The Role of Galectin-3 in Heart Failure-The Diagnostic, Prognostic and Therapeutic Potential-Where Do We Stand?

Heart failure (HF) is a clinical syndrome with high morbidity and mortality, and its prevalence is rapidly increasing. Galectin-3 (Gal-3) is an important factor in the pathophysiology of HF, mainly due to its role in cardiac fibrosis, inflammation, and ventricular remodeling. Fibrosis is a hallmark of cardiac remodeling, HF, and atrial fibrillation development. This review aims to explore the involvement of Gal-3 in HF and its role in the pathogenesis and clinical diagnostic and prognostic significance. We report data on Gal-3 structure and molecular mechanisms of biological function crucial for HF development. Over the last decade, numerous studies have shown an association between echocardiographic and CMR biomarkers in HF and Gal-3 serum concentration. We discuss facts and concerns about Gal-3's utility in acute and chronic HF with preserved and reduced ejection fraction for diagnosis, prognosis, and risk stratification. Finally, we present attempts to use Gal-3 as a therapeutic target in HF.

Involvement of circRNAs in the Development of Heart Failure.

In recent years, interest in non-coding RNAs as important physiological regulators has grown significantly. Their participation in the pathophysiology of cardiovascular diseases is extremely important. Circular RNA (circRNA) has been shown to be important in the development of heart failure. CircRNA is a closed circular structure of non-coding RNA fragments. They are formed in the nucleus, from where they are transported to the cytoplasm in a still unclear mechanism. They are mainly located in the cytoplasm or contained in exosomes. CircRNA expression varies according to the type of tissue. In the brain, almost 12% of genes produce circRNA, while in the heart it is only 9%. Recent studies indicate a key role of circRNA in cardiomyocyte hypertrophy, fibrosis, autophagy and apoptosis. CircRNAs act mainly by interacting with miRNAs through a "sponge effect" mechanism. The involvement of circRNA in the development of heart failure leads to the suggestion that they may be promising biomarkers and useful targets in the treatment of cardiovascular diseases. In this review, we will provide a brief introduction to circRNA and up-to-date understanding of their role in the mechanisms leading to the development of heart failure.

Serum copeptin and copeptin/NT-proBNP ratio - new tools to differentiate takotsubo syndrome from acute myocardial infarction.

BACKGROUND: Today no established biomarkers are available for the early diagnosis of takotsubo syndrome and its differentiation from ST-segment elevation myocardial infarction. We hypothesized that copeptin and copeptin/NT-proBNP ratio may serve a routine marker combination for non-invasive differentiation. METHODS: The study compared the serum concentrations of copeptin, troponin I (TnI) and NT-proBNP in 19 consecutive women diagnosed with takotsubo syndrome according to the Mayo Clinic criteria and 10 consecutive women diagnosed with ST-segment elevation myocardial infarction. RESULTS: Copeptin concentrations were significantly lower in patients with takotsubo syndrome than in patients with ST-segment elevation myocardial infarction. The diagnostic accuracy to distinguish takotsubo syndrome from ST-segment elevation myocardial infarction is highest for copeptin/NTproBNP ratio, copeptin/TnI at admission ratio and copeptin alone (AUC 0.8713, 0.8538, 0.8480, respectively). CONCLUSIONS: The serum copeptin to NTproBNP ratio could be an additional tool in the non-invasive differentiation between takotsubo syndrome and ST-segment elevation myocardial infarction. However, further researches are needed.

Mycophenolic acid attenuates the tumour necrosis factor-α-mediated proinflammatory response in endothelial cells by blocking the MAPK/NF-κB and ROS pathways.

BACKGROUND: Mycophenolate mofetil (MMF) has beneficial effects in cardiac transplant patients beyond the suppression of tissue rejection. Moreover, mycophenolic acid (MPA), its active metabolite, has been associated with positive effects on atherosclerosis in animal models. The attachment of leukocytes to the vascular endothelium and the subsequent migration of these cells into the vessel wall are early events in inflammation and atherosclerosis. The aim of this study was to investigate the effects of MPA on tumour necrosis-α (TNF-α)-induced, endothelial cell proinflammatory responses and the underlying mechanisms. METHODS AND RESULTS: Human aortic endothelial cells (HAECs) were treated with different concentrations (primarily 50 µM) of MPA before treatment with TNF-α. The surface protein and mRNA expressions of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were determined by flow cytometry and real-time RT-PCR, respectively. Adhesion of leukocytes to TNF-α-treated HAECs was evaluated by an adhesion assay. Activation of mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) was evaluated by measuring the levels of their phosphorylation using flow cytometry. NF-κB p65 translocation was detected by Western blotting. The production of reactive oxygen species (ROS) was determined by reduction in fluorescent 2',7'-dichlorofluorescein diacetate (H2 DCFH-DA). MPA significantly inhibits TNF-α-induced ICAM-1, VCAM-1 surface protein and mRNA expression as well as adhesion of mononuclear leukocytes to HAEC. ICAM-1 and VCAM-1 expressions were also reduced by antioxidants such as pyrrolidine dithiocarbamate, diphenylene iodonium and apocynin. MPA inhibited TNF-α-stimulated ROS generation similarly to apocynin. TNF-α increased ICAM-1 and VCAM-1 expression via c-Jun NH2 -terminal kinase (JNK), extracellular signal-regulated kinase (ERK1/2) and p38 MAPK. MPA and apocynin inhibited TNF-α-induced phosphorylation of all three MAP kinases. Furthermore, TNF-α-induced NF-κB activation was attenuated by SP600125 (JNK inhibitor), PD98059 (ERK1/2 inhibitor, SB203580 (p38 MAPK inhibitor) and MPA. MPA also inhibited TNF-α-induced nuclear translocation of NF-κB p65. CONCLUSION: These results suggest that, in addition to the prevention of rejection, MPA may be a promising approach for the treatment of inflammatory vascular disease.

2024 Guidelines of the Polish Society of Laboratory Diagnostics and the Polish Lipid Association on laboratory diagnostics of lipid metabolism disorders.

Lipid disorders are the most common (even 70%) and worst monitored cardiovascular risk factor (only 1/4 of patients in Poland and in CEE countries are on the low-density lipoprotein cholesterol (LDL-C) goal). To improve this, clear and simple diagnostic criteria should be introduced for all components of the lipid profile. These are the updated guidelines of the two main scientific societies in Poland in the area - the Polish Society of Laboratory Diagnostics (PSLD) and the Polish Lipid Association (PoLA), which, in comparison to those from 2020, introduce few important changes in recommendations (two main lipid targets, new recommendations on LDL-C measurements, calculations new goals for triglycerides, new recommendations on remnants and small dense LDL) that should help the practitioners to be early with the diagnosis of lipid disorders and in the effective monitoring (after therapy initiation), and in the consequence to avoid the first and recurrent cardiovascular events.

Ischaemia modified albumin in patients with acute coronary syndrome and negative cardiac troponin I.

BACKGROUND: Approximately 40-60% of patients with acute coronary syndrome (ACS) have normal cardiac troponin I (cTnI) concentrations on admission. Ischaemia modified albumin (IMA) has been suggested as a new biomarker of myocardial ischaemia. METHODS: A total of 43 patients presenting with symptoms suggestive of ACS but with normal (< 0.1 µg/L) cTnI concentrations and 45 healthy subjects were studied. The patients from the study group were divided into two groups: STEMI (n = 28) and NSTEMI (n = 15). All these patients were undergoing percutaneous coronary intervention (PCI) with stenting. The concentrations of cTnI, myoglobin and IMA were determined on admission and 4 h after PCI. RESULTS: Mean (SD) IMA concentrations were higher in patients with ACS (114.39 ± 25.18 U/ml) as compared to the control group (96.24 ± 6.28 U/ml, p < 0.005). IMA concentrations ≥ 104.0 U/ml demonstrated 72.1% sensitivity and 75.6% specificity for the diagnosis of ACS. The area under the receiver operator characteristic curve was 0.766 (95% CI 0.664-0.868) for ACS patients (NSTEMI + STEMI). In both groups increased median (IQR) cTnI concentration after PCI was observed (STEMI patients to 65.4 (10.9-106.9) µg/L and NSTEMI to 17.6 (0.77-84.0) µg/L). In contrast, no increase in IMA concentration was observed. CONCLUSIONS: IMA may be a useful biomarker for the identification of ACS patients presenting with typical acute chest pain and/or abnormal electrocardiograms but negative cTnI.

[Enantiomers: a new problem in pharmacotherapy of depression?]. / Enancjomery: nowy problem w farmakoterapii depresji?

Enantiomers as a optically active forms of drugs now have a big impact on most areas of pharmacotherapy. They arouse a large interest in the field of psychiatry and especially in the treatment of depression. This is due to the fact that enantiomers (chiral forms) of many drugs may have a different pharmacokinetic, pharmacological or pharmacogenetic profiles. Therefore, in many cases the use of a single enantiomer of the drug may have huge advantages over previously used forms and lead to strong improvement of the current treatments. An example is the stereoselective property of such a psychotropic drug fluoxetine as belonging to a group of selective serotonin reuptake inhibitors (SSRI).

Mitochondrial Quality Control: the Role in Cardiac Injury.

The heart is a highly energy-dependent organ, and most of its energy is provided by mitochondrial oxidative phosphorylation. Therefore, maintaining a well-functioning mitochondrial population is of paramount importance for cardiac homeostasis, since damaged mitochondria produce less adenosine triphosphate (ATP) and generate higher amounts of reactive oxygen species (ROS). Mitochondrial dysfunction is associated with the development of many diseases, including cardiovascular disorders. In this article, we review the role of mitochondria as key determinants of acute myocardial ischemic/reperfusion injury (IRI) and also diabetic cardiomyopathy. The structure and function of mitochondria are regulated by the mitochondrial quality control (MQC) system. Mitochondrial quality control mechanisms involve a series of adaptive responses that preserve mitochondrial structure and function as well as ensure cardiomyocyte survival and cardiac function after injury. This review summarizes the basic mechanisms of MQC, including mitochondrial dynamics (fusion and fission), mitophagy and mitochondrial biogenesis. Mitochondrial dynamics are mainly controlled by the level of fission and fusion proteins and also by their post-translational modifications. In addition, this review aims to provide a contemporary view of the importance of miRNA molecules in the regulation of mitochondrial dynamics at the post-transcriptional level. Thus, miRNAs play an important role not only in the pathogenesis and prognosis of cardiac diseases, but can also be an important therapeutic target.

Bovine corneal epithelial primary cultures as an in vitro model for ophthalmic drugs studies.

In the recent years a significant development of investigations with regard to bioavailability of ocular drugs has been noticed. The corneal epithelial barrier is the main pathway for ocular penetration of topically applied ophthalmic drugs into the anterior chamber. To work out an in vitro model of bovine corneal epithelial primary cultures and exercise it for permeability research with lipophilic and hydrophilic markers, permeability coefficients estimation of the 6-carboxyfluorescein and rhodamin B was made. The corneal epithelial cultures of the 3th or 4th passage were chosen for layered culture with inserts based on the liquid-liquid interface (for the first week) and the air-liquid interface (for the two following weeks). On the 7th, 12th, 18th, 21st experiment day TER values, and on the 21st day drug permeability coefficients, were determined. The mean TER values of the 7th, 12th, 18th, 21st day of corneal epithelial culture were: 122.14, 155.14, 198.43 and; 247.43 Wcm2, respectively. The mean values of permeability coefficients on the 21st day of culture for 6-carboxyfluorescein and rhodamin B were 3.87 +/-0.10 x 10(-6)cm/s and 3.65 +/- 0.06 x 10(-6)cm/s, respectively. We state that the in vitro bovine corneal epithelial primary culture model is useful for ocular studies.

A Review of the Molecular Mechanisms Underlying Cardiac Fibrosis and Atrial Fibrillation.

The cellular and molecular mechanism involved in the pathogenesis of atrial fibrosis are highly complex. We have reviewed the literature that covers the effectors, signal transduction and physiopathogenesis concerning extracellular matrix (ECM) dysregulation and atrial fibrosis in atrial fibrillation (AF). At the molecular level: angiotensin II, transforming growth factor-ß1, inflammation, and oxidative stress are particularly important for ECM dysregulation and atrial fibrotic remodelling in AF. We conclude that the Ang-II-MAPK and TGF-ß1-Smad signalling pathways play a major, central role in regulating atrial fibrotic remodelling in AF. The above signalling pathways induce the expression of genes encoding profibrotic molecules (MMP, CTGF, TGF-ß1). An important mechanism is also the generation of reactive oxygen species. This pathway induced by the interaction of Ang II with the AT2R receptor and the activation of NADPH oxidase. Additionally, the interplay between cardiac MMPs and their endogenous tissue inhibitors of MMPs, is thought to be critical in atrial ECM metabolism and fibrosis. We also review recent evidence about the role of changes in the miRNAs expression in AF pathophysiology and their potential as therapeutic targets. Furthermore, keeping the balance between miRNA molecules exerting anti-/profibrotic effects is of key importance for the control of atrial fibrosis in AF.

The Diagnostic and Therapeutic Potential of Galectin-3 in Cardiovascular Diseases.

Galectin-3 plays a prominent role in chronic inflammation and has been implicated in the development of many disease conditions, including heart disease. Galectin-3, a regulatory protein, is elevated in both acute and chronic heart failure and is involved in the inflammatory pathway after injury leading to myocardial tissue remodelling. We discussed the potential utility of galectin-3 as a diagnostic and disease severity/prognostic biomarker in different cardio/cerebrovascular diseases, such as acute ischemic stroke, acute coronary syndromes, heart failure and arrhythmogenic cardiomyopathy. Over the last decade there has been a marked increase in the understanding the role of galectin-3 in myocardial fibrosis and inflammation and as a therapeutic target for the treatment of heart failure and myocardial infarction.

Interindividual variability in the response to oral antiplatelet drugs: a position paper of the Working Group on antiplatelet drugs resistance appointed by the Section of Cardiovascular Interventions of the Polish Cardiac Society, endorsed by the Working Group on Thrombosis of the European Society of Cardiology.

Oral antiplatelet drugs are a cornerstone of modern pharmacotherapy in cardiovascular atherothrombotic diseases. The efficacy of acetylsalicylic acid (ASA, aspirin) and clopidogrel in decreasing the risk of adverse events in coronary heart disease patients has been well established in the past 20 years. Despite chronic oral antiplatelet therapy, a number of atherothombotic events continue to occur. In recent years, a number of reports in the literature have shown possible relationships between residual platelet activity, as measured with a variety of laboratory tests, and clinical outcome, raising the possibility that 'resistance' to oral antiplatelet drugs may underlie many such clinical adverse events. The present position paper, conveyed within a group of clinical cardiologists with expertise in thrombosis appointed by the Section of Cardiovascular Interventions of the Polish Cardiac Society, has been further elaborated and endorsed by the Working Group on Thrombosis of the European Society of Cardiology. It aims at summarizing the main findings in this complex area, issuing opinions in cases of high controversy, and fostering future research in this area to obtain reliable laboratory and clinical data for the resolution of the many problems still open.

Molecular mechanisms of organ damage in sepsis: an overview.

Sepsis is one of the most common reasons for hospitalization. This condition is characterized by systemic inflammatory response to infection. International definition of sepsis mainly points out a multi-organ dysfunction caused by a deregulated host response to infection. An uncontrolled inflammatory response, often referred to as "cytokine storm", leads to an increase in oxidative stress as a result of the inhibition of cellular antioxidant systems. Oxidative stress, as well as pro-inflammatory cytokines, initiate vascular endothelial dysfunction and, in consequence, impair microcirculation. Microcirculation damage leads to adaptive modifications of cell metabolism. Moreover, mitochondrial dysfunction takes place which results in increased apoptosis and organ damage. Non-coding RNA fragments, especially miRNA molecules, may play an important role in the pathomechanism of sepsis. Numerous studies have indicated altered expression of various miRNAs in sepsis. miRNAs can be used as markers in the diagnosis and prognosis of disease development. In turn, intracellular miRNAs regulate the TLR4/NFκB pathway responsible for the expression of pro-inflammatory cytokine genes involved in the inflammatory response in sepsis. The understanding of detailed molecular mechanisms leading to organ damage can contribute to the development of specific therapy methods thereby improving the prognosis of patients with sepsis.

MicroRNAs in the development of left ventricular remodeling and postmyocardial infarction heart failure.

Acute myocardial infarction (AMI) induces unfavorable left ventricular remodeling (LVR), a complex process that involves molecular, cellular, and geometric alterations leading to important changes in heart structure and function. Heart failure (HF) is a frequent complication of AMI, and it remains a serious clinical, epidemiological, and economic challenge. Despite advances in the therapy and management of HF, many patients still suffer from severe symptoms. The underlying molecular mechanisms of the post­AMI LVR are not yet fully understood. Numerous studies have indicated that dysregulation in the expression of microRNA (miRNA) molecules leads to changes in several pathological processes in the heart, which are associated with post­AMI transition from cardiac hypertrophy to HF. In this review, we summarize the current knowledge on the role of miRNAs in the regulation of basic processes, such as excessive myocardial fibrosis, pathological cardiomyocyte hypertrophy, and myocardial cell apoptosis. Moreover, the significance of circulating miRNAs as noninvasive prognostic biomarkers in the prediction of LVR and HF after AMI has also been discussed. In conclusion, miR­29 family members (miR­29a and miR­29b), miR­150, and miR­30a­5p represent different groups of miRNAs, but all of them are involved in the regulation of the fundamental processes associated with post­AMI left ventricular dysfunction and HF. Furthermore, these miRNA molecules may serve as a potential therapeutic target during disease progression.

Circulating miR-30a-5p as a prognostic biomarker of left ventricular dysfunction after acute myocardial infarction.

Left ventricular (LV) dysfunction after acute myocardial infarction (AMI) is associated with an increased risk of heart failure (HF) development. Diverse microRNAs (miRNAs) have been shown to appear in the bloodstream following various cardiovascular events. The aim of this study was to identify prognostic miRNAs associated with LV dysfunction following AMI. Patients were divided into subgroups comprising patients who developed or not LV dysfunction within six months of the infarction. miRNA profiles were determined in plasma and serum samples of the patients on the first day of AMI. Levels of 14 plasma miRNAs and 16 serum miRNAs were significantly different in samples from AMI patients who later developed LV dysfunction compared to those who did not. Two miRNAs were up-regulated in both types of material. Validation in an independent group of patients, using droplet digital PCR (ddPCR) confirmed that miR-30a-5p was significantly elevated on admission in those patients who developed LV dysfunction and HF symptoms six months after AMI. A bioinformatics analysis indicated that miR-30a-5p may regulate genes involved in cardiovascular pathogenesis. This study demonstrates, for the first time, a prognostic value of circulating miR-30a-5p and its association with LV dysfunction and symptoms of HF after AMI.

Significance of aspirin and clopidogrel resistance in patients undergoing percutaneous coronary interventions.

Dual antiplatelet therapy (aspirin plus clopidogrel) is mandatory in patients treated with coronary stent implantation. This strategy is highly effective in prevention of stent thrombosis until its struts are covered with endothelium. However, a substantial number of patients still suffer from recurrent ischemic coronary events despite adequate antiplatelet therapy. These events fall into three categories: stent thrombosis, in stent restenosis and events related to other non-stented coronary lesions. Some data suggest that beside other local and systemic factors resistance to aspirin and clopidogrel may be a possible cause of stent thrombosis and ischemic events in patients after coronary interventions. Several mechanisms of antiplatelet drug resistance have been reported including poor compliance, interactions with other drugs, genetic polymorphism or increased platelet turnover. More research is needed to adequately assess the clinical significance and prognostic value of antiplatelet drug resistance detected by laboratory tests in patients undergoing percutaneous intervention. We review published data on mechanisms and the clinical significance of aspirin and clopidogrel resistance in patients after coronary interventions.

Expression of platelet surface receptors and early changes in platelet function in patients with STEMI treated with abciximab and clopidogrel versus clopidogrel alone.

BACKGROUND: Platelets play a crucial role in the pathogenesis of acute coronary syndromes (ACS). The efficacy of antiplatelet treatment is pivotal in the success of percutaneous coronary intervention (PCI) performed in patients with ACS. OBJECTIVE: The aim of the study was to investigate the effects of clopidogrel with or without abciximab on the expression of platelet surface receptors and platelet function in patients with ST-segment elevation myocardial infarction (STEMI) undergoing PCI. MATERIALS AND METHODS: Thirty patients with STEMI were included in the study. During acute primary coronary intervention, patients received aspirin (acetylsalicylic acid) and clopidogrel in a loading dose of 300mg. Clopidogrel was the only antiplatelet therapy used by nine patients (group B). Twenty-one patients (group A) received additional abciximab. Blood samples were collected and analyzed twice: before and up to 22 hours after administration of antiplatelet therapy. The platelet aggregation was established as primary platelet-related hemostasis (closure time [CT] assessed using the PFA100 system). The absolute number of platelet surface antigens as CD41a, CD42a, CD42b, CD61, and CD62P were determined by flow cytometry analysis. RESULTS: The study revealed a statistically significant increase in CT induced by adenosine diphosphate and adrenaline (epinephrine) +130 seconds (p < 0.0001) and +94 seconds (p < 0.0001), respectively, in group A patients post-therapy. While in group B the parameters of CT did not change after treatment. In addition, the absolute number of CD41a antigens (glycoprotein [GP] IIb/IIIa) increased significantly after treatment in group A. No significant changes were observed after treatment in the expression of CD62P (P-selectin) antigens in either treatment group. There was a significant reduction in the percentage of CD62P-positive platelets in group B after antiplatelet therapy. CONCLUSIONS: The absolute number of GP IIb/IIIa receptors increases and platelets are not activated up to 12 hours after cessation of abciximab therapy. Treatment of STEMI patients undergoing PCI with a loading dose of clopidogrel reduces the percentage of active platelets but does not influence the CT.

Galectin-3 in Patients with Acute Heart Failure: Preliminary Report on First Polish Experience.

BACKGROUND: Galectin-3 (Gal-3) as a biomarker of fibrosis and inflammation has been implicated in the development and progression of heart failure (HF) and may predict increased morbidity and mortality in society. OBJECTIVES: In this preliminary report we investigated the utility of a novel serum marker for the diagnosis of acute HF (AHF). MATERIAL AND METHODS: The study involved 14 AHF patients aged 67.0 ± 14.6 yrs. with left ventricular ejection fraction (LVEF) 29.29 ± 10.73%, hospitalized at the Intensive Coronary Care Unit, where the research took place. In addition, a control group consisting of 19 volunteers who were age, gender and ethnically matched to the HF group was recruited. In the study group, the concentrations of Gal-3, NT-proBNP, hsCRP and basic clinical parameters, such as prevalence of dyspnea and LVEF were determined. The concentration of Gal-3 in serum was examined by an automated quantitative test (VIDAS® Galectin-3, bioMerieux SA, France) using the ELFA technique. The survival rate was assessed after a 12-month follow-up. RESULTS: The median (IQR) Gal-3 concentrations in patients with AHF were higher (nearly 2.1-times) than in the control group - 17.8 (10.3-27.8) ng/mL vs. 8.4 (6.5-11.0) ng/mL; p = 0.0007. In our study group, the median (IQR) of concentrations of NT-proBNP 4723 (1415-29725) pg/mL and hsCRP 10.0 (4.9-13.9) mg/L were observed. In those patients, the statistically significant correlation (Spearman's rank-correlation coefficient) between the concentrations of Gal-3 and NT-proBNP (Rs = 0.565; p = 0.035) as well as the value of LVEF and the concentration of hsCRP (Rs = -0.663; p = 0.020) were stated. The serum Gal-3 concentrations were significantly higher among the 4 HF patients (28.6%) who had died than among the HF patients who were alive after this time (n = 10) (55.6 ± 37.6 ng/mL vs. 15.0 ± 7.04 ng/mL; p = 0.005). CONCLUSIONS: Higher expression of Gal-3 is an indicator of myocardial fibrosis and remodeling in decompensated HF. Therefore, galectin-3 seems to be an interesting and valuable marker of AHF.

Interindividual variability of atorvastatin treatment influence on the MPO gene expression in patients after acute myocardial infarction.

Myeloperoxidase (MPO) and C-reactive protein (CRP) may play critical roles in generation of oxidative stress and the development of the systemic inflammatory response. The aim of the study was to determine the effect of atorvastatin therapy on the MPO gene expression and its plasma level in relation to lipids level lowering and an anti-inflammatory response in patients after acute myocardial infarction. The research material was represented by 112 samples. Thirty-eight patients with first AMI receiving atorvastatin therapy (40 mg/day) and followed up for one month were involved in the study. The relative MPO gene expression in peripheral blood mononuclear cells (PBMCs) was examined using RT-qPCR in 38 patients before-, 38 patients after-therapy and in 36 patients as the control group. The plasma concentrations of MPO and serum concentrations of biochemical parameters were determined using commercially available diagnostic tests. After one month of atorvastatin therapy, in 60.5% patients a decrease of MPO gene expression, whereas in 39.5% patients an increase, was observed. The plasma MPO levels behaved in the same way as the MPO gene expression. However, the serum lipids and CRP concentrations were significantly lower after one month of atorvastatin therapy in both groups of patients - with decreased and increased MPO gene expression. Atorvastatin exhibited a different effect on MPO gene expression and its plasma level. Short-term atorvastatin therapy resulted in lipid lowering and anti-inflammatory activity in patients after AMI, independently of its effect on MPO gene expression. The molecular mechanisms of this phenomenon are not yet defined and require further research.