Circulating levels of inflammatory parameters pentraxin-3, cyclophilin and heparin-binding epidermal growth factor-like growth factor in patients with ST-elevation myocardial infarction.

Inflammatory biomarkers - pentraxin-3 (PTX3), cyclophilin A (CypA) and heparin-binding epidermal growth factor-like growth factor (HB-EGF) were examined in patients with ST-segment elevation myocardial infarction (STEMI) undergoing revascularization with primary percutaneous coronary intervention (pPCI) and stent implanting. Investigated parameters were compared between patients with and without obstructive coronary artery disease (CAD). In addition, their changes were tested in circulation before and immediately after pPCI. The study group consisted of 81 STEMI patients. Patients were classified in the STEMI-CAD group if they had significant obstructive CAD or in MINOCA group if they had no significant stenosis. In STEMI-CAD patients inflammatory parameters were determined prior to and after pPCI intervention. Immediately after pPCI, in STEMI-CAD patients levels of PTX3 were significantly lower (1.52 vs. 2.17 µg/L, p < .001), while the levels of HB-EGF (14.61 vs. 12.03 pg/L, p < .001) and CyPA (15.95 vs. 8.62 µg/L, p < .001) were significantly higher compared to levels before pPCI. STEMI-CAD patients had lower PTX3 values 2.17 µg/L (1.55-5.10 µg/L) than MINOCA patients 5.06 µg/L (2.77-6.7 µg/L), p = .046. Diagnostic accuracy of PTX3 for discrimination MINOCA from STEMI-CAD patients was low (area under receiver operating characteristic curve = 0.770). Evaluation of PTX3 values may be helpful in the understanding of MINOCA aetiology but they couldn't distinguish stenosis severity in STEMI patients. Inflammatory biomarkers significantly changed after pPCI but the possibility of clinical use of these biomarkers needs to be evaluated in a larger prospective study.

Clinoptilolite for Treatment of Dyslipidemia: Preliminary Efficacy Study.

OBJECTIVES: A tribomechanically activated clinoptilolite (natural aluminosilicate mineral) has been used to increase growth in meat-producing animals, as an adjuvant in cancer therapy, and a heavy metal remover in humans. Because of its unique cation exchanging and chelating properties, we hypothesized that clinoptilolite may be beneficial for the treatment of dyslipidemia in the manner similar to bile acid sequestrants. Thus, specific aims of this pilot study were to orally administer clinoptilolite in different doses and granule size combinations to determine magnitude and time profile of changes in blood lipids. DESIGN: A phase I/IIa prospective, open-label, uncontrolled, dose/granule size-ranging study (treatment phase 8 weeks, follow-up 6 weeks). Blood lipids were examined every 2 weeks. SETTINGS: Outpatient clinic of a university-affiliated hospital. SUBJECTS: Forty-one subjects (all white, mean age 57.6 ± 6.8 years, 17 women) with blood lipids above the normative limits divided into three groups. INTERVENTION: A tribomechanically activated clinoptilolite was administered in three dose/grind combinations: 6 g/day of fine grind (6gF), 6 g/day of coarse grind (6gC), and 9 g/day of coarse grind (9gC). OUTCOME MEASURES: Blood concentrations of total cholesterol (TC), low-density lipoprotein cholesterol (LDLc), high-density lipoprotein cholesterol (HDLc), and triglycerides (TG). RESULTS: For the 3 groups combined, all lipid fractions significantly improved after 8 weeks of treatment (20-25%, p < 0.001), which reversed to baseline after 6 weeks of clinoptilolite withdrawal. Early (week 2) and the most pronounced decrease in TC and LDLc was observed in the 6gF group (19% and 23% in week 8, respectively), with no difference in HDLc and TG between the three dose/grind groups. No side effects were reported. CONCLUSIONS: These pilot results suggest that oral administration of clinoptilolite may improve lipid profile in individuals with dyslipidemia, which warrants further investigations.

Oxidative stress induced by chlorpromazine in patients treated and acutely poisoned with the drug.

Background/Aim: Although chlorpromazine (CPZ) is an antipsychotic drug widely used in clinical practice for a long time, its mechanism of action has not been entirely defined. An extremely difficult managing of patients acutely poisoned with CPZ is additional reason for detailed studying its toxicity mechanisms. In this clinical study, we investigated whether the oxidative stress (OS) mediates CPZ toxic effects in the exposed patients. Methods: The patients were organized into 3 groups: the T-group - hospitalized patients receiving therapeutic doses of 75-150 mg CPZ/day; the overdosed group, divided into two subgroups: the group M and the group S - mildly (CPZ serum concentration: 0.21 ± 0.05 mg/L) and severely (CPZ serum concentration: 2.66 ± 0.25 mg/L) poisoned patients, respectively, and the group C (control group of healthy volunteers). Oxidative stress parameters [total antioxidative status (TAS) and malondialdehyde (MDA) in plasma)] and superoxide dismutase (SOD) activity in erythrocytes were measured spectrophotometrically, and CPZ concentrations in serum were monitored chromatographically. One set of measurements was performed in the group C and T, whereas two sets of measurements (after 24 hours and 48 hours) were done in the poisoned patients, groups M and S. Results: A decrease of TAS and increase of SOD activity were obtained in both subgroups of the poisoned patients, compared to the controls and the group receiving therapeutic doses of CPZ. A significant increase of MDA was achieved in severely poisoned patients, compared to all other groups. Conclusion: Changed oxidative stress parameters in patients poisoned with chlorpromazine indicate involvement of oxidative stress in the toxicity mechanism(s) of chlorpromazine.

Association of Serum Pentraxin-3 and High-Sensitivity C-Reactive Protein with the Extent of Coronary Stenosis in Patients Undergoing Coronary Angiography.

BACKGROUND: We compared factors of inflammation - high sensitivity C-reactive protein (hsCRP) and pentraxin-3 (PTX3), and we explored their relationship with coronary artery disease (CAD). Also, we tested the usefulness of hsCRP and PTX3 in the risk assessment of coronary stenosis development and the diagnostic ability of these biomarkers to detect disease severity. METHODS: The study group consisted of 93 CAD patients undergoing coronary angiography. Patients were divided into CAD(0), representing subclinical stenosis, and CAD (1-3), representing significant stenosis in one, two or three vessels. RESULTS: We determined the concentration of lipid status parameters, hsCRP and PTX3. We found significantly lower PTX3 and hsCRP concentrations in CAD(0) than in CAD(1-3) group. Concentration of PTX3 showed an increasing trend with the increasing number of vessels affected. The area under ROC curve (AUC) for the combinations of hsCRP and PTX3 with lipid parameters had useful accuracy for detecting CAD(1-3) patients (AUC=0.770, p<0.001). CONCLUSION: PTX3 is a promising independent diagnostic marker for identifying patients with CAD, and a useful indicator of disease progression. In all the analyses PTX3 showed better performance than hsCRP. A combination of PTX3, hsCRP with the lipid status parameters provides risk stratification of the development of coronary stenosis and better classification than their individual application.