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Aims The coronavirus disease‐2019 (COVID‐19) pandemic has changed the landscape of medical care delivery worldwide. We aimed to assess the influence of COVID‐19 pandemic on hospital admissions and in‐hospital mortality rate in patients with acute heart failure (AHF) in a retrospective, multicentre study. Methods and results From 1 January 2019 to 31 December 2020, a total of 101 433 patients were hospitalized in 24 Cardiology Departments in Poland. The number of patients admitted due to AHF decreased by 23.4% from 9853 in 2019 to 7546 in 2020 (P

Non-adherence to prescribed medication is a serious limitation of long-term treatment in patients after myocardial infarction (MI), which can be associated with medical, social and economical consequences. Improvement of medication adherence has been shown to be a challenge for healthcare providers. The aim of this study was to evaluate changes in medication adherence and variability of adherence determinants during follow-up in patients after MI. A single-center, cohort observational study was conducted in 225 post-MI patients treated with primary coronary intervention (PCI) (27% women and 73% men) aged 30–91 years. Adherence was defined as availability of evaluated drugs within 1-year after discharge from hospital, based on completed prescriptions data obtained from the National Health Fund. The analysis of therapeutic plan realization (adherence to medication prescribed at discharge from hospital) embraced only reimbursed drugs: ACEIs (ramipril, perindopril), P2Y12 receptor inhibitors (clopidogrel) and statins (atorvastatin, simvastatin, rosuvastatin). Sufficient adherence was defined as ≥ 80%. During 1-year follow-up, adherence for all three drug classes was 64 ± 25%, with 67 ± 32% for ACEIs, 62 ± 34% for P2Y12 receptor inhibitor and 64 ± 32% for statins. A gradual decline in adherence was observed from 65% ± 26% in the first quarter of follow-up to 51% ± 34% in the last quarter of follow-up (p 65 years and having a history of prior CABG more often had an insufficient adherence to drugs, married and hypertensive patients, city inhabitants and patients with higher education tended to have a sufficient drug adherence. Adherence to pharmacotherapy after myocardial infarction decreases over time in a similar manner for all pivotal groups of drugs prescribed after MI. A number of socioeconomic and clinical factors have been identified to affect medication adherence over time.

Background: Carbamazepine (CBZ) is a first-generation anticonvulsant drug. Hence, in certain cases, therapeutic drug monitoring (TDM) supports pharmacotherapy. Methods: The presented research was based on a retrospective analysis including 710 ambulatory and hospitalized patients treated with CBZ between the years 1991 and 2011. The method used for the determination of the CBZ concentration was fluorescence polarization immunoassay (FPIA) performed using an Abbott GmbH TDx automatic analyzer, with the therapeutic range for carbamazepine being 4–12 µg/mL. Results: The therapeutic range was observed more often in patients between 3 and 17 years of age compared with the population ≥18 years of age (73.5% vs. 68.8%). The therapeutic level was exceeded less frequently in the population between 3 and 17 years of age despite them being given a significantly higher dose per kilogram of body weight than in the population ≥18 years of age (13.64 mg/kg vs. 10.43 mg/kg, p &lt, 0.0001). Patients ≥18 years of age were statistically significantly more likely to be in the group with a suspected drug overdose (73.9% vs. 26.1%), and suicide attempts only occurred in elderly patients (100.0% vs. 0.0%, p = 0.003). Conclusion: The results of the TDM of CBZ showed that only 71% of all samples were at the therapeutic level. To ensure the maximum efficacy and safety of the therapy, it is necessary to monitor the concentration of CBZ regardless of sex and age.

Several mechanisms have been suggested to explain positive cardiovascular effects observed in studies with sodium-glucose co-transporter 2 (SGLT2) inhibitors. The reduction in glucose reabsorption in proximal tubuli induced by SGLT2 inhibitors increases urinary glucose and sodium excretion resulting in increased osmotic diuresis and consequently in decreased plasma volume, followed by reduced preload. In addition, the hemodynamic effects of SGLT2 inhibition were observed in both hyper and euglycemic patients. Due to the complex and multidirectional effects induced by SGLT2 inhibitors, this originally antidiabetic group of drugs has been successfully used to treat patients with heart failure as well as for subjects with chronic kidney disease. Moreover, their therapeutic potential seems to be even broader than the indications studied to date.

Diagnosis of deficient areas in the functioning of patient with chronic disease is necessary to undertake the adequate therapeutic actions. The aim of the study was to validate a new self-reported questionnaire for patients with chronic disease assessing the impact of the disease on the patient, the patient’s impact on the disease and the impact of the disease on patient’s attitudes. Results: The internal consistency of the questionnaire expressed by a-Cronbach coefficient = 0.855, indicates its high reliability and homogeneity. The set of 24 items fulfilled the assumption of factor analysis: the determinant of correlation matrix was 0.001, Kaiser-Mayer-Olkin (K-M-O) statistic was 0.843 and the Bartlett’ test of sphericity was statistically significant. The factor analysis was conducted using the principal component analysis with Varimax rotation. The scale and subscale levels were determined based on the percentiles scale. Conclusion: The validation procedure revealed that FCIS is a reliable and homogeneous tool to measure patient’s physical and mental functioning in the chronic illness. The set of items divided into 3 subscales allows evaluation of: the impact of the disease on the patient, the patient’s impact on the disease and the impact of the disease on the patient’s attitudes.

Background Digoxin is the oldest drug used in the pharmacotherapy of heart failure (HF). However, digoxin remains an important therapeutic option for patients with persistent symptoms of HF occurring despite the implementation of standard pharmacotherapy. Digoxin concentration serum (SCD) should equal 1–2 ng/ml. The aim of our study was to measure of SCD among the hospitalized patients as well as to determine the selected factors influencing the concentration of the digoxin in the blood. Methods The presented research was based on a retrospective analysis including 2149 patients treated with digoxin and hospitalized between 1980 and 2000. Was used for the determination of SCD automatic analyzer TDX ABBOTT GmbH – fluorescence polarization immunoassay (FPIA), with therapeutic range for digoxin of 0.8–2.0 ng/ml. Results Average SCD result in the study population was located within the therapeutic range and amounted 1.06 ng/ml (55.7% of patients). Statistically significant differences in digoxin level were observed depending on the way of medicine administration ( p = 0.000001) and the daily amount ( p = 0.001). Moreover, statistically significant differences in digoxin level were observed depending on sex ( p = 0.00002). Conclusions An elevated level of digoxin was observed in the case of patients who received the medication both orally and intravenously, together with an increase in the daily amount of digoxin doses. It was confirmed that an elevated digoxin level occurs in the course of treatment in the case of women.

The article presents the case of a 55-year-old woman who suffered from anterior myocardial infarction and chronic complications of the underlying disease, heart failure with reduced left ventricular ejection fraction, severe secondary mitral regurgitation, and paroxysmal atrial fibrillation. Due to the severity of symptoms, which persisted despite the optimal pharmacotherapy, after exclusion of reversible causes, the patient was qualified for different advanced percutaneous treatment methods. Within two years from the onset of the disease, three percutaneous procedures were performed: mitral valve correction with the MitraClip system, left atrial appendage occlusion using the Watchman system, and implantation of cardioverter-defibrillator.

Introduction. Subarachnoid hemorrhage (SAH) is currently one of the most serious diseases of the central nervous system. To reduce the negative consequences of SAH and help clinicians to assess the patient’s condition, there are attempts to search for new diagnostic markers, which quickly and accurately allow for the proper diagnosis. The aim of this research was the concentration and activity of Vascular Endothelial Growth Factor A (VEGF-A) and selected parameters of coagulation and fibrinolysis in the blood of patients with SAH. Serum levels of VEGF-A in patients diagnosed with SAH are measured to assess the correlation between VEGF-A and the clinical condition of patient. This may help with proper therapeutics and better prognosis. Methods. The study involved 85 patients with subarachnoid hemorrhage. The control group consisted of 45 healthy subjects, sex and age matched. The following parameters were determined: APTT (Activated Partial Thromboplastin Time), INR (International Normalized Ratio), D-dimers and fibrinogen concentration, and the concentration of VEGF-A by ELISA (R&D USA). Results. The average concentration of VEGF-A in the study group was significantly lower compared to the control group. The D-dimer concentration was higher in patients with SAH but the difference was not significant. Coagulation parameters such as INR, APTT, and fibrinogen did not show significant differences between investigated groups. Conclusions. VEGF-A cannot be an independent marker of SAH. Selected parameters of coagulation and fibrinolysis such as D-dimers, INR, APTT, and fibrinogen should not be used as markers of SAH.

Introduction. Autotransfusions of ozonised blood or infusions of gaseous ozone into blood vessels andbody cavities are believed to exert therapeutic effects in some pathological states. Investigations on thereaction of ozone with biological molecules and membrane structures are a subject of crucial importance. The present study aimed to yield more precise data about the alterations, which occur in different erythrocytemembrane regions subjected to medical ozone. This could provide some additional informationabout the structural changes in the membrane at a molecular level. Material and methods. Blood was obtained from 22 healthy volunteers (aged 21 to 63) by vein puncture andmixed with 1/10 volume of 0.13 M trisodium citrate. Erythrocytes were isolated from fresh blood by centrifugationat 4°C, at 1,500 × g and purified by three cycles of resuspension and washing with PBS. Ozone was generatedby passing pure gaseous oxygen at 30 l/h through an apparatus producing silent electric discharges. EPRspectra were obtained at X-band (9.4 GHz), at modulation frequency of 100 kHz. The scan time was 4 min, and the time constant 0.3 s. Since biological membranes are heterogeneous systems composed of severalcoexisting domains, EPR spectra are superimpositions of several spectra with different fluidity parameters. Results. The effects of ozone at two concentrations (10 and 45 g/m3) on fluidity and phospholipid domainstructure of erythrocyte membranes were investigated by electron paramagnetic resonance (EPR). Atincreased ozone concentration (45 g/m3), the portion of the least ordered domains (WLO) increased, witha corresponding decrease of ordered (WMO, WO), more rigid regions. The order of lipid acyl chains of twoordered (MO and O) as well as the least ordered (LO) domains diminished, as expressed by smaller orderparameters. For ozone concentration of 10 g/m3 values of order parameter were slightly increased, whichindicates a tendency to rigidisation of lipid bilayer at this ozone concentration. This change was, however,statistically insignificant. There were no statistically significant differences in the thermotropic behaviour ofweight factor of ordered domains (WMO, WO) between ozonised and control red cells. Conclusion. The obtained data shows that ozonation of erythrocytes results in cell membrane fluidisationand an increase in red cell deformability. On the other hand, these results could suggest that ozonationof erythrocytes leads to structural changes in the membranes, especially in cytoskeletal proteins, but thiseffect is probably dose-dependent.

Introduction. The aim of the current study was to verify the impact of statin therapy on evaluation of the inflammatory process and cortisol concentration in patients with the first episode of ST-segment elevation myocardial infarction undergoing coronary angioplasty with bare metal stent implantation. Material and methods. The study was designed as a prospective, single-center cohort study, with a total number of 200 patients enrolled between 2005 and 2008. Results. Seventeen patients with ongoing statin therapy and 167 patients without those agents underwent pPCI with BMS implantation. The cortisol concentration on admission was significantly lower in statin therapy subgroup — median 14.9 μg/dL (9.5–23.3 IQR) vs. 28,1 μg/dL (17.2–39.9 IQR) for patients without lipid lowering drug, p = 0.01. The level of cortisol after 23h was also significantly lower in statin receiving subgroup: 10.4 μg/dL (8.3–19 IQR) vs. 17.3 μg/dL (10.1–25.9 IQR) adequately, p = 0.021. Those two groups did not differ significantly in relation to CRP, IL-6, IL-10 concentrations and to anti-inflammatory cytokine ratio [IL-6/IL-10] on admission, after 24h and at discharge. Significant differences were observed in the concentrations of cTnI and activities of CK and CK-MB. Conclusions. Ongoing statin therapy before an episode of myocardial infarction has an influence on cortisol concentration and cardiac markers. No significant effect on serum levels of cytokines has been observed.

Background Ischemia and reperfusion remain inseparable elements of numerous medical procedures such as by-pass surgery, organ transplantation or other cardiology and intervention radiology. The contraction of the smooth muscle of the vessel is considered to be one of the basic components leading to impaired perfusion, an increase in the oxygen deficit of the endothelium of the vessel, and subsequently also to tissues vascularized by the vessel. Main aim of this study was to evaluate the effect of ischemia and reperfusion on vascular smooth muscle cells stimulated pharmacologically with mastoparan-7 (direct G-protein activator) in comparison to stimulation of G-protein coupled receptor agonist - phenylephrine, and direct calcium channel activator - Bay K8644. Material and methods Experiments were performed on isolated and perfused tail artery of Wistar rats. Contraction force in our model was measured by increased level of perfusion pressure with a constant flow. Results Concentration-response curves obtained for phenylephrine, mastoparan-7 and Bay K8644 presented a sigmoidal relation. Ischemia induced hyporreactivity of vessels, whereas during reperfusion the significant time related hyperreactivity for phenylephrine and mastoparan-7 only but not for Bay K8644. These reactions were secondary to the modulation of calcium influx from intra- and extracellular calcium stores. Conclusions Results of our experiments suggest that mastoparan-7 significantly induces contraction of vascular smooth muscle cells not only for controls but in the presence of ischemia and reperfusion too. Potential therapeutic applications of the observed reactions are important. They may include regenerative processes within the nervous system, studies on the improvement of blood flow within the microcirculation, or antimicrobial activity. Modulation of the G protein-phospholipase C response may also be an interesting point of action of future drugs modifying the response to stimulation during ischemia in particular, such activities could take place during the transport of organs for transplantation.

Morning increase in the occurrence of myocardial infarction, stroke and sudden cardiac death is a well-recognized phenomenon, which is in line with a morning enhancement of platelet aggregation. We investigated whether platelet inhibition during clopidogrel and aspirin therapy varies during the day. Fifty-nine consecutive patients (45 men and 14 women) with first ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary interventions (pPCI) on dual antiplatelet therapy were prospectively enrolled into the study. Blood samples were collected 4 days after start of clopidogrel treatment at 6.00 a.m., 10.00 a.m., 2.00 p.m. and 7.00 p.m. Arachidonic acid and adenosine diphosphate (ADP)-induced platelet aggregation were assessed by impedance aggregometry. Platelet inhibition by clopidogrel was lowest in the midmorning: median ADP-induced platelet aggregation was 55%, 17% and 27% higher at 10.00 a.m. compared to 6.00 a.m., 2.00 p.m. and 7.00 p.m., respectively ( p < 0.002). Nonresponsiveness to clopidogrel defined according to the device manufacturer was 2.4-fold more frequent in the midmorning than in the early morning. We observed a more pronounced midmorning increase in ADP-induced platelet aggregation in diabetic patients when compared to non-diabetics. In contrast, no diurnal variation in the antiplatelet effect of aspirin was observed. In conclusion, in patients presenting with STEMI undergoing pPCI, platelet inhibition by clopidogrel is less strong in the midmorning hours. This periodicity in platelet aggregation in patients on dual antiplatelet therapy should be taken into consideration when assessing platelet function in clinical studies.

Background Despite its commonly recognized benefits in the cardiovascular disease setting, an issue of resistance to this drug has lately emerged. The aim of this research was assessment of the phenomenon of acetylsalicylic acid (ASA) resistance and its risk factors in patients treated for myocardial infarction. Methods This study is a post-hoc analysis of a previous prospective study with approximately 200 patients treated for myocardial infarction with a coated formulation of ASA. The population was divided into two subgroups according to the response to ASA. ASA responsiveness was assessed using the arachidonic acid-dependent platelet aggregation (ASPI-test). The measurements were performed using the technique of impedance aggregometry. Results The prevalence of aspirin resistance among the study population was 6.2%. All analyzed aggregometric parameters (including ASPI-test, adenosine diphosphate dependent platelet aggregation – ADP-test, bleeding time measurement) showed significant differences between both subgroups. ASA resistant patients had higher concentrations of brain natriuretic peptide (BNP), high-sensitivity C-reactive protein (hs-CRP), leukocytes (WBC) and platelets (PLT) but lower concentrations of hemoglobin (HGB). The temporal point analysis for both subgroups showed aspirin resistance incidence peak in patients at 9 months after myocardial infarction. Conclusions The prevalence of aspirin resistance in our study population is comparable with rates reported in literature among patients with cardiovascular diseases. There is a possible relation between aspirin resistance and clopidogrel resistance. Presence did not affect the incidence of the clinical end-points.

Background: The aim of this study was to assess antiplatelet effect of prasugrel in acute coronary syndrome (ACS) patients with high on-treatment platelet reactivity (HTPR) on clopidogrel, undergoing percutaneous coronary intervention (PCI). Methods: A prospective, platelet reactivity-guided, parallel-group, open-label study including 71 patients pretreated with clopidogrel 600 mg and assigned either to prasugrel (30 mg loading dose, 10 mg maintenance dose; n = 46) or clopidogrel (150 mg maintenance dose for 6 days and thereafter 75 mg maintenance dose; n = 25) regimen, based on vasodilator-stimulated phosphoprotein (VASP)-assessed platelet reactivity index (PRI; > 50% vs. ≤ 50%) measured next morning post-PCI. Results: Median PRI value after switch to prasugrel sharply declined at 24 h (70.0 [61.3–75.6] vs. 11.9 [6.8–25.7]%; p < 0.000001) and slightly but significantly rose between 24 h and 30 days (27.9 [15.5–46.8]%; p < 0.0006). In contrast, median PRI values in the clopidogrel group were similar at baseline and at 24 h (25.1 [13.7–40.2] vs. 22.0 [18.4–36.8]%; p = NS) and then modestly rose at 30 days (30.3 [20.4–45.7]%; p < 0.03). The prevalence of HTPR decreased in the prasugrel group between baseline and 24 h measurements (100.0 vs. 4.3%; p < 0.0001). Rates of patients with HTPR at 24 h and 30 days were similar in both groups, so were the tendencies in patterns of platelet inhibition evaluated with multiple electrode aggregometry as compared with the VASP assay. Conclusions: Our study indicates that prasugrel overcomes HTPR on clopidogrel in the acute phase of interventionally treated ACS and maintains its antiplatelet potency in 30-day follow-up. Potential clinical benefits of personalized antiplatelet prasugrel-based therapy warrant further investigation in clinical ACS trials. Normal 0 21 false false false PL X-NONE X-NONE MicrosoftInternetExplorer4