Cardiovascular, Pulmonary, and Neuropsychiatric Short- and Long-Term Complications of COVID-19.

Beginning with the various strategies of the SARS-CoV-2 virus to invade our bodies and manifest infection, and ending with the recent long COVID, we are witnessing the evolving course of the disease in addition to the pandemic. Given the partially controlled course of the COVID-19 pandemic, the greatest challenge currently lies in managing the short- and long-term complications of COVID-19. We have assembled current knowledge of the broad spectrum of cardiovascular, pulmonary, and neuropsychiatric sequelae following SARS-CoV-2 infection to understand how these clinical manifestations collectively lead to a severe form of the disease. The ultimate goal would be to better understand these complications and find ways to prevent clinical deterioration.

Relationships between Circulating Matrix Metalloproteinases, Tissue Inhibitor TIMP-2, and Renal Function in Patients with Myocarditis.

INTRODUCTION: Under physiological conditions, the myocardial extracellular matrix (ECM) is maintained by matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). However, changes in the balance between MMPs and TIMPs can lead to pathological remodeling of the ECM, which contributes to cardiovascular and kidney diseases. The aim of our study was to assess levels of MMPs and TIMP-2 in patients with myocarditis and their relationship to renal function. MATERIALS AND METHODS: Forty five patients with myocarditis who underwent CMR were included, comprising 11 with concurrent chronic kidney disease (CKD). Blood samples were obtained to assess serum levels of MMP-2, MMP-3, MMP-9, and TIMP-2. RESULTS: Serum MMP-2, MMP-3, and TIMP-2 levels negatively correlated with the ejection fraction in patients with myocarditis, while MMP-3 levels correlated with longitudinal deformation (p < 0.05). Serum MMP-2, MMP-3, and TIMP-2 levels also negatively correlated with renal function, as assessed by the estimated glomerular filtration rate (eGFR) (p < 0.05). Patients with myocarditis and concurrent CKD had higher levels of MMP-2 and TIMP-2 than those without kidney damage. CONCLUSIONS: (1) We demonstrated that MMP-2, MMP-3, and TIMP-2 concentrations were related to left-ventricular ejection fraction, and MMP-3 levels correlated with longitudinal deformation, indicating MMPs play an important role in the post-inflammatory remodeling of the myocardium. (2) A negative correlation between the eGFR and MMP-2, MMP-3, and TIMP-2 and a positive correlation between creatinine and MMP-3 levels indicate the role of MMPs and TIMP-2 in renal dysfunction.

Molecular Mechanism of Thymidylate Synthase Inhibition by N4-Hydroxy-dCMP in View of Spectrophotometric and Crystallographic Studies.

Novel evidence is presented allowing further clarification of the mechanism of the slow-binding thymidylate synthase (TS) inhibition by N4-hydroxy-dCMP (N4-OH-dCMP). Spectrophotometric monitoring documented time- and temperature-, and N4-OH-dCMP-dependent TS-catalyzed dihydrofolate production, accompanying the mouse enzyme incubation with N4-OH-dCMP and N5,10-methylenetetrahydrofolate, known to inactivate the enzyme by the covalent binding of the inhibitor, suggesting the demonstrated reaction to be uncoupled from the pyrimidine C(5) methylation. The latter was in accord with the hypothesis based on the previously presented structure of mouse TS (cf. PDB ID: 4EZ8), and with conclusions based on the present structure of the parasitic nematode Trichinella spiralis, both co-crystallized with N4-OH-dCMP and N5,10-methylenetetrahdrofolate. The crystal structure of the mouse TS-N4-OH-dCMP complex soaked with N5,10-methylenetetrahydrofolate revealed the reaction to run via a unique imidazolidine ring opening, leaving the one-carbon group bound to the N(10) atom, thus too distant from the pyrimidine C(5) atom to enable the electrophilic attack and methylene group transfer.

Advanced Spectroscopy and APBS Modeling for Determination of the Role of His190 and Trp103 in Mouse Thymidylate Synthase Interaction with Selected dUMP Analogues.

A homo-dimeric enzyme, thymidylate synthase (TS), has been a long-standing molecular target in chemotherapy. To further elucidate properties and interactions with ligands of wild-type mouse thymidylate synthase (mTS) and its two single mutants, H190A and W103G, spectroscopic and theoretical investigations have been employed. In these mutants, histidine at position 190 and tryptophan at position 103 are substituted with alanine and glycine, respectively. Several emission-based spectroscopy methods used in the paper demonstrate an especially important role for Trp 103 in TS ligands binding. In addition, the Advanced Poisson-Boltzmann Solver (APBS) results show considerable differences in the distribution of electrostatic potential around Trp 103, as compared to distributions observed for all remaining Trp residues in the mTS family of structures. Together, spectroscopic and APBS results reveal a possible interplay between Trp 103 and His190, which contributes to a reduction in enzymatic activity in the case of H190A mutation. Comparison of electrostatic potential for mTS complexes, and their mutants, with the substrate, dUMP, and inhibitors, FdUMP and N4-OH-dCMP, suggests its weaker influence on the enzyme-ligand interactions in N4OH-dCMP-mTS compared to dUMP-mTS and FdUMP-mTS complexes. This difference may be crucial for the explanation of the "abortive reaction" inhibitory mechanism of N4OH-dCMP towards TS. In addition, based on structural analyses and the H190A mutant capacity to form a denaturation-resistant complex with N4-OH-dCMP in the mTHF-dependent reaction, His190 is apparently responsible for a strong preference of the enzyme active center for the anti rotamer of the imino inhibitor form.

The Links between Cardiovascular Diseases and Alzheimer's Disease.

The root cause of non-inherited Alzheimer's disease (AD) remains unknown despite hundreds of research studies performed to attempt to solve this problem. Since proper prophylaxis remains the best strategy, many scientists have studied the risk factors that may affect AD development. There is robust evidence supporting the hypothesis that cardiovascular diseases (CVD) may contribute to AD progression, as the diseases often coexist. Therefore, a lack of well-defined diagnostic criteria makes studying the relationship between AD and CVD complicated. Additionally, inflammation accompanies the pathogenesis of AD and CVD, and is not only a consequence but also implicated as a significant contributor to the course of the diseases. Of note, АроЕε4 is found to be one of the major risk factors affecting both the cardiovascular and nervous systems. According to genome wide association and epidemiological studies, numerous common risk factors have been associated with the development of AD-related pathology. Furthermore, the risk of developing AD and CVDs appears to be increased by a wide range of conditions and lifestyle factors: hypertension, dyslipidemia, hypercholesterolemia, hyperhomocysteinemia, gut/oral microbiota, physical activity, and diet. This review summarizes the literature and provides possible mechanistic links between CVDs and AD.

Response to antiplatelet therapy in patients undergoing invasive treatment due to acute coronary syndrome complicated by cardiogenic shock.

INTRODUCTION: There are limited data on platelet reactivity and response to antiplatelet drugs in patients with cardiogenic shock. AIM: To assess platelet reactivity on dual antiplatelet therapy with acetylsalicylic acid (ASA) and ticagrelor, a novel potent P2Y12 receptor inhibitor, in patients with cardiogenic shock in the course of acute coronary syndrome (ACS) who received invasive treatment. MATERIAL AND METHODS: We enrolled 12 consecutive patients with ACS complicated by cardiogenic shock. To assess response to antiplatelet therapy during cardiogenic shock, only patients with symptoms persisting for at least 3 days and who completed a 5-day follow-up were included in the study. Patients received a loading dose of ASA (300 mg) and ticagrelor (180 mg), followed by a maintenance dose (ASA, 1 × 75 mg; ticagrelor, 2 × 90 mg). Blood samples for platelet function tests were collected. Platelet aggregation was assessed with a Multiplate whole-blood impedance aggregometer. Arachidonic acid (AA), adenosine diphosphate (ADP), and thrombin receptor-activating peptide (TRAP) were used as aggregation agonists. RESULTS: Response to antiplatelet therapy assessed by aggregometry showed numerically higher on-ASA platelet reactivity on day one and statistically significant higher on-ticagrelor platelet reactivity on day one in comparison with following days. There were 2 patients with high on ASA platelet reactivity and 3 with high on ticagrelor platelet reactivity, but only on the day one. CONCLUSIONS: Some patients with cardiogenic shock in the course of ACS treated invasively show a lower response to ASA and ticagrelor only on the first day after invasive treatment, with a good response on subsequent days.

Münchausen Syndrome as an Unusual Cause of Pseudo-resistant Hypertension: A Case Report.

Münchausen syndrome can be characterized by simulated illness, pathological lying and wandering from place to place (the patient typically presents to numerous hospitals). Individuals with elevated blood pressure due to non-adherence to medication have the so-called pseudo-resistant hypertension. A 45-year-old woman was admitted to hospital on an emergency basis because of a hypertensive crisis. Despite combination antihypertensive treatment, normalization of blood pressure was not achieved and a device to produce a therapeutic arteriovenous fi stula was implanted. Aft er the procedure, a signifi cant increase in pulmonary artery pressure was observed and closure of the fistula was performed by implantation of the stent graft . The suspicion was raised that the patient had not been taking her prescribed medications. Therefore, blood samples were taken and the serum was analyzed for presence of the prescribed drugs (atorvastatin, bisoprolol, chlorthalidone, clonidine, doxazosin, furosemide, nitrendipine, oxazepam and valsartan). The results confirmed suspected failure of the patient to take the prescribed medications. Münchausen syndrome is usually first suspected when inexplicable laboratory test results are noted. To our knowledge, this is the first reported case of Münchausen syndrome with pseudo-resistant hypertension leading to the implantation of a device to produce a therapeutic arteriovenous fi stula.

Thymidylate synthase-catalyzed, tetrahydrofolate-dependent self-inactivation by 5-FdUMP.

In view of previous crystallographic studies, N4-hydroxy-dCMP, a slow-binding thymidylate synthase inhibitor apparently caused "uncoupling" of the two thymidylate synthase-catalyzed reactions, including the N5,10-methylenetetrahydrofolate one-carbon group transfer and reduction, suggesting the enzyme's capacity to use tetrahydrofolate as a cofactor reducing the pyrimidine ring C(5) in the absence of the 5-methylene group. Testing the latter interpretation, a possibility was examined of a TS-catalyzed covalent self-modification/self-inactivation with certain pyrimidine deoxynucleotides, including 5-fluoro-dUMP and N4-hydroxy-dCMP, that would be promoted by tetrahydrofolate and accompanied with its parallel oxidation to dihydrofolate. Electrophoretic analysis showed mouse recombinant TS protein to form, in the presence of tetrahydrofolate, a covalently bound, electrophoretically separable 5-fluoro-dUMP-thymidylate synthase complex, similar to that produced in the presence of N5,10-methylenetetrahydrofolate. Further studies of the mouse enzyme binding with 5-fluoro-dUMP/N4-hydroxy-dCMP by TCA precipitation of the complex on filter paper showed it to be tetrahydrofolate-promoted, as well as to depend on both time in the range of minutes and the enzyme molecular activity, indicating thymidylate synthase-catalyzed reaction to be responsible for it. Furthermore, the tetrahydrofolate- and time-dependent, covalent binding by thymidylate synthase of each 5-fluoro-dUMP and N4-hydroxy-dCMP was shown to be accompanied by the enzyme inactivation, as well as spectrophotometrically confirmed dihydrofolate production, the latter demonstrated to depend on the reaction time, thymidylate synthase activity and temperature of the incubation mixture, further documenting its catalytic character.

MMP-2 and TIMP-2 in Patients with Heart Failure and Chronic Kidney Disease.

The aim of the study was to assess MMP-2 (matrix metalloproteinase-2) and TIMP-2 (tissue inhibitor of metalloproteinase-2) serum levels in patients with diverse types of heart failure (HF) and chronic kidney disease (CKD). 101 patients with chronic HF were enrolled. Each patient has assessed the serum levels of MMP-2, TIMP-2, and NT-proBNP. Patients were initially classified into 2 groups based on their LVEF. 43 patients were classified into the HFREF group (HF with Reduced Ejection Fraction) and 58 characterized as HFPEF (HF with Preserved Ejection Fraction). Next, all patients were subdivided into 4 groups according to the degree of diastolic dysfunction. 38 patients with CKD were classified into HF/CKD(+) group. The HF/CKD(-) (HF without CKD) group comprised 61 patients. This study provides original data on positive correlation between ejection fraction and MMP-2 levels in all patients with heart failure. Elevated levels of MMP-2 and TIMP-2 were found in serum from patients with chronic kidney disease; in addition, serum levels of MMP-2 were correlated with the degree of kidney failure. In all groups of patients there was positive correlation between MMP-2 and TIMP-2. Among patients with heart failure etiology was not related to MMP-2 and TIMP-2 serum levels.

Determinants of the beneficial effect of mineralocorticoid receptor antagonism on exercise capacity in heart failure with reduced ejection fraction.

BACKGROUND: The determinants of the impact of mineralocorticoid receptor antagonism (MRA) on exercise tolerance in heart failure with reduced ejection fraction (HFrEF) have not been sufficiently characterised. AIM: We sought to investigate the factors associated with improvement in exercise capacity following the introduction of spironolactone to therapy in HFrEF patients, as well as to assess the association between improvement in exercise capacity and changes in cardiac functional characteristics with treatment. METHODS: In 120 patients (age 62 ± 11 years) with stable chronic HFrEF, remaining on optimal pharmacotherapy, spironolactone 25 mg/d was added to treatment. Echocardiographic assessment, including myocardial deformation, and treadmill exercise tests were performed at baseline and at six-month follow-up. RESULTS: According to the functional improvement at follow-up, patients were stratified into two groups: with increase in exercise capacity > 20% (IMPRpos, n = 68) and < 20% (IMPRneg, n = 52) of the baseline value. The IMPRpos subset demonstrated significantly larger improvement in left ventricular systolic and diastolic functions at follow-up, as assessed by global longitudinal deformation (GLS), ejection fraction, and tissue e' velocity. Functional improvement > 20% was independently predicted by diabetes (odds ratio [OR] 5.62, p = 0.011), estimated glomerular filtration rate (OR 0.95, p = 0.008), and B-type natriuretic peptide (BNP) at baseline (OR 0.54, p = 0.027), and associated with increase in GLS at follow-up (OR 1.40, p = 0.019). CONCLUSIONS: In patients with HFrEF, improvement in exercise capacity in response to the addition of spironolactone to treatment is more evident in the presence of diabetes, decreased renal function and lower BNP, and improvement in GLS is a contributor to this beneficial effect of MRA.

A synergistic effect of phosphate, pH and Phe159 substitution on the formycin A association to the E. coli purine nucleoside phosphorylase.

A steady-state absorption and emission spectroscopy was used to create a comprehensive work and to study the interaction of the wild type Escherichia coli purine nucleoside phosphorylase and its mutants, PNPF159Y and PNPF159A, with a potent E. coli PNP inhibitor - formycin A. The absorption and emission spectra were recorded in the presence and absence of the phosphate at the 50 mM concentration. From the collected sets of data dissociation constants (Kd), apparent dissociation constants (Kapp) and Hill's coefficients (h) were calculated. Additionally, the temperature dependence of the enzymes emission quenching at two temperatures, 10 °C and 25 °C, was examined. To verify the calculations, total difference absorption spectra were computed for all types of the complexes. A prominent quenching of the PNPF159Y emission indicates a complex formation, with the strongest association in the phosphate buffer, pH 7, relative to the wild type enzyme. On the other hand, results testify to a deterioration of the interactions in the E. coli PNP/PNPF159Y and formycin A complexes in the presence of the phosphate, pH 8.3. Moreover, data obtained for the PNPF159A-FA complexes confirm a weak association of the FA to the mutant's active center.

Towards understanding the E. coli PNP binding mechanism and FRET absence between E. coli PNP and formycin A.

The aim of this study is threefold: (1) augmentation of the knowledge of the E. coli PNP binding mechanism; (2) explanation of the previously observed 'lack of FRET' phenomenon and (3) an introduction of the correction (modified method) for FRET efficiency calculation in the PNP-FA complexes. We present fluorescence studies of the two E. coli PNP mutants (F159Y and F159A) with formycin A (FA), that indicate that the aromatic amino acid is indispensable in the nucleotide binding, additional hydroxyl group at position 159 probably enhances the strength of binding and that the amino acids pair 159-160 has a great impact on the spectroscopic properties of the enzyme. The experiments were carried out in hepes and phosphate buffers, at pH7 and 8.3. Two methods, a conventional and a modified one, that utilizes the dissociation constant, for calculations of the energy transfer efficiency (E) and the acceptor-to-donor distance (r) between FA and the Tyr (energy donor) were employed. Total difference spectra were calculated for emission spectra (λex 280nm, 295nm, 305nm and 313nm) for all studied systems. Time-resolved techniques allowed to conclude the existence of a specific structure formed by amino acids at positions 159 and 160. The results showed an unexpected pattern change of FRET in the mutants, when compared to the wild type enzyme and a probable presence of a structure created between 159 and 160 residue, that might influence the binding efficiency. Additionally, we confirmed the indispensable role of the modification of the FRET efficiency (E) calculation on the fraction of enzyme saturation in PNP-FA systems.

Characteristics of chaotic processes in electrocardiographically identified ventricular arrhythmia.

BACKGROUND: The theory of chaos proves a deterministic mechanism of induction of multiple complex processes previously thought to be random in nature. This research explains how these complex processes develop. The aim of the study was to test the hypothesis of the chaotic nature of myocardial electrical events during ventricular tachycardia (VT) and ventricular fibrillation (VF). METHODS: Original hardware and software was developed for digitalization of on-line electrocardiography (ECG) data, with the functions of automatic and manual identification as well as categoriza-tion of specific ventricular arrhythmias. Patient ECGs were recorded by specially developed measuring equipment (M2TT). Available ECG sampling frequency was 20,000 Hz, and it was possible to analyze the signal retrospectively. Digital ECG of the sinus rhythm (SR) was analyzed with non-sustained VT, VT and VF. The signals were then subjected to mathematical analysis. Using wavelet analysis, signals carrying frequencies from various ranges were isolated from baseline and each of these isolated signals was subjected to Fourier transformation to check on differences in the Fourier power spectra of the analyzed VT and VF signals. RESULTS: Ventricular tachycardia identified based on ECG fulfills the criteria of a chaotic process, while no such properties were found for SR and VF. Information obtained by the ECG is used to record myo-cardial electrical signals, but they are not sufficient to differentiate between an advanced chaotic state and the process of linear expansion of electrical activation within the myocardium. CONCLUSIONS: Electrophysiological study requires advanced methods to record the signal of myocardial electrical activity, as ECG is not sufficiently sensitive to identify the features of a chaotic process during VF. (Cardiol J 2017; 24, 2: 151-158).

A suicide attempt by intoxication with Taxus baccata leaves and ultra-fast liquid chromatography-electrospray ionization-tandem mass spectrometry, analysis of patient serum and different plant samples: case report.

BACKGROUND: Taxus (yew) is one of the most frequently reported plants causing potentially fatal outcome when taken incidentally or for suicidal reasons. A fast and reliable method of detection of poisonous compounds or their metabolites is critical in life-saving procedures in cases of yew ingestion. Previously, several chromatographic analytical procedures have been described usually taking longer than one hour of total analysis time. CASE PRESENTATION: In this report we describe a suicide case study and an ad hoc developed fast method of detection and quantitation of 3,5-dimethoxyphenol - the main taxane metabolite in the blood plasma from the patient as well as the determination of major taxine components in the plant material (Taxus baccata). At present, there is no reasonable alternative for mass spectrometry that could match its high sensitivity and accuracy, and Multiple Reaction Monitoring could be adequate and useful mass spectrometry technique in analyzing and identification of plants material compounds that cause severe poisoning in humans. In the reported case, intensive cardiac care together with the astuteness of the treating physicians not only saved the patient's life, but also allowed for his complete recovery and return to work. CONCLUSIONS: The development of ultra fast liquid chromatography tandem mass spectrometry UFLC-MS/MS method provides a fast means to confirm yew alkaloids and their metabolite in various material. The applied analytical procedure allows early detection of main metabolite in patient material as well as comparing to those extracted from the plant. In our study, the taxanes remained undetected, probably due to the time elapsing from the patient admittance and collection of plasma. In cases like those reported in this study, retaining the gastric material should be obligatory to confirm the ingestion of yew. The possibility of using this approach in detection of native taxine compounds in human plasma remains to be verified.

Expression of Proinflammatory Factors, Proangiogenic Factors and Endostatin in Patients with Heart Failure and Different Grades of Collateral Circulation Development.

BACKGROUND: The process of collateral vessel maturation is stimulated by numerous factors affecting the endothelium and smooth muscle cells building the vessel wall. Looking for arteriogenesis stimulating factors means looking for a potential innovative heart failure treatment method in the patients unresponsive to traditional therapies. OBJECTIVES: The purpose of this study was to assess the changes in serum concentrations of pro-inflammatory factor IL-6, growth factors FGF (FGFa, FGFb, FGFbH), HGF, VEGF and endostatin in heart failure patients in relation to the coronary collaterals development stage. MATERIAL AND METHODS: This study included 22 patients with chronic heart failure NYHA II or III (mean age 62.5 ± 11.6 years) and 8 control patients (mean age 58.4 ± 10.7 years). Coronary angiography was performed and the presence and grade of collateral circulation was assessed by a four-level scale proposed by Rentrop and Cohen. The level of the studied factors was determined in the blood samples collected during the angiographic procedure. RESULTS: The concentration of IL-6 was significantly higher in the heart failure patients than in the control group (p < 0.001) and in NYHA III vs. NYHA II patients (p < 0.02). Patients with heart failure and collaterals grade 1 or 2 exhibited higher serum concentrations of FGFbH (from p < 0.03 to p < 0.01). The serum VEGF level in NYHA III patients was significantly higher than in NYHA II individuals (from p < 0.03 to p < 0.01). CONCLUSIONS: Higher levels of IL-6 and FGFbH were observed in patients with heart failure. Collaterals formation seems to be associated with the activation of pro-inflammatory factors, growth factors and endostatin.

Influence of aggregation and route of injection on the biodistribution of mouse serum albumin.

Protein aggregates are a major risk factor for immunogenicity. Until now most studies on aggregate-driven immunogenicity have focused on linking physicochemical features of the aggregates to the formation of anti-drug antibodies. Lacking is however, basic knowledge on the effect of aggregation on the biodistribution and clearance of therapeutic proteins in vivo. The aim of current study was to get insight into the effect of aggregation on biodistribution in mice using different routes of administration. Fluorescently labeled stressed and unstressed mouse serum albumin was injected via different routes in mice and detected via in vivo fluorescence imaging up to 48 hrs post-injection. We found that biodistribution of stressed MSA significantly differed from its unstressed counterpart. Subcutaneous and intramuscular administration resulted in accumulation of protein at the site of injection, from which clearance of stressed MSA was considerably slower than clearance of unstressed MSA. Upon intravenous and intraperitoneal injection of stressed MSA, fluorescent "hotspots" were observed in the spleens, livers and lungs. Further and more detailed examination of biodistribution after intraperitoneal injection showed higher fluorescence in most of tested organs suggesting more efficient diffusion and/or lymphatic uptake from peritoneum of unstressed MSA than the stressed formulation.

Effect of intravenous dopamine infusion on pituitary and thyroid function and on nephroprotection.

UNLABELLED: INTRODUCTION; Catecholamines, including dopamine, are used in cardiac intensive care. OBJECTIVES: The aim of the study was to assess the effect of intravenous dopamine infusion on the function of pituitary gland in patients with acute cardiac failure. We analyzed changes in the serum levels of thyroid-stimulating hormone (TSH) and adrenocorticotropic hormone (ACTH), as well as potential nephroprotection. PATIENTS AND METHODS: The study involved 29 patients with chronic decompensated heart failure (New York Heart Association class III/IV; mean age 77.4 ± 13.3 years). Dopamine was administered intravenously in doses varying from 1 to 5 µg/kg/min. Measurements of TSH, free triiodothyronine (FT3), free thyroxine (FT4), and ACTH were taken directly before dopamine infusion, after 12 hours of continuous infusion, and 12 hours after the 72-hour infusion was completed. RESULTS: Serum FT3 levels were significantly higher before dopamine infusion than at 12 hours post infusion (5.12 ± 1.16 vs. 4.27 ± 0.89 pmol/l, P < 0.005). Serum FT4 levels before the infusion were significantly higher than after 12 hours of continuous infusion as well as after 12 hours post infusion (18.79 ± 5.33 vs. 17.06 ± 4.61 pmol/l, P < 0.05; 18.79 ± 5.33 vs. 16.26 ± 4.53 pmol/l, P < 0.05, respectively). There were no statistically significant differences between serum TSH and ACTH levels or in creatinine clearance before, during, and 12 hours post infusion. CONCLUSIONS: Intravenous infusion of dopamine may downregulate endocrine thyroid function; however, it has no significant effect on the pituitary gland-derived TSH and ACTH. There was no significant nephroprotective effect of low-dose dopamine infusion in patients with chronic decompensated chronic heart failure.

[Myocardial infarction without coronary arteries stenoses in a patient with Jervell and Lange-Nielsen syndrome--diagnostic dilemmas]. / Zawal serca bez przewezen w tetnicach wiencowych u pacjentki z zespolem Jervella i Lange-Nielsena--dylematy diagnostyczne.

According to the rules of differential diagnostics an acute coronary syndrome (ACS) often constitutes an initial diagnosis while a subsequent patient's follow-up with troponin determination results in further verification of the diagnosis. A 55 year-old female with congenital hearing loss, poorly controlled hypertension, type 2 diabetes treated with oral medications, and hypothyreosis was admitted to the Department of Cardiology with 6 h long severe chest pain radiating over her back with concomitant dyspnea. She underwent urgent coronary angiography which showed no epicardial coronary narrowing. Acute heart failure symptoms occurred immediately after coronary angiography in the form of cardiogenic shock. Even though an ACS was diagnosed on the basis of typical biochemical, electrocardiographic and clinical criteria, a further follow-up suggested a possibility of a co-existance of other diseases which occurred to be a Jervell and Lange-Nielsen syndrome.

[Cardiac tamponade of unknown aetiology in a dialyzed patient]. / Tamponada serca u pacjenta dializowanego.

A case of a 58 year-old male with renal failure and recurrent cardiac tamponade is presented. In spite of extensive work-up, aetiology of pericardial effusion remained unknown. Diagnostic difficulties in this setting are discussed.