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Dive into the research topics where Zbigniew Gasior is active.

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Featured researches published by Zbigniew Gasior.


Haemophilia | 2007

Percutaneous coronary intervention with stent implantation in haemophilic A patient with unstable angina.

G. Smolka; Andrzej Kułach; Dabek J; A. Szulc; Zbigniew Gasior

Summary.  The prevalence of coronary artery disease (CAD) and acute coronary syndromes in patients with haemophilia is much lower than in general population and there is a lack of information regarding safe interventional or surgical treatment of CAD in haemophiliacs. This report presents a case of patient with moderate haemophilia A and unstable angina pectoris, who underwent successful coronary angioplasty. The patient was pretreated with factor VIII (before and after the procedure) and the incision site was sealed with vessel closure device. Additionally, the article discusses the issue of the safety of standard, postpercutaneous coronary intervention antiplatelet therapy in patients with haemophilia.


Internal Medicine Journal | 2008

Expression of genes encoding kinin receptors in peripheral blood mononuclear cells from patients with acute coronary syndromes

Dabek J; Andrzej Kułach; G. Smolka; Tadeusz Wilczok; J. Scieszka; Zbigniew Gasior

Background:  Inflammation plays a critical role in all stages of atherogenesis, including plaque destabilization leading to the rupture and local thrombosis, clinically manifested as unstable angina (UA) or myocardial infarction (MI). Recent data report enhanced expression of numerous pro‐inflammatory genes in patients with acute coronary syndrome (ACS) both in plaque and in inflammatory cells. Kinins are peptides involved in vasodilation, vascular permeability, pain and inflammation. Their effects are mediated by two receptors, B1 and B2. As the role of kinins in ACS is not clear, the aim of the study was to assess the expression of the genes encoding kinin receptors in patients with ACS.


Advances in Experimental Medicine and Biology | 2013

Cardiovascular Effects of the Valsalva Maneuver During Static Arm Exercise in Elite Power Lifting Athletes

Aleksandra Zebrowska; Zbigniew Gasior; Dariusz Jastrzębski

The objective of the study was to investigate whether a blood pressure increase during static exercises might affect the left ventricular function and whether a possible pressure overload might decrease cardio-respiratory adaptation to aerobic exercise in power lifting athletes. Nine resistance-trained athletes and ten age-matched untrained men participated in high intensity isometric exercise performed during the Valsalva maneuver and in an incremental arm cranking test. All subjects underwent echocardiographic evaluation. The combine effect of exercise and increased intrathoracic pressure due to the Valsalva maneuver was a significant increase in systolic blood pressure in the athletes compared with controls. Echocardiography demonstrated significant differences in left ventricular mass and left ventricular mass index; both being higher in the athletes than in controls. The intraventricular septum diameter and left ventricular posterior wall thickness were significantly greater and the myocardial performance index was lower in the athletes compared with controls, indicating a better left ventricular function in the athletes. A cumulative effect of mechanical compression of peripheral blood vessels by contracting muscles and intrathoracic pressure increase during the Valsalva maneuver did not compromise myocardial contractility and cardiorespiratory adaptation to incremental arm exercise in power lifting athletes.


Scandinavian Cardiovascular Journal | 2007

Gene expression of kinin receptors B1 and B2 in PBMC from patients with cardiac syndrome X

Dabek J; Tadeusz Wilczok; Zbigniew Gasior; Sylwia Kucia-Kuzma; Romuald Twardowski; Andrzej Kułach

Introduction. Cardiac syndrome X (CSX) is defined by typical chest pain, ST segment depression on ECG and normal coronary angiography. Pathology of CSX may involve microvascular dysfunction related to inflammation and abnormal pain sensitivity. Kinins are labile peptides participating in vasodilation, inflammation and pain. Their effects are mediated by two receptors: B1 and B2. The aim of the study was to assess gene expression of kinin receptors in peripheral blood mononuclear cells (PBMC) from patients with CSX. Methods. The study was carried out in 34 patients with cardiac syndrome X, 13 with unstable angina and ten healthy subjects. Total mRNA was extracted from PBMC and the number of mRNA copies was assessed by quantitive reverse transcriptase polymerase chain reaction. Results and Conclusion. The study showed 7-fold higher transcriptional activity of B1R in CSX vs. control and 3.5 higher vs. UA. B2R expression was 2.5-fold higher in CSX group vs. control and UA, while in the letter two groups it was similar. Such disturbance in kinin signaling may participate in local vasoconstriction and may reflect disturbances in kinin signaling leading to nociceptive disturbances in these patients.


Archives of Medical Science | 2010

Altered transcriptional activity of gene encoding GAPDH in peripheral blood mononuclear cells from patients with cardiac syndrome X - an important part in pathology of microvascular angina?

Dabek J; Jakub Wilczok; Andrzej Kułach; Zbigniew Gasior

Introduction Cardiac syndrome X (CSX) is characterized by anginal pain with ECG suggestive of ischaemia and normal coronary arteries at angiography. Pathology of CSX involves microvascular dysfunction and is possibly linked with metabolic syndrome. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is an enzyme involved in glycolysis. The GAPDH gene is a “housekeeping” gene and is used for normalization in quantitative gene expression assays. The aim of the study was to evaluate GAPDH gene expression in CSX. Material and methods The study was performed in 35 CSX patients and 10 control subjects. mRNA was extracted from peripheral blood mononuclears and the mRNA was assessed by QRT-PCR. Results GAPDH gene expression was enhanced in CSX patients vs. controls (93022 ±23837 copies/μg vs. 1067 ±240 copies/μg respectively; p < 0.001). Moreover, transcriptional activity of the GAPDH gene was heterogeneous within the CSX group. Conclusions GAPDH gene expression is markedly enhanced in CSX, which reflects carbohydrate metabolism disturbances and makes the GAPDH gene unsuitable as an endogenous control in patients with CSX.


Journal of Nuclear Cardiology | 2008

Coronary artery calcium score assessed by a 64 multislice computed tomography and early indexes of functional and structural vascular remodeling in cardiac syndrome X patients.

Katarzyna Mizia-Stec; Maciej Haberka; Magdalena Mizia; Artur Chmiel; Joanna Wierzbicka-Chmiel; Mariusz Skowerski; Zbigniew Gasior

Background. Regardless of normal coronary angiograms, coronary artery calcium (CAC) can be found in cardiac syndrome X (CSX) patients. According to some data, a relationship between the CAC score and markers of early atherosclerosis in CSX has been observed. Our aim was to assess whether the extent of the CAC score assessed by multislice computed tomography (MSCT) with a 64-slice system in CSX patients is related to brachial artery reactivity, intima-media thickness (IMT), and arterial compliance indexes.Methods and Results. High-resolution ultrasound was used to measure flow-mediated dilatation (FMD) and nitroglycerin-mediated vasodilatation, as well as the following parameters of arterial structural changes: IMT, pulse wave velocity, total arterial compliance, and stiffness index. MSCT was used to assess the presence and the quantity of CAC. The study group consisted of 46 CSX patients (mean age, 56.3±9 years), whereas the control group comprised 21 healthy subjects (mean age, 54.9±7 years). The assessment of the vascular parameters showed significantly decreased FMD and increased IMT in the CSX subjects (9.06%±3.2% and 0.67±0.1 mm, respectively) in comparison to the control subjects (17.42%±8.4% [P=.008] and 0.57 ± 0.2 mm [P=.021], respectively). CAC was detectable in 19 CSX patients (41%) (CAC range according to Agatston score, 2–500; mean, 101.6; median, 26.5) and in 1 control subject (4.8%) (CAC value, 13). CSX patients with detectable CAC were characterized by a significantly higher age (P=.001), lower body mass index (P=.017), and increased stiffness index (P=.020); there were no differences in FMD and IMT values. In a multivariate logistic and linear regression analysis, age was the only risk factor independently associated with the presence of CAC (P=.001) and the log(CAC+1) value (P=.01). In the subgroup of women, log(CAC+1) significantly correlated with age (r=0.587, P=.002) and stiffness index (r=0.427, P=.024), and in a borderline significant manner, it correlated with weight (r=−0.329, P=.07) and waist-hip ratio (r=0.315, P=.07). There were no significant correlations in the male subgroup.Conclusions. Low ranges of CAC are frequently detectable in CSX patients, and the results are age-related and independent of impaired early indexes of functional and structural vascular remodeling.


Heart and Vessels | 2013

Copeptin constitutes a novel biomarker of degenerative aortic stenosis.

Katarzyna Mizia-Stec; Bartosz Lasota; Magdalena Mizia; Artur Chmiel; Tomasz Adamczyk; Jerzy Chudek; Zbigniew Gasior

Copeptin is a new biomarker of cardiovascular diseases. Its diagnostic value in degenerative aortic valve stenosis (AS) with preserved left ventricle systolic function is unknown. We aimed to assess the association of serum copeptin levels with AS severity and coexistence of coronary artery disease (CAD). Sixty-four patients with AS and preserved left ventricle systolic function including 40 with severe degenerative AS (group sAS, effective orifice area EOA = 0.67 cm2) and 24 with moderate degenerative AS (group mAS, EOA = 1.40 cm2) were enrolled into the study. Twenty-three patients without AS and heart failure, matched for age, sex, and CAD occurrence served as the control group (group C). Serum levels of copeptin and N-terminal pro-brain natriuretic peptide (NT-proBNP) were measured using enzyme-linked immunosorbent assay. The mean serum copeptin concentrations were significantly higher in patients with AS: sAS (405 pg/ml) and mAS (351 pg/ml; sAS vs mAS P < 0.05), compared with group C (302 pg/ml, P < 0.05). Serum copeptin levels correlated inversely with EOA (r = −0.55; P < 0.001) in AS patients. There was no correlation between copeptin and NT-proBNP or association with the coexisting CAD. Receiver-operating characteristics analysis showed that copeptin was a good marker of severe/moderate AS (sensitivity 71 %; specificity 87 %), with the optimized cut-off value of 354 pg/ml. Serum copeptin concentration constitutes a novel biomarker of degenerative AS. Coexisting CAD does not interfere with copeptin level.


Journal of the American College of Cardiology | 2016

TCT-581 Plaque redistribution after stenting: data from NIRS-IVUS imaging

Tomasz Roleder; Magdalena Dobrolińska; Elzbieta Pociask; Wojciech Wanha; Grzegorz Smolka; Tomasz Bochenek; Wojciech Walkowicz; Mariusz Lebek; Radosław Parma; Andrzej Ochała; Zbigniew Gasior; Michal Tendera; Wojtek Wojakowski

Plaque redistribution after stent implantation may cause distal embolization. There is no data as to the longitudinal plaque shift with relation to the stent in context of plaque morphology. The study aimed to measure plaque redistribution after stent implantation with relation to its composition


Journal of the American College of Cardiology | 2012

TCT-789 Optimizing plugs size for transcatheter paravalvular leak closure with Amplatzer Vascular Plug III devices

Grzegorz Smolka; Piotr Pysz; Ewa Peszek-Przybyła; Przemyslaw Zurek; Zbigniew Gasior; Andrzej Ochała

Transcatheter paravalvular leak closure (TPVLC) has become a well-established alternative to reoperation. Implantation of multiple smaller plugs is postulated to outperform a single large one. Still, the procedural success pivots on optimal choice of occluding devices, which has not been


Archives of Medical Science | 2010

Changes in transforming growth factor β and its receptors' mRNA expression in monocytes from patients with acute coronary syndromes.

Andrzej Kułach; Dabek J; Tadeusz Wilczok; Zbigniew Gasior

Introduction Transforming growth factor β (TGF-β) is thought to be a vasoprotective cytokine. Numerous reports confirm its significance in blood and plaques. There is, however, a lack of information on the molecular mechanisms involving TGF-β in circulating inflammatory cells in atherogenesis. sThe aim of the study was to assess gene expression of TGF-β and its receptors in monocytes from patients with acute coronary syndromes (ACS) and the effect of standard treatment on the studied genes. Material and methods The study was carried out in 32 patients with ACS and 15 healthy subjects. Gene expression of TGF-β and receptors TGF-βRI and TGF-βRII was evaluated on day 1 and 5 in the study group and once in controls. The number of mRNA copies isolated from monocytes was assessed by QRT-PCR. Results Monocytes of ACS patients showed slightly elevated transcriptional activity of TGF-β1 and its receptors RI and RII genes (0.29 ±0.043 vs. 0.08 ±0.020, p = 0.05; 0.071 ±0.022 vs. 0.036 ±0.023, p < 0.05; 0.134 ±0.020 vs. 0.048 ±0.016, p < 0.05, respectively). After 5-day standard treatment modest reduction of TGF-βRI expression was observed. The studied genes’ expression was unrelated to ejection fraction, myocardial necrosis markers, GRACE score, time from the onset of pain to percutaneous coronary intervention and angiographic findings. Among risk factors family history of CAD was associated with increased TGF-βRI expression. Moreover, the presence of 4 or more classic risk factors correlated with higher TGF-βRI expression. Conclusions Monocytes of ACS patients demonstrate overexpression of TGF-β1 and its receptors’ genes. Five-day standard treatment downregulated the TGF-βRI gene but did not affect TGF-β1 and TGF-βRII.

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Andrzej Ochała

Medical University of Silesia

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Grzegorz Smolka

Medical University of Silesia

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Andrzej Kułach

Medical University of Silesia

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Dabek J

Medical University of Silesia

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Wojciech Wojakowski

Medical University of Silesia

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Tomasz Roleder

Medical University of Silesia

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Wojciech Wanha

Medical University of Silesia

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Katarzyna Mizia-Stec

Medical University of Silesia

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Michal Tendera

Medical University of Silesia

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Tadeusz Wilczok

Medical University of Silesia

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