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Introduction: Recently resistance to an acetylsalicylic acid (ASA) administration has been a frequently mentioned problem. However, to identify ASA nonresponsive patients (ASA resistance) is difficult and common examination procedures can contain important preanalytic, analytic and postanalytic mistakes. Recently a possibility to use aggregometry after induction with cationic propyl gallate (CPG) has been discussed in this context; it's a robust, highly sensitive, and specific method for ASA resistance estimates. We asked ourselves following questions during our work:, Goal: a) Experience patients with acute coronary syndrome (ACS) ASA resistance more often than healthy volunteers?; b) Are aggregation values in both patients with different metabolic homeostasis disorders and patients with risk factors for atherosclerotic complications different?; c) Change results of measured aggregation induced by CPG in patients treated with identical ASA therapy during a several years long monitoring; respectively are patients assessed differently during the monitoring?; d) Is it possible to use one-shot aggregation assessment following CPG to estimate ASA resistance or is it necessary to repeat the examinations?; e) Is recurrence of ACS complications more frequent during two years of monitoring of patients with ACS history resistant to 100 mg doses of ASA per day?, Method: 103 patients of an average age 69 were assessed. All of them suffered from ACS without ST segment elevations and were treated conservatively; in addition to it all of them were treated with 100 mg ASA/day. They were assessed at the onset of ACS and after 3, 12 and 24 months. The examination consisted of taking patient history, clinical examination, BMI determination, laboratory test for cholesterol, HDL, LDL, triacylglycerols, and glucose, and of an aggregation of thrombocytes assessment under standard conditions (spontaneous and after CPG induction)., Results and Conclusion: a) ASA resistance is more frequent in patients with ACS compared to healthy volunteers (45% to 6%, p < 0.001). b) Patients with type II DM, smokers, patients with low HDL cholesterol levels or high triacylglycerols levels are ASA resistant more often (< 0.05). c) Results of measured aggregation of thrombocytes don't change during administration of the identical dose of 100 mg ASA/day during 2 years of monitoring. Respondents usually are assessed identically during monitoring (responsive/ASA nonresponsive). d) ASA resistance can be estimated from one-shot aggregation assessment following induction with CPG. e) Two years after diagnosing the ASA resistance a percentage of cardiovascular complications recurrence is higher in patients with history of ACS (p < 0.001). One-shot assessments of the CPG induced thrombocytes aggregation and the spontaneous aggregation are sensitive in 81% of patients with ACS history and specific in 100% of patients at risk of recurrence of cardiovascular complications. If these results are confirmed it could lead to a change in interventions in patients with ASA resistance proved by this method.

Introduction and Objective: Recently in the literature information is found on estimation of natriuretic peptides in the differential diagnosis of dyspnoea. Because in the Czech Republic since the beginning of 2002 routine estimation of NT-proBNP is available (analyzer Elecsys 2010), the objective of our work was to find out whether it is possible to use in the everyday practice of a district hospital estimation of NT-proBNP to differentiate dyspnoea with affection of the heart muscle from other types of dyspnoea., Method: A group of 33 patients from the medical department of the Sternberk hospital was examined who attended on account of dyspnoea and lacked signs of acute coronary syndrome. All probands were diagnosed on the basis of defined criteria; according to the final diagnosis the patients were divided into three groups: group "LV" was formed by dyspnoic patients with organic affection of the left ventricle and signs of congestion in the lesser circulation, group "non-LV" was formed by patients where no organic affection of the left ventricle was found but other heart disease was present. Group "non-C" was formed by patients where a cardiac cause of dyspnoea was ruled out. In all patients on admission NT-proBNP was assessed., Results: 33 probands were examined, 18 men and 15 women, mean age 74.5 years. 25 probands the dyspnoea was classified as dyspnoea with affection of one of the cardiac compartments [19 of them had signs of organic affection of the left ventricle (group "LV")]; in 6 probands no signs of organic left ventricular affection were found (group "Non-LV"). The remaining 8 patients had no signs of any disease of the heart muscle, valves, septa, endocardium and pericardium (group "Non-C). The baseline values of NTpro-BNP were closely associated with the NYHA classification (grade II--median 55.3 pmol/l (469 ng/l, grade III--median 399.3 pmol/l (3384 ng/l), grade IV--median 724.7 pmol/l (6294 ng/l), the differences were statistically significant, p < 0.05). The dyspnoic probands with concurrent affection of some cardiac compartment (groups "LV" and "Non-LV") had a NT-pro BNP concentration significantly higher than probands without affection of the heart (group "Non-C") (median 589.5 pmol (4996 ng/l as compared with 62.9 pmol/l (533 ng/l, p < 0.01). In the group of probands with heart disease probands with affections of the left ventricle (group "LV") had significantly higher NT-proBNP values than subjects without affection of the LV and without any heart disease (groups "Non-LV" and "Non-C") (median 670.6 pmol/l (5683 ng/l) as compared with 187.5 pmol/l (1589 ng/l), p < 0.01). In hospitalized probands after treatment along with improved cardiopulmonary compensation also a significant drop of NT pro-BNP occurred (median 303 pmol/l (3967.7 ng/l to 211 pmol/l (2561 ng/l), p < 0.05). When looking for associations between anamnestic, laboratory and clinical data we found that the value of NT-proBNP is associated with dyspnoea with cardiac affection (groups "LV" + "Non-LV", correlation coefficient 0.48), with the left ventricular ejection fraction (correlation coefficient 0.52) and the baseline NYHA classification (correlation coefficient 0.36). In the examined group we did not find an association between NT-proBNP and age, sex, diabetes mellitus, hypertension, the presence of atrial arrhythmias, aortal stenosis, or the width of the left atrium. When using as cut-off for NT-proBNP 59 pmol/l (500 ng/l), the sensitivity of NT-proBNP for dyspnoea with affection of the cardiac compartments was 92% and the specificity 67%., Conclusion: Assessment of NT-proBNP is an important diagnostic acid in the differential diagnosis of dyspnoea.

Introduction and Aim of the Study: Acetylsalicylic acid (ASA) is one of basic preparations used in the therapy of cardiovascular diseases. Application of ASA leads to irreversible reduction of platelet aggregation. The aim of the present study was to verify monitoring of effectiveness of ASA therapy using the measurement of platelet aggregability in vitro after induction by cationic propyl gallate (CPG), which is considered to be a highly potent inducer of aggregation., Methods: We examined a group of 27 healthy volunteers, divided into two subgroups (n = 19, n = 8). The first subgroup was examined for thrombocyte aggregation before and 24 hours after administration of 400 mg of ASA after induction by ADP, collagen, adrenalin and CPG. The second subgroup was examined for thrombocyte aggregation before and after a three-day administration of ASA in a dose of 100 mg/day., Results and Conclusion: In the group of 27 healthy volunteers we determined normal values of aggregability for individual inducers. Low stability of the used methods was proved (weak or insignificant correlation of results of the same method before and after administration of ASA). The most advantageous parameter for monitoring of effectiveness of 400 and 100 mg of ASA was CPG slope (paired t test, p < 0.00000002, resp. p < 0.001). The parameter of CPG slope we determined in both subgroups the cut-off value (< 53s), by means of which it is possible to discriminate probands according to ASA therapy (in contrast to other routinely used inducers). The obtained results indicate that measurement of thrombocyte aggregation after CPG induction reveals a significantly lower percentage of ASA non-responders ASA than after other inducers. Measurement of thrombocyte aggregation after CPG induction is predicted to be highly promising for monitoring the effectiveness of anti-aggregation therapy.

Osteoprotegerin, RANK (Receptor Activator of Nuclear factor kappa B) and RANKL (Receptor Activator of Nuclear faktor kappa B ligand) became the aim of intensive research. RANK is considered as a hematopoietic surface receptor controlling osteoclastogenesis and calcium metabolism. RANKL may promote osteoresorption by induction of cathepsin K gene expression. The present paper summarizes the most significant data in osteoprotegerin, RANK and RANKL problems obtained.

Introduction and Objective: Acetylsalicylic acid (ASA) is one of the basic preparations which are used in the treatment of cardiovascular diseases. ASA administration leads to irreversible restriction of platelet aggregation. The objective of our work was to test possibilities of monitoring the effectiveness of ASA therapy by measuring the platelet aggregability in vitro after induction with cationic propyl gallate (CPG) which is considered a very potent aggregation inductor., Method: We examined a group of 27 healthy volunteers divided into two sub-groups (n = 19, n = 8). In the first sub-group the platelet aggregation was examined before and after 24 hours following ingestion of 400 mg ASA after induction with ADP, collagen, adrenaline and CPG. In the second sub-group the platelet aggregation was examined before and after three-day administration of ASA--100 mg/day., Results and Conclusion: In a group of 27 volunteers we assessed normal values of aggregation after different inductors. A low stability of the methods used was proved (low stability or insignificant correlation of results of the same method before and after ASA ingestion. The most useful parameter by means of which it was possible to monitor the effectiveness of administration of 400 or 100 mg ASA was the C/G slope (paired t-test, p < 0.0000002, and p < 0.001 resp.). In parameter CPG slope we were able to assess in both groups the cut-off value (< 53%/min.) by means of which it is possible to discriminate probands according to ASA therapy (contrary to the other commonly used inductors). From the results ensues that when assessing the thrombocyte aggregation after CPG induction we find a significantly lower percentage of so-called ASA non-respondents than after other inductors. We consider the use of assessment of thrombocyte aggregation after CPG induction when monitoring antiaggregation therapy a very promising procedure.

The estimated risk of development of complications of atherosclerosis (coronary or cerebral ischaemia) is one of the activities every physician should include in the diagnostic and therapeutic algorithm. Treatment with hypolipidaemic agents is indicated according to the European consensus if the danger of a coronary or cerebral event is 20%/10 years. The objective of preventive provisions should be reduction of this risk to < 5%/10 years in younger subjects (< 45 years in men and < 50 years in women) and < 10%/10 years in elderly subjects. These recommendations obviously do not apply to secondary prevention (in case of complications of atherosclerosis) where treatment with hypolipidaemic agents is indicated already when the LDL-cholesterol level is 2.3 mmol/l or when triacylglycerols are 2.3 mmol/l, combined with a drop of HDL-cholesterol to < 0.9 mmol/l.

Assessment of carbohydrate-deficient serum transferrin CDT) is considered a very useful indicator of alcohol abuse. There is a number of methods for assessment of CDT. In clinical practice most frequently assessment of the percentage ratio of CDT in transferrin is used. In our hospital we assessed CDT by the method of homogeneous immunoanalysis (Boehringer Mannheim (CDT-BM). Because we obtained a relatively high percentage of false results and because we found in the literature reference to a new method of homogeneous immunoanalysis (The Sanqui BioTech-CD-SB) with a different cut-off, we decided to compare the results of the estimations by the two methods and assess the percentage of false results. We examined a group of 49 patients incl. 16 who admitted alcohol abuse (> 60 g alcohol more than four times per week). As anticipated, we found that the %CDT assessed by the CDT-BM method was significantly higher than the percentage CDT-SB. After classification of the group into sub-groups with regard to alcohol intake the two sub-groups differed significantly only in values of CDT-SB and CDT-BM. In the group of patients with alcohol abuse we found relations between CDT-MB and indicators of hepatic lesions. In CDT-SB we found only an association with AST. This finding could suggest a greater specificity of CDT-SB. We confirmed data in the literature that GMT is independent on CDT and the mean corpuscular volume is independent on CDT in subjects with alcohol abuse. In abstainers who negated alcohol intake we found also when assessing CDT-SB a significant gender differentiation which is described in the literature (the reason is probably the fact that the CDT-SB method analyzes, contrary to CDT-BM, only asialo,-monosialo and disialylic isoforms of transferrin and women have higher levels of monosialylic forms). In our group the examination of %CDT by the new method, the Sanqui Biotech for alcohol abuse, had an almost absolute specificity and sensitivity. Contrary to the older Boehringer-Mannheim method we did not record any false increase in any patient with signs of hepatopathy nor any false negative results). We assume that the described methodical innovation of the analysis could facilitate the differential diagnosis of various diseases in different medical disciplines (internal medicine, neurology, psychiatry, assessment of work capacity).

Unlabelled: During the last decade several papers were published where obesity in included among the building stones of the so-called metabolic cardiovascular syndrome (along with hypertension, dyslipidaemia, impaired glucose tolerance and hyperinsulinaemia). Several months ago it was also revealed that some patients with the metabolic syndrome suffer from hyperleptinaemia. Leptinaemia is considered by some authors as independent indicator of the risk of accelerated atherosclerosis. The cause of these hypothesis were (in addition to the known conclusions on the occurrence frequent incidence of leptin resistance and insulin resistance) in particular the results of experimental studies where evidence was provided that infusion induced hyperleptinaemia leads in animals to hypertension due to its direct effect on sympathicotonia and peripheral vascular resistance. The authors of these hypothesis assume that hyperleptinaemia (in particular in subjects with metabolic syndrome) in one of the basic causes of hypertension which is frequently encountered in these patients., Objective: To assess the relations between leptinaemia and the blood pressure reading (actual and mean values) and leptinaemia and the classification of hypertension according to WHO., Method: The authors examined 35 hypertensive subject and 10 subject with tetanies (without hypertension). The blood pressure was assessed under standard conditions (rest, semi-recumbent position, three readings). The mean blood pressure readings during the last three months were obtained from case records. Leptin was assessed by the ELISA method of Bio Vendor Co., Results: The group of hypertonic can be classified as subjects with mild obesity (BMI 30.1). The values of leptin were elevated but did not differ significantly from those of the normal population. No correlations were found between leptinaemia (incl. values calculated for BMI) and the actual and mean blood pressure readings. No correlations were found between leptinaemia (incl. BP calculated with regard to BMI) and the stage of hypertension according to WHO., Conclusion: Hypertonic subject do not differ significantly as to the serum leptin concentration from the general population. Leptinaemia does not correlate with the actual or mean blood pressure reading nor with stage of hypertension according to the WHO classification. Thus the authors did not confirm the hypothesis on the fundamental effect of leptinaemia on the genesis and development of hypertension. It is probable that leptin is only one of the many factors which have an impact on blood pressure.

Introduction: Leptin is a protein, determined by the ob-gene which influences in a fundamental way the energy metabolism of the organism. A significant effect of leptin on the haematopoietic, immunological and endocrinological system cannot be ruled out nor its effect on the course of pregnancy and maturation of the organism. In humans leptinaemia correlates with the amount of subcutaneous fat which is due to a receptor or post-receptor disorder, obese subjects suffer frequently from hyperleptinaemia., Objective: To assess the mean leptinaemia of the general population, seek relations between leptinaemia and anthropological indicators and age., Methods: Using the method of random sampling the authors examined a group of 538 probands (252 males, 286 females) incl. 12% healthy students of the Faculty of Physical Culture in Olomouc, 37% subjects without acute or chronic complications feeling in good health and 37% patients of the metabolic and diabetological ambulance of the hospital in Sternberk. In each patient a detailed case-history was recorded, an anthropological examination was made and a venous blood sample was taken for leptin analysis (serum, ELISA-sandwich method of BIOVENDOR Co.), Results: Spectrum of patients, whose condition and age distribution in our group corresponded to the general population of the Czech Republic. The mean age of the probands was 51 years (18 to 82 years), the examined group can be characterized as subjects lacking signs of obesity. Leptinaemia was on average about 10 ng/ml (minimum 0, maximum 97.9 ng/ml), whereby men had values round 6 and women round 14 ng/ml (women had also a greater adipose tissue mass). Non-obese subjects (BMI<26) had a mean leptinaemia of 5 (women cca 6, men cca 2 ng/ml), obese subjects (BMI>30) have a leptinaemia of cca 19 ng/ml (women about 26, men about 13 ng/ml). With advancing age the leptinaemia in adults rises up to the age of 70, in subjects above 70 years it does not change (in women it declines significantly). The dynamics of leptinaemia imitate the changes of BMI and percentage of adipose tissue (in men also a rise in WHR). Leptinaemia is associated with the BMI (correlation coefficient 0.55), with the percentage of body fat (correlation coefficient 0.75), and in men with the WHR (correlation coefficient 0.82). The association between ageand leptinaemia is only indicated (correlation coefficient 0.29) and is not very close. According to the authors results subcutaneous body fat is responsible for cca 60% of the variability of leptinaemia (in women as much as 74%), BMI for 23%, age and sex for cca 9% of the vriability of leptinaemia. In men the WHR is responsible for 66% of the variability of leptinaemia. With an increase of subcutaneous adipose tissue by 1% the leptinaemia increases by some 0.54 ng/ml (in men by 0.22 ng/ml, in women by 0.84 ng/ml), with increasing BMI leptinaemia rises by 0.44 ng/ml/u (in men by 1.3 ng/ml, in women by 1.72 ng/ml), with advancing age leptin rises by 0.24 ng/ml/year (in men by 0.16 ng/ml, in women by 0.28 ng/ml), changes of leptinaemia imitate changes of BMI and the percentage of body fat. With increasing WHR in men the leptinaemia rises by 2.6 ng/ml/0.1 WHR., Conclusion: Standards of leptinaemia for the general population of the Czech Republic were elaborated. Leptinaemia correlates most closely of all anthropometric indicators with subcutaneous fat and in men with the WHR index. With advancing age between 20 and 70 years leptunaemia rises and then decliunes insignificantly (in women the changes are however significant). The primary cause of the mentioned differencesare probably changes of the bodily constitution.

Introduction: According to contemporary estimates diabetes is present in 120 million subjects. This disease is associated with the incidence of a number of very serious organ complications and very frequently is diagnosed late (several years after its development). Because despite increased diagnostic and therapeutic efforts the number of diabetic patients is increasing, new diagnostic and therapeutic means are sought. Evidence was provided that some complications of diabetes develop not only in case of poor compensation but also in hyperinsulinaemia (hypertension, ischaemic heart and coronary artery disease etc.). In clinical practice it is however possible to assess hyperinsulinaemia or incipient insulin resistance only with difficulty because classical examinations (insulin and C-peptide on fasting) have a very low specificity and sensitivity. Therefore for estimation of insulin resistance loading tests are used (e.g. examination of insulin after stimulation with glucose, or C-peptide after stimulation with glucagon, insulin tolerance and suppression tests, or in research projects so-called minimal models or clamp techniques). Any loading test is however demanding from the aspect of time, money, technical aspects and staff and therefore possibilities are sought how to estimate the degree of insulin resistance and sensitivity in a specimen of biological material under basal conditions. OBJECTIVE OF INVESTIGATION: Because in the literature only sporadically assessment of intact proinsulin is mentioned as the ideal marker of insulin resistance under basal conditions, the authors decided to assess the relations between intact proinsulin (PI) and other biochemical parameters in patients with type 2 diabetes and dyslipidaemia (200 probands) and to assess whether PI correlates with the results of loading tests (modified oGTT with calculation of the sum and delta-insulin--120 probands)., Results: It was revealed that PI (contrary to insulin, C-peptide and total proinsulin) correlates with the results of the loading test characterizing insulin resistance (sum and delta insulin, correlation coefficient 0.84) (n=120 subjects). It was furthermore found that probands (n=200 subjects) who are followed up on account of type 2 diabetes or dyslipidaemia (or both) differ from the control group (n=20 subjects) as regards biochemical parameters only in the PI concentration (dispensarized patients have higher levels, p>0.99), whereby in other standard basal characteristics of insulin secretion and resistance the groups did not differ. The differences were correlated with HOMA models of insulin secretion and resistance and no correlations were found. The PI concentration in this group correlated significantly with the cholesterol, fibrinogen and triacylglycerol concentration. No relations were found between the values of intact proinsulin with C-peptide and insulin., Conclusion: Based on the results of their study the authors assume that examination of intact proinsulin is a valid "basal" indicator of insulin resistance. From the results ensues also that intact proinsulin is probably a very good predictor as regards the risk of development of cardiovascular disease.

Leptin receptors are supposed to have signal effects and are located in most tissues in the organism but we failed to find literary data on concentration (measurement) of leptin receptors in the system circulation. We examined by the method of randomized selection the group of 20 patients with manifested atherosclerosis in whom BMI was calculated. Then we analyzed concentration of leptin receptor (double sandwich ELISA, standard recombinant human leptin), leptin, glucose, insulin, proinsulin, CRP and uric acid in the serum. The control group consisted of 103 probands without signs of atherosclerosis or other manifested diseases. The control group was subjected to determination of BMI, leptin and leptin receptor in the serum. Concentration of leptin receptor does not differ significantly between the patients with atherosclerosis and normal population. Probands with atherosclerosis showed a very close negative correlation between concentration of leptin receptor and leptinemia which is absent in normal population.

Treatment of dyslipidemia and its frequently associated complications (manifest atherosclerosis) is very pretentious from the economic aspect. Diagnostic and therapeutic criteria are based mainly on biochemical analyses. Although demands on laboratories are relatively strict (respecting defined laboratory errors, analytical and preanalytical conditions), when defined diagnostic criteria are used, the results of biochemical analyses are not yet satisfactory. A typical example is the stratification of risk patients according to the LDL concentration which in our country is very often preferred, although the LDL concentration is based only on calculation (contrary to investigations from which the majority of recommendations was derived where the LDL concentration was assessed directly). We know from our own experience that a large percentage of results of estimated and assessed LDL differs significantly. Therefore we wanted to know whether the assessed LDL concentration correlates with its estimate according to Friedewald s formula and which analytes have the greatest impact on the LDL concentration. Our objective was also to assess th percentage of incorrectly listed patients (according to the LDL stratification scale). In 1997-1998 we examined a group of 4578 probands, patients of the consultant out-patient departments of the Sternberk hospital. Their mean age was 56 years. On average subjects with as slightly atherogenic phenotype were involved (classification A according to EAS). The values of lipid parameters did not differ significantly in the two sexes. The cholesterol, LDL and triacylglycerol concentrations increased with advancing age. The LDL values obtained by assessment and calculation correlated closely. The LDL value was influenced most by ApoB and total cholesterol. Triacylglycerols correlated with LDL assessment only up to a concentration of .3 mmol/l. HDL, ApoA-1 and higher triacylglycerol concentrations (1.3 mmol/l) did not correlate with the LDL value. The authors provided evidence that in subjects where it was possible to calculate LDL lege artis (2458 probands) were listed according to LDL calculation into a wrong group (stratification according to NCEP) whereby up to an LDL concentration .11 mmol/l this parameter cannot be predicted at all by calculation (error up to 85%). A satisfactory estimate is assumed only at LDL concentrations 5.2 mmol/l. Because the estimated LDL values are in the majority of patients lower than the calculated values, it may be assumed that during stratification of LDL obtained by calculation the patients are treated too aggressively. Assuming pharmacological treatment of all mentioned patients, it may be estimated that by using analyses of direct LDL for stratification of probands the costs of hypolipidaemic treatment will by reduced by about 1/4-1/3 (in the catchment area of the Sternberk hospital this would save more than 10 million crowns). The costs of LDL analyses per year are about 180,000 crowns (in the Sternberk hospital--which amounts to cca 1.5% of the money saved on pharmacotherapy).

The purpose of the study was to verify whether the currently reported relationship between leptinemia and adipose tissue mass can be applied to cases of acute coronary attack. An increased number of cytokines has been reported in severe acute myocardial infarctions so that correlation between cytokines and leptin was investigated. Correlation between standard coronary markers and leptinemia was also studied. We examined 48 probands, patients of the Coronary Unit, Hospital, Sternberk, who were hospitalized for acute myocardial infarction (AMI--16 probands) or for unstable angina pectoris (UAP--22 probands). The persons with AMI had leptinemia and a higher concentration of interleukine-6 (Il-6) and of cardial troponine-I (cTn-I) than individuals without coronary accident (UAP). Early after the acute coronary lesion, leptinemia in persons with AMI displayed a statistically significant positive correlation with concentration of interleukine-6 and subsequently of markers of coronary lesion severity (cTnI). No correlation between leptinemia and body weight was found in those probands. This study proved that leptinemia in the AMI individuals is influenced directly by concentration of cytokines which leads to leptin superproduction by fat cells and leptin resistance.

Leptin is a small protein produced mainly by adipocytes. Recently, its relationship to obesity has been studied extensively. It was proved that obese individuals have either relative or absolute leptin deficiency. Several years ago, leptin was found to be produced also by the placenta. This stimulated us to study relationship between leptinemia and placental hormones in 85 women in the second gravidity trimester. Within the prenatal screening, these pregnant women were subjected to analysis of AFP, hCG, SP-1 glycoprotein and leptin and the results obtained were processed statistically. The control group consisted of 20 nonpregnant women with tetany. Women in the second gravidity trimester were found to have a significantly higher leptinemia than nongravid women (even with respect to body weight). This may be due to a larger amount of adipose tissue during gravidity and also leptin-resistance. Moreover, we recorded a negative correlation between leptinemia related to body weight and concentration of SP-1 glycoprotein. This finding supports the presumption that mother's leptinemia correlated negatively in the second gravidity trimester with quality and quantity of the placental syncytiotrophoblast. Our findings can be explained as follows: the biological effect of leptin is metabolically unfavourable for the growth of the foetus and the placenta. An increased leptinemia with advancing gravidity can be caused by a larger fatty mass and an increased activity of adipocytes when leptin presence increases in system circulation but the organism begins to be leptin-resistant and an "unfavourable" metabolic effect fort the gravid woman and the foetus is not distinct. These findings thus support the hypothesis postulating the nonsignificance of leptin production in human placenta and on the contrary the necessity of leptin-resistance for foetus development from the metabolic point of view. Thus, a decreased leptinemia immediately before and after the delivery could be caused by the still unclear regulators of leptin sensitivity. This is again a metabolically highly favourable state (reduced appetite, decreased body weight, increased energy output and others).

Acute myocardial infarction (AMI) is a disease with high morbidity and mortality. Diagnosis of AMI using common methods (classical biochemistry, ECG) fails even in the fifth part of patients so that other noninvasive diagnostic methods are preferred. Recently, the biochemical analysis has been restored in the case of AMI diagnostics and also in prediction of coronary reperfusion after administration of a fibrinolytic agent. A suitable markers of AMI diagnostics is a combination of myoglobin and cardial troponin-I which is reported as a marker with high specificity and sensitivity. To determine coronary reperfusion, the examination of cardial troponin-T and CK-MB mass is recommended. In the literature, there exist isolated papers dealing with dynamics of cTn-I suitable for prediction of coronary revascularization. However, these papers do not report any adequate algorithm and subsequently mathematical differences between successful thrombolysis and failing thrombolysis. Therefore the aim of our study was to describe dynamics of cTn-I changes in AMI patients treated by thrombolysis. The study comprised of 8 AMI patients with delay from the occurrence of pains to fibrinolysis application under 4 hours (delay 4 hrs). These probands were examined for concentration of cTn-I and CK-MB mass in 3-hour intervals in the first 48 hours after admission to the clinic and further in 6-hour intervals from the hour 48 to the hour 90 after admission. All probands had a successful reperfusion (estimated using CK-MB peak, in 4 patients reperfusion was verified by subsequent coronarography). However, a simple mathematical prediction of coronary reperfusion after acute myocardial infarction by means of cTn-I dynamics determination is not possible due to relatively low cTn-I differences in individual analyses (CK-MB mass analysis shows more significant differences). Thus, in order to determine coronary revascularization, we recommend to use common analyses of dynamics of cTn-T or CK-MB mass.