Andrzej Minczykowski
New York Academy of Medicine
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Featured researches published by Andrzej Minczykowski.
International Journal of Cardiology | 1995
Henryk Laskowski; Andrzej Minczykowski; Henryk Wysocki
There is increasing evidence that free radical scavengers limit reperfusion injury in animal experiments. We randomly administered 250 ml 20% mannitol infusion and 10.0 g ascorbic acid infusion, potent free radical scavengers to 42 patients with acute myocardial infarction receiving streptokinase. A control group of 42 patients received only standard fibrinolytic therapy. We found that additional antioxidant treatment with ascorbic acid and mannitol decreased the number of some complications of acute myocardial infarction.
International Journal of Cardiology | 1996
Juliusz Smielecki; Andrzej Wykretowicz; Andrzej Minczykowski; Miroslaw Kazmierczak; Henryk Wysocki
We studied the influence of electrical cardioversion on unstimulated and stimulated superoxide anion production by polymorphonuclear neutrophils in 22 patients with atrial flutter or atrial fibrillation. We also estimated hydrogen peroxide plasma level, as well as malondialdehyde serum concentration, in these subjects. We noted an increase in spontaneous production of superoxide anions from 14.9 +/- 1.8 nmol/10(6) neutrophils per 20 min to 21.37 +/- 2.7 nmol/10(6) neutrophils per 20 min (P = 0.002) in neutrophils obtained after electrical cardioversion. Similarly, stimulated production of O2- also increased after electrical cardioversion (41.8 +/ 3.4 nmol/10(6) neutrophils per 20 min vs. 59.0 +/- 5.9 nmol/10(6) neutrophils per 20 min, P = 0.0027). Moreover, hydrogen peroxide plasma level increased significantly after electrical cardioversion (39.9 +/- 6.2 mumol/l vs. 53.4 +/- 7.6 mol/l, P = 0.003). Serum malondialdehyde concentration also increased after countershock (2.56 +/- 0.26 nmol/ml vs. 2.94 +/- 0.26 nmol/ml, P = 0.023). These results seem to indicate that electrical cardioversion may lead to polymorphonuclear neutrophils activation, increased H2O2 production and lipid peroxidation.
Coronary Artery Disease | 1995
Miroslaw Kazmierczak; Henryk Wysocki; Andrzej Wykretowicz; Andrzej Minczykowski
Background.Prolonged ischemia leads to myocardial infarction and increased formation of toxic oxygen radicals. These substances exert deleterious effects on myocardial cells, contributing to reperfusion injury and generation of arrhythmia. Little information is available, however, concerning the toxic oxygen species generated during transient ischemia. The purpose of our study was to estimate hydrogen peroxide plasma levels in patients subjected to short-lasting ischemia induced by a dipyridamole stress test used for the diagnosis of coronary artery disease. Evaluation of the performed test was carried out with 99mTc-SestaMIBI followed by single photon emission computed tomography (SPECT). Methods.Blood was obtained from peripheral veins of 53 patients (37 men and 16 women, mean age 49 ± 11 years). Plasma hydrogen peroxide levels were estimated by spectrophotometric methods: immediately before a dipyridamole challenge and after drug infusion. Results.Hydrogen peroxide plasma levels in patients with a negative SPECT test were 23.5 ± 3.0 μmol/l (mean ± SEM) and 21.0 ± 2.9 after the dipyridamole infusion (P= 0.474). Plasma concentrations of hydrogen peroxide in patients with a positive SPECT test were 30.5 ±4.6 and increased after dipyridamole challenge to 50.3±5.4 (P= 0.004). Further analysis revealed that the observed difference cannot be attributed to previous history of myocardial infarction. Conclusions.Even transient myocardial ischemia can generate toxic oxygen derivatives. Evaluation of plasma levels of hydrogen peroxide may be of clinical relevance in patients with suspected coronary artery disease.
International Journal of Cardiology | 2014
K. Katulska; M. Wykrętowicz; Andrzej Minczykowski; Tomasz Krauze; Agata Milewska; Jaroslaw Piskorski; R. Marciniak; M. Stajgis; Henryk Wysocki; Przemyslaw Guzik; Andrzej Wykretowicz
a Department of Radiology, University School of Medicine, 49 Przybyszewskiego, 60-355 Poznan, Poland b Department of Cardiology-Intensive Therapy, University School of Medicine, 49 Przybyszewskiego, 60-355 Poznan, Poland c Institute of Physics, University of Zielona Gora, 4a Szafrana, 65-516 Zielona Gora, Poland d Department of Surgery, University School of Medicine, 49 Przybyszewskiego, 60-355 Poznan, Poland
Academic Radiology | 1996
Andrzej Minczykowski; Wlodzimierz Paprzycki; Juliusz Smielecki; Piotr Sosnowski; Adam Szczepanik; Michal Eder; Henryk Wysocki
RATIONALE AND OBJECTIVES Limited research has been performed on the effects of magnetic resonance (MR) imaging on the immune system. To our knowledge, there are no reported studies of MR imaging effects on the polymorphonuclear neutrophil (PMN) system. Therefore, we evaluated the influence of MR imaging exposure on PMNs. METHODS In vivo and in vitro studies were performed on 36 patients undergoing MR imaging. The following were estimated in blood samples: leukocyte and PMN count, PMN phagocytosis and bactericidal capacity, percentage of cells with expression of surface receptor for the Fc fragment of immunoglobulin G (IgG), PMN superoxide, hydrogen peroxide production, and plasma lysozyme activity. Another sample of patients was used to eliminate temperature as an influence on changes in PMN functions. RESULTS Both in vitro and in vivo MR imaging led to a decrease in PMNs and an increase in PMN phagocytosis, bactericidal capacity, hydrogen peroxide production, and percentage of cells with expression of surface receptor for Fc IgG. Superoxide anion production did not change significantly. Elevated temperature, stress, and anxiety were excluded as influences on our results. CONCLUSION The PMN system is affected seriously by MR imaging.
International Journal of Cardiology | 2016
Agata Milewska; Andrzej Minczykowski; Tomasz Krauze; Jaroslaw Piskorski; James A. J. Heathers; Adam Szczepanik; Agnieszka Banaszak; Przemyslaw Guzik; Andrzej Wykretowicz
BACKGROUND The value of modern non-invasive indices of the left ventricle (LV) and arterial system function, and their interaction for determining prognosis in contemporarily treated patients with acute coronary syndrome (ACS) is not well established. The study aimed to determine the association of ventricular-arterial (VA) coupling, LV global longitudinal peak systolic strain (GLPSS), global strain rate (GSR) and end-diastolic volume at end-diastolic pressure 30mmHg (V30) with long-term clinical outcomes in patients with ACS. METHODS Echocardiography was applied in 569 ACS patients followed up for >12months after hospitalization. Univariate Cox proportional hazard regression models adjusted to various clinical factors, including reduced LV ejection fraction <40%, were used to compare patients between the first and third tertiles of various indices of LV and arterial systems function and their interaction for the prediction of a combined end-point (defined as either stroke, myocardial infarction or death). Results are presented as hazard ratio (HR) with 95% confidence interval (CI). RESULTS There were 57 clinical outcomes during a median follow-up of 625days. Increased VA coupling >1.68 (HR 2.4; 95% CI: 1.04-5.6); V30>107mL (HR 4.5; 95% CI: 1.9-10.6), GLPSS > -12.8% (HR 2.4; 95% CI: 1.02-5.7), GSR > -0.96 1/s (HR 3.8; 95% CI: 1.6-9.1) were robustly associated with increased hazard. CONCLUSIONS With a sample of contemporarily treated ACS patients, abnormal values of non-invasive indices of LV function and their interaction with arterial system, predict adverse clinical outcomes, independently of LV ejection fraction.
International Journal of Cardiology | 1998
Henryk Wysocki; Miroslaw Kazmierczak; Andrzej Wykretowicz; Adam Szczepanik; Andrzej Minczykowski
BACKGROUND We have previously reported that transient myocardial ischemia induced during exercise or dipyridamole challenge leads to the release of increased amounts of hydrogen peroxide into circulating blood. It would indicate that the temporary functional changes within myocardial cells may constitute there a sterile inflammatory area. Therefore we decided to evaluate the chemotactic properties of plasma in patients undergoing dipyridamole provocative test, as a sign of released inflammatory mediators. The ischemia occurrence was evaluated with 99mTc-SestaMIBI followed by single photon emission computed tomography (SPECT). METHODS Blood samples were obtained from the peripheral vein of 42 patients (18 men and 24 women, mean age 61 years). Plasma chemotactic activity was determined by the use of the Boyden chamber method: immediately before dipyridamole challenge (time 0), 7, and 30 min after drug infusion. The migration of control polymorphonuclear neutrophils towards evaluated plasma samples was estimated. RESULTS Chemotaxis of control PMNs towards plasma isolated from patients without signs of myocardial ischemia 7 min after dipyridamole administration was significantly diminished in comparison with baseline values (p=0.003). Plasma obtained 7 min after dipyridamole infusion from patients manifesting signs of myocardial ischemia by SPECT attracted control PMNs significantly more intensively in comparison to plasma isolated at time 0 (p=0.0005). CONCLUSIONS The obtained results indicate that transient myocardial ischemia induced by dipyridamole challenge leads to generation of chemotactic factors detectable in peripheral blood plasma.
International Journal of Cardiology | 2005
Andrzej Minczykowski; Maria Gryczyńska; Katarzyna Ziemnicka; Jerzy Sowiński; Henryk Wysocki
Kardiologia Polska | 2007
Przemyslaw Guzik; Dorota Rogacka; Janusz Tarchalski; Andrzej Minczykowski; Marek Baliński; Andrzej Wykretowicz; Henryk Wysocki
Polish archives of internal medicine | 2017
Agata Schneider; Joanna Gawęcka; Andrzej Minczykowski; Tomasz Krauze; Przemyslaw Guzik; Jaroslaw Piskorski; James A. J. Heathers; Andrzej Wykretowicz