Willebrand factor (136.8 +/- 40.32% versus 104.1 +/- 24.9%, P < 0.05). No significant difference was found in the levels of inhibitor of activator of plasminogen-1 and vasoadhesive molecules. The results indicated that members of families with familial combined hyperlipidemia represent a high-risk group from the standpoint of early manifestation of arteriosclerosis.

Adult↗
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

[Dyslipoproteinemia and diabetes mellitus].

Diabetes mellitus is, as compared with the non-diabetic population, associated with a much higher mortality of ischaemic heart disease and other cardiovascular diseases. In this risk participates in a major way also diabetic dylipidaemia. The latter is characterized in particular by hypertriglyceridemia which reflects the increase of VLDL and IDL lipoproteins. Elevated and prolonged postprandial lipaemia participates in the development of qualitative lipoprotein changes. Highly athergenic "small dense LDL" are formed which are liable to an oxidative modification and are then in an unregulated manner taken up in the vascular wall. Reduction of HDL-cholesterol and a change in the different HDL sub-populations leads then to a deteriorated reverse cholesterol transport. Type 2 diabetes mellitus is associated with dyslipidaemia in the majority of patients even under conditions of satisfactory compensation of diabetes, in particular during the postprandial stage. On the other hand, in type 1 diabetes the lipid values usually become normal when the blood sugar level becomes normal, however qualitative changes of lipoproteins frequently persist. Increased glycation and oxidation of lipoproteins is a common sign of both types of diabetes. For prevention of cardiovascular complications treatment of diabetic dyslipidaemia is at least equally important as efforts to achieve optimal compensation of diabetes. Successful treatment of diabetic dyslipidaemia includes efforts to achieve compensation of diabetes, optimation of body weight, increase of physical activity, modification of diet, treatment of other secondary causes of hyperlipidaemia, and if these provisions are not successful, pharmacological hypolipidaemic treatment. The risk of macrovascular complications is so high in diabetics that according to recent knowledge it is not necessary to differentiate between primary and secondary prevention but aggressive treatment is necessary to achiebe target values of total cholesterol < 5.0 mmol/l and LDL-cholesterol < 3.0 mmol/l. Triglycerides > 2 mmol/l and HDL-cholesterol < 1 mmol/l are signs of a high cardiovascular risk. Optimation of the whole lipid profile is ideal.

Cardiovascular Diseases↗
PubMed2000

[Dyslipoproteinemia and chronic kidney failure].

Lipoprotein abnormalities are a regular part of metabolic changes associated with chronic renal failure. The character of dyslipoproteinaemia changes with the severity of disorders of renal functions, from initial deviations in the composition and distribution of circulating lipoprotein particles (a decline of glomerular filtration to 0.7-0.8 ml/s) to differently expressed changes of plasma lipid concentrations in terminal renal failure. The basis of the pathogenetic mechanism of these lipid abnormalities is the negative effect of the uraemic environment on the formation and catabolism of triglyceride-risk lipoproteins and on the function of the reverse cholesterol transport. An important part is also played by the modification of lipoprotein particles by oxidation and glycation. To a different extent also the nutritional status is manifested via the unfavourable composition of dietary fats, reduced effectiveness of antioxidant factors and in some instances also carnitine deficiency. Haemodialysis treatment and in particular peritoneal dialysis modify these lipid abnormalities. From the quantitative aspect renal dyslipoproteinaemia is not very striking, despite this its quantitative changes are important. It may have a negative impact on the progression of renal disease by its participation in the development of glomerular sclerosis and tubulointerstitial fibrosis. As one of the important risk factors it participates also in the acceleration of atherosclerosis in patients with chronic renal failure and in their much higher cardiovascular mortality as compared with the general population. These factors justify efforts to influence uraemic dyslipoproteinaemia. Fibrates or statins are indicated in conjunction with the supporting effect of diet and modification of the dialysis regimen. In tables and figures some results assembled by the authors are presented obtained in a group of dialyzed patients (characteristic of the lipid profile under basal conditions on fasting and after an oral lipid load and experience with influencing dysliopoproteinaemia by fenofibrates and atorvastatin).

Disease Progression↗
PubMed1997

Complementary insulin therapy improves blood glucose and serum lipid parameters in type 2 (non-insulin-dependent) diabetic patients. I. Effects on blood glucose control.

Aim of the present prospective study was to assess the potential benefits of complementary insulin therapy, consisting of a single dose of 1 to 8 units of shortacting insulin before each meal, on blood glucose, serum lipid parameters and on patient's well-being. A group of 251 type 2 (non-insulin-dependent) diabetic patients completed the study. The complementary insulin therapy was introduced in hospital in the course of one week. Number of injections per day was increased, the average dose of insulin per day and the average dose of glibenclamide decreased, amount of carbohydrates in food (adapted by patients themselves) diminished, mean blood glucose, number of hyperglycaemia's and number of hypoglycaemia's decreased. At a check-up 8 to 10 weeks later, a decrease of haemoglobin A1c, glycated proteins in serum and body mass index together with improved patient's well-being have been shown. These results demonstrate a good effectiveness of complementary insulin therapy in type 2 (non-insulin-dependent) diabetic patients. We assume this kind of therapy should be more often recommended.

Adult↗
PubMed1997

Complementary insulin therapy improves blood glucose and serum lipid parameters in type 2 (non-insulin-dependent) diabetic patients. II. Effects on serum lipids, lipoproteins and apoproteins.

The aim of the present study was to evaluate the effects of complementary insulin therapy, consisting of a single dose of 1 to 8 units of shortacting insulin before each meal (4-6x daily) and sometimes at 02.30 h, on concentrations of serum lipids, lipoproteins and apoproteins in type 2 (non-insulin-dependent) diabetic patients, unsatisfactorily controlled either by oral hypoglycemic agents (OHA) or by longacting insulin 1-2x daily (INS 1-2). Compared means +/- SD. Patients on INS 1-2 (n = 82) had better baseline glycemic control than patients on OHA (n = 68) (HbAlc: 9.33 +/- 1.76% vs. 10.59 +/- 1.83%, p < 0.001 and fructosamine: 3.34 +/- 0.74 mmol/l vs. 3.85 +/- 0.84 mmol/l, p < 0.001) and serum triglyceride concentrations (3.03 +/- 2.05 mmol/l vs. 4.95 +/- 4.48 mmol/l, p < 0.001), in spite of longer duration of diabetes (13.35 +/- 8.07 years vs. 10.1 +/- 6.9 years, p < 0.001). After 8-10 weeks of complementary insulin therapy, OHA patients (n = 33) improved both the glycemic control (HbA1c: 10.5 +/- 1.78% vs. 9.0 +/- 1.75%, p < 0.001) and fructosamine: 4.0 +/- 0.85 mmol/l vs. 3.5 +/- 0.76 mmol/l, p < 0.001) and most of the lipid parameters (decreased serum triglyceride: 5.8 +/- 5.64 mmol/l vs. 3.6 +/- 4.69 mmol/l, p < 0.001, total cholesterol/HDL-cholesterol: 6.8 +/- 3.13 vs. 5.6 +/- 2.23, p < 0.01 and increased HDL-cholesterol: 1.0 +/- 0.30 mmol/l vs. 1.2 +/- 0.30 mmol/l, p < 0.001, apo AI: 1.6 +/- 0.26 g/l vs. 1.8 +/- 0.28 g/l, p < 0.001, LpAI particles: 0.6 +/- 0.1 g/l vs. 0.7 +/- 0.12 g/l, p < 0.001 and LDL-cholesterol/apo B: 2.1 +/- 0.67 vs. 2.7 +/- 0.67, p < 0.001). In patients previously on INS 1-2x (n = 34), complementary insulin therapy with reduced dose of insulin per day (49.6 +/- 22.5 U/d vs. 36.6 +/- 13.3 U/d, p < 0.001) did not further improve glycemic control but improved the number of proatherogenic and antiatherogenic lipoprotein particles (decreased apo B: 1.7 +/- 0.52 g/l vs. 1.5 +/- 0.94 g/l, p < 0.01, apo AI/Lp AI: 2.9 +/- 1.01 vs. 2.3 +/- 0.98, p < 0.01 and increased Lp AI particles: 0.6 +/- 0.10 g/l vs. 0.7 +/- 0.12 g/l, p < 0.0001); BMI also decreased (29.4 +/- 4.28 kg/m2 vs. 28.9 +/- 4.24 kg/m2, p < 0.05). These results demonstrate that complementary insulin therapy probably induces antiatherogenic lipoprotein changes in NIDDM patients previously treated by either OHA or INS 1-2x. Thus, this type of therapy should be used more often and start earlier, and should be preferred to longacting insulins.

Adult↗
PubMed1997

Medullary and mixed medullary-papillary carcinoma of the thyroid gland.

Concurrent medullary and papillary carcinomas of the thyroid gland are rare and occurrence of the medullary and medullary-papillary carcinoma, as far as we know, has not been previously described. The medullary carcinoma was found in the upper part of the right lobe and the mixed medullary-papillary carcinoma in the left lobe of thyroid gland. Immunohistochemistry revealed calcitonin positivity in the medullary parts of the carcinoma and thyroglobulin positivity in papillary structures. Both light microscopy and immunohistochemistry observation distinguished these two cell lineages. The patient was treated with radiotherapy but died 18 months after first symptoms. Metastases were identified in the liver, mediastinal lymph nodes and soft tissues and micro-metastases in the lungs. The authors discuss histogenesis of mixed thyroid carcinomas.

Biomarkers, Tumor↗
PubMed1997

[Simultaneous occurrence of 2 thyroid gland carcinomas].

The concurrent finding of two thyroid carcinomas is rare. The authors present two patients with the concurrent occurrence of two tumours. In the first case--a 51-year-old man--the authors found a medullary carcinoma in the right lobe and a medullary papillary carcinoma in the left thyroid lobe. The medullary papillary carcinoma metastatized into the mediastinal lymph nodes and into the mediastinal tissues in the area above the tracheal bifurcation. From the morphological and immunohistological aspect in the primary tumour of the left lobe as well as in the mediastinum two different clones of tumour cells were found (the medullary component of the tumour responded positively to antibodies against calcitonin and the papillary component to serum against thyroglobulin. The patient was treated by radiotherapy. The tumour progressed however markedly in its medullary component and the patient died one and a half year after the first symptoms from generalization of the tumour. The second patient, a woman, had an occult papillary carcinoma in the right lobe and in the left lobe a of a medullary papillary carcinoma (follicular variant). This type of tumour also metastatized into a cervical lymph node in the area of the left lobe. The patient was treated by radioiodine. Nine months after bilateral thyroidectomy she has no signs of progression of the tumour.

Adult↗
PubMed1996

[Lipid risk factors and their role in the pathogenesis of atherosclerosis].

The author presents an account on the main lipid risk factors of ischaemic heart disease. She emphasizes the causal role of cholesterol and low density lipoproteins (LDL), incl. the VLDL subclass and oxidized LDL in the pathogenesis of atherosclerosis. The atherogenic action of elevated concentrations of triacylglycerols is discussed (the importance of heterogenity of lipoproteins rich in triacyglycerols, postprandial hypertriacylglycerolaemia, combination with low concentrations of high density lipoproteins (HDL) and prothrombogenic changes). The protective role of HDL is mediated not only by their participation in the reverse cholesterol transport but also other antiatherogenic changes (antioxidant, increased prostacycline secretion, effect on the vascular tonus). Low HDL cholesterol concentrations in subjects with ischaemic heart disease indicate not only loss of these protective properties but also a pathological metabolism of lipoproteins rich in triacylglycerols with which they are metabolically associated. The author emphasizes the antiatherogenic importance of the sub-population HDL2 and of lipoprotein particles Lp AI. Lipoprotein (a) is another independent risk factor of ischaemic heart disease. The genetic determination and ratio of factors of the external environment in the variability of concentrations of all these lipid risk factors in the population is discussed.

Cholesterol↗
PubMed1996

[Personal experience with 200mg of micronized fenofibrate (Lipanthyl 200 M) in the treatment of primary dyslipidemias].

Micronized phenofibrate 200 mg was administered in clinical trial to 30 patients with dyslipidaemia. Their average age was 51.9 years (10 with type 2a, 12 with type 2b and 8 with types 4 and 5). After 12 weeks of treatment significant improvement of the whole lipid profile was achieved. The total cholesterol declined in different sub-groups by 16, 17 and 20% resp. LDL cholesterol declined by 20 and 18 per cent in types 2a and 2b, in types 4 and 5 it was not assessed (it was not possible to use Friedewald's equation). Triglycerides declined by 39, 45 and 75%. The HDL concentration increased by 16, 27 and 25%. The atherogenic indexes TCh/HDL-Ch declined by 28, 36 and 32%. LDL-Ch/HDL-Ch dropped by 30 and 34%. The extent of the hypolipidaemic effect depended on the baseline value: the more pathological the baseline value, the more marked the improvement. As to other investigated indicators there was a significant rise of the apolipoprotein AI and Lp AI particle concentration. Apoprotein B declined insignificantly. Uric acid declined significantly by 28%. Fibrinogen dropped significantly only in type 2a. The lipoprotein(a) concentration did not change significantly. The drug was very well tolerated and undesirable effects were minimal. Micronized phenofibrate (Lipanthyl 200 M) due to its comprehensive favourable effect on the entire lipid profile and other risk factors can prove useful in the treatment of all types of dyslipidaemias (with the exception of type I). As compared with Lipanthyl 100, the better pharmacokinetic properties make it possible to reduce the dose from 300 mg/day and it can be administered in a single daily dose.

Dosage Forms↗
PubMed1995

[Lipoprotein (a): a genetic risk factor with atherogenic and thrombogenic properties].

Lipoprotein (a) is a relatively new independent risk factor of early atherosclerosis with atherogenic and thrombogenic properties. From the structural aspect it resembles LDL-lipoprotein and differs from the latter by the presence of another glycoprotein-apolipoprotein (a). Due to the great similarity of apolipoprotein (a) and plasminogen, lipoprotein (a) is bound to plasminogen receptors on the fibrin surface (fibrinogen) and thus prevents the cumulation and activation of local fibrinolysis. Its levels are under strict genetic control and are very little influenced by external factors and available hypolipidaemic treatment. There is a great interindividual variability of lipoprotein(a) concentrations which is due above all to the structural variability of apolipoprotein (a). At present at least 34 isoforms of apolipoprotein(a) were described which differ as to the size of the molecule. This great structural variability has an impact not only on the function and pathogenicity of lipoprotein (a) but also on methods of its assessment. High lipoprotein(a) concentrations are found in subjects with early clinical manifestations of atherosclerosis, in nephrotic syndrome, in chronic renal insufficiency, in haemodialyzed patients and other diseases. They rise in women after the menopause and are favourably influenced by hormonal substitution therapy. There is a number of immunochemical methods used for its estimation which are very well reproducible within the same laboratory. The high interlaboratory coefficients of variation indicate, however, that unification of lipoprotein(a) analyses is urgent.

Arteriosclerosis↗
PubMed1995

[Hyperlipoproteinemia as a risk factor for ischemic heart disease. Epidemiologic and interventional studies].

The author reviews the main epidemiological studies which identified a number of risk factors of ischaemic heart disease and became the basis for widely accepted ranges of lipids where dietary or medicamentous intervention should be used. She emphasizes in particular the evaluation of the total risk not only from the aspect of various lipid indicators but also non-lipid risk factors. The author reviews the main hypolipidaemic intervention studies and their meta-analyses. She emphasizes the importance of hitherto not widely accepted hypolipidaemic treatment in secondary prevention of ischaemic heart disease, which reduced not only cardiovascular but also total mortality. The author gives also an account of coronarography-based intervention studies which provide evidence that intensive hypolipidaemic treatment leads not only to arrested progression but may induce regression of atherosclerotic vascular changes.

Coronary Artery Disease↗
PubMed1993

[Reaven's metabolic syndrome X in the families of individuals with premature cerebrovascular attacks].

In families of subjects with premature ischaemic cerebrovascular attacks (a total of 45 families with 190 members) the authors detected a high incidence of dyslipidaemia, arterial hypertension, impaired glucose tolerance and non-insulin dependent diabetes mellitus, frequently with striking cumulation. The authors investigated therefore the relationship of the insulin level as an indirect reflection of insulin resistance with these risk factors. The fasting insulin levels correlated significantly positively with triglyceride levels, apolipoprotein B, atherogenic indices and negatively with HDL-cholesterol. The probands and siblings with arterial hypertension had significantly higher fasting insulin levels, as compared with subjects without hypertension which was due to a more frequent incidence of overweight. Patients with an impaired glucose tolerance and NIDDM had significantly higher fasting insulin levels and insulin levels after two hours (the latter value was not assessed in diabetes) and unfavourable "atherogenic" lipid and lipoprotein values, as compared with subjects without glucose intolerance and the control group. Overweight (BMI > 26) had an adverse impact on all investigated indicators of lipid and carbohydrate metabolism whereby a W/H ratio > 0.85 as a manifestation of central obesity further accentuated this adverse effect. The authors draw from these results therapeutic conclusions as regards the mentioned risk factors in these families. They emphasize the importance of non-pharmacological intervention of the metabolic X syndrome by weight reduction and more physical activity not only in families of subjects with early atherosclerosis but in the entire population which has a high prevalence of cardiovascular diseases.

Cerebrovascular Disorders↗