Treatment with atorvastatin reduces serum adipocyte-fatty acid binding protein value in patients with hyperlipidaemia.

BACKGROUND: Adipocyte-fatty acid binding protein (A-FABP) is a circulating protein expressed in adipocytes and macrophages. Several recent studies demonstrated that A-FABP might be involved in the pathogenesis of metabolic syndrome, particularly in dyslipidaemia, insulin resistance and atherosclerosis. The aim of this study was to investigate the influence of atorvastatin treatment (20 mg day(-1) for 3 months) on serum A-FABP value in subjects with hyperlipidaemia. MATERIALS AND METHODS: Anthropometric and serum analyses were performed for body mass index, A-FABP, triglycerides, total cholesterol, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, uric acid, alanine aminotransferase (ALT), aspartate aminotransferase (AST), high sensitive C-reactive protein (hs-CRP), creatine kinase (CK) and glucose on 26 subjects (BMI 30.3 +/- 6.0, mean age 62 +/- 10 years) with hyperlipidaemia who met the criteria: total cholesterol > 5.2 mmol L(-1), LDL cholesterol > 3.3 mmol L(-1) and triglycerides < 3 mmol L(-1). RESULTS: After the 3-month therapy, a significant reduction in total cholesterol (P < 0.001), LDL cholesterol (P < 0.001), glucose (P < 0.001), A-FABP (from 44.6 +/- 26.2 to 38.6 +/- 19.3 g L(-1), P < 0.01), uric acid (P < 0.05), AST (P < 0.05) and triglycerides (P < 0.05) values was observed. No difference was found in BMI, CK, ALT, hs-CRP, or HDL cholesterol values. A significant difference in the serum A-FABP value before and after the therapy remains after the correction for total cholesterol value (P < 0.001). A positive correlation between serum A-FABP and glucose was found (P < 0.05). CONCLUSIONS: In conclusion, our study confirmed in vivo that atorvastatin reduces serum A-FABP by a pleiotropic mechanism and supports the hypothesis that A-FABP is involved in atherosclerotic actions.

[Adiponectin and insulin sensitivity]. / Adiponektin a inzulínová senzitivita.

BACKGROUND: Adiponectin is a fat tissue protein that plays a role in maintaining the homeostasis of glucose and lipids, along with counteracting a number of risk factors associated with atherosclerosis and obesity. In addition, adiponectin has an effect on insulin sensitivity. The aim of this work was to assess concentrations of adiponectin in predefined groups of individuals and to analyse the associations between adiponectin and other metabolic parameters. METHODS AND RESULTS: The studied population comprised four groups of individuals, A-D. A--healthy controls, B--patients with impaired lipid metabolism, C--the obese, and D--patients with metabolic syndrome. When comparing the levels of adiponectin in groups of patients with impaired lipid metabolism (B), the obese (C), and patients with metabolic syndrome (D) with healthy controls (A), no statistically significant difference was observed between groups B and C and healthy individuals. In contrast, statistically significant difference was found when concentrations of adiponectin in patients with metabolic syndrome (D) were compared to those in healthy controls. Individuals with metabolic syndrome had the lowest levels of adiponectin - 5.3 mg/1 (men) and 5.6 mg/1 (women). The correlation coefficient for the association between adiponectin and HDL was R=0.57, for adiponectin and triglycerides R=-0.46, for adiponectin and BMI R=-0.37, for adiponectin and glycemia R=-0.34, for adiponectin and insulinemia R=-0.39, and for adiponectin and the QUICKI index R=0.44. CONCLUSIONS: One possible method of the complex evaluation of the metabolic syndrome development and its metabolic consequences is the assessment of adiponectin levels. Low levels of adiponectin indicate the development of insulin resistance.

[Use of assessment of aggregation of thrombocytes induced by cationic propyl gallate to estimate recurrence of cardiovascular complications]. / Vyuzití stanovení agregability trombocytu po indukci kationickým propylgalátem v odhadu recidiv kardiovaskulárních komplikací.

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.

[First experience with the cobalt binding capacity (ACB) test in the diagnosis of acute coronary syndrome (a pilot study)]. / První zkusenosti se stanovením vazebné kapacity pro kobalt (ACB) v diagnostice akutního koronárního syndromu (pilotní studie).

INTRODUCTION: Commonly used laboratory markers of coronary damage in individuals with acute coronary syndrome (ACS) are not specific for myocardial ischemia and prove only irreversible myocardial damage. There have been concerns recently of a laboratory test able to distinguish sufficiently an individual with myocardial ischemia and typical IHD symptoms from patients without IHD. Since 1994 several works about cobalt binding capacity of albumin (ACB) have been published in which a unique diagnostic sensitivity and specificity of this test for estimations of the presence of myocardial ischemia has been described. In February 2003 this test was approved by FDA for making an early diagnosis of ACS. GOAL OF THE WORK: To verify a possibility to use ACB test for making an early diagnosis of ACS. METHOD: 98 individuals, patients of the Department of Internal Medicine of the hospital in Sternberk, hospitalised for suspicion of ACS but not indicated for direct PTCA, have been examined. Respondents with ACS diagnosis were examined via coronarography. All the respondents were examined for cTnI, myoglobin, and ACB immediately at the admission (0) and 2, 6, and 12 hours after admission. Cobalt binding capacity of albumin has been given in absorbance units. The group of respondents was subsequently divided into subgroups according to presence of ACS and subgroups of respondents with/without AMI. RESULTS: 55 respondents (56%) have been diagnosed with ACS. 16 respondents (16%) from them suffered from non-Q AMI and 39 respondents (40%) suffered from unstable AP (UAP). 43 respondents (44%) suffered from noncoronary sternal pain. Patients with ACS had ACB values significantly higher at admission and 2 and 6 hours after admission compared to respondents without ACS (0: 0.62 +/- 0.17 vs. 0.4 +/- 0.11, 2: 0.61 +/- 0.13 vs. 0.44 +/- 0.12, 6: 0.58 +/- 0.16 vs. 0.45 +/- 0.1, p < 0.01). In ACB dynamics monitoring in defined groups of respondents no significant differences have been identified among ACB values of individual takings. There were no significant differences in ACB values 12 hours after admission (0.53 +/- 0.12 vs. 0.44 +/- 0.16) in cut-off absorbance ACB 0.5 the diagnostic sensitivity at admission was 69% and specificity 89%, 2 hours later 87% and 71% and 6 hours after admission 64% and 69%. 12 hours after admission ACB assessment has not been possible to be used for ACS diagnosing (AUC of 0.55). First 2 hours after admission ACB test was more specific and sensitive for diagnosing ACS compared to cTnI test (0: AUC 0.83 vs. 0.61, p = 0.015, 2: AUC 0.87 vs. 0.71, p = 0.04). However, ACB test could not be used in respondents with ACS to distinguish between acute myocardial infarction and unstable angina pectoris (UAP) (AUC: ACB-0 0.51, ACB-2 0.56, ACB-6 0.51, ACB-12 0.57). CONCLUSION: ACB test is a quick, cheap and easy examination which is very specific and sensitive for early diagnosing of acute coronary syndrome without regard whether it is caused by UAP or AMI (up to 6 hours after admission) compared to commonly used markers. This test could significantly contribute to the next fate of a patient (diagnostic procedures, patient's prognosis).