Wyniki wyszukiwania

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Human skeletal muscle-derived stem/progenitor cells modified with connexin-43 prevent arrhythmia in rat post-infarction hearts and influence gene expression in the myocardium

100%

Rugowska A., Wiernicki B., Maczewski M., Mackiewicz U., Chojnacka K., Bednarek-Rajewska K., Kluk A., Majewski P., Kolanowski T., Malcher A., Rozwadowska N., Kurpisz M.

Journal of Physiology and Pharmacology

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2019

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tom 70

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nr 6

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Pathophysiological mechanism of cardiac arrhytmias as a key for optimal nonpharmacological treatment

100%

Kozluk E.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

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nr 11

69-77

Pathological automatism and triggered activity had focal origin. Thus, the treatment has to be aimed at ablation of the arrhythmogenic region. Some arrythmogenic places can be precisely characterized by analysis of ECG patterns. Among them are foci located close to the pulmonary veins, sinus node, ventricular outflow tracts or mitroaortic commissura. Classical ablation of these loci is highly successful. In other types of focal arrhythmias electroanatomical systems make possible to create 3D map, with activation sequence allowing for identification of the place where the arrhythmia could be eliminated. In reentrant mechanism of the arrhythmia the impulse circulates around the loop via the cardiac muscle. In case of the atrioventricular nodal reentrant tachycardia, atrial flutter or bundle branch ventricular tachycardia the loop can be easily outlined. Ablation can be performed using the anatomical method without induction of the tachycardia. In patients with the ventricular tachycardia with multiple forms or hemodynamically unstable it is possible to perform electranatomical map with visualization of the scar and the border zones. In this case the proarrhythmic region in the borderline zone is the aim of linear ablation without induction of tachycardias. In the chaotic tachycardias (atrial or ventricular fibrillation), the arrythmogenic substrate is too much dispersed to destroy them. Therefore, the ablation is aimed at the trigger which is initiating the arrhythmia (for instance the pathological Purkinje fibers). The excitability of the substrate may be also modified by pacemakers (ventricular or atrial resynchronization). In the life-threatening arrhythmias implantable cardioverter-defibrillator is necessary.

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Diameter of the cavo-sinus-tricuspid area in relation to type I atrial flutter

100%

Kozlowski D., Hreczecha J., Skwarek M., Piwko G., Kosinski A., Gawrysiak M., Grzybiak M.

Folia Morphologica

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2003

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tom 62

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nr 2

Cardiac arrhythmias have troubled patients and fascinated physicians for centuries. The twentieth century was an era of progress, when the mechanism of cardiac disorders became more commonly recognised. Arrhythmias may be due to abnormalities of automaticity, to abnormalities of conduction, or to a combination of both. In order for re-entry to occur, an area of slowing conduction combined with unidirectional block must be present. Much investigation has centred on the underlying re-entry mechanisms of atrial flutter. In the light of these facts, it would seem that a close acquaintance with the detailed topography of the vena cava orifice (cavo), coronary sinus orifice (sinus) and the attachment of the septal leaflet of the tricuspid valve (tricupid) area could be of great interest, especially for invasive cardiologists. The research was conducted on material consisting of 41 hearts of humans of both sexes from the age of 12 to 80 (6 female, 35 male). Classical macroscopic methods of anatomical evaluation were used. The following measurements were made: the shortest distance between the Eustachian valve and the attachment of the tricuspid valve on the left margin of the coronary sinus orifice (diameter 1), the distance between the attachment of the tricuspid valve and the inferior margin of the sinus orifice (diameter 2), the distance between the Eustachian valve and the attachment of the tricuspid valve on the right margin of the coronary sinus orifice (diameter 3), the distance between the inferior margin of the vena cava inferior and the attachment of the tricuspid valve (diameter 4) and, finally, the diameter between the attachment of the septal cups of the tricuspid valve and the external border of the vena cava inferior (diameter 5). No correlation was found between the age and sex of the three groups of the material. The dimensions of the structure examined were similar in the three groups of hearts. In young adult hearts all the diameters measured ranged from 4 to 47 mm The average diameters were, respectively: 15.02 mm (diameter 1), 8.97 mm (diameter 2), 17.27 mm (diameter 3), 26.87 mm (diameter 4), 36.42 mm (diameter 5). In the mature adult hearts all the diameters measured ranged from 8 to 45 mm: 18.19 mm (diameter 1), 10.54 mm (diameter 2), 19.95 mm (diameter 3), 28.90 mm (diameter 4), 39.63 mm (diameter 5). In the older adults hearts all the diameters measured ranged from 4 to 47 mm. The average diameters were, respectively: 15.65 mm (diameter 1), 8.70 mm (diameter 2), 7.25 mm (diameter 3), 26.80 mm (diameter 4), 35.85 mm (diameter 5).

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Cardiac ion channel gene mutations in Greek long QT syndrome patients

80%

Kotta C.-M., Anastasakis A., Gatzoulis K., Papagiannis J., Geleris P., Stefanadis C.

Journal of Applied Genetics

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2010

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tom 51

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nr 4

The long QT syndrome (LQTS) is an inherited cardiac arrhythmia that may lead to sudden death in the absence of structural heart disease. Mutations in the cardiac potassium and sodium channel genes can be found in approximately 70% of patients with a highly probable clinical diagnosis. In this study, we aimed to genotype and explore the yield of genetic testing of LQTS patients from Greece, for whom there are no collective published data available. We clinically evaluated and genetically screened 17 unrelated patients for mutations in the KCNQ1, KCNH2, SCN5A, KCNE1, and KCNE2 cardiac ion channel genes. Genetic testing was positive in 6 out of 8 patients with a highly probable clinical diagnosis of LQTS and negative for all the other patients. Two patients carried KCNQ1 mutations (c.580G>C, c.1022C>T), while 4 patients carried KCNH2 mutations (c.202T>C, c.1714G>A, c.3103delC, c.3136C>T). To the best of our knowledge, the last mentioned mutation (c.3136C>T) is novel. Moreover, 27 single-nucleotide polymorphisms (SNPs) were detected, 5 of which are novel. Our preliminary data indicate a low genetic diversity of the Greek LQTS genetic pool, and are in accordance with international data that genetic testing of the major LQTS genes is efficient in genotyping the majority of patients with a strong clinical diagnosis. Therefore, the transition of an LQTS genetic screening program from research to the diagnostic setting within our ethnic background is feasible.

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Action potential clamp and mefloquine sensitivity of recombinant IKs' channels incorporating the V307L KCNQ1 mutation

80%

El Harchi A., Mcpate M. J., Zhang Y. H., Zhang H., Hancox J. C.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 2

The slow delayed rectifier potassium current, 'IKs', contributes to repolarisation of cardiac ventricular action potentials and thereby to the duration of the QT interval of the electrocardiogram. Mutations to IKs channel subunits occur in clinically significant cardiac repolarisation disorders. The short QT syndrome (SQTS) is associated with accelerated ventricular repolarisation and with an increased risk of arrhythmia and sudden death. The SQT2 variant of the SQTS has been linked to a gain-of-function amino-acid substitution (V307L) in the KCNQ1-encoded IKs channel -subunit. This study reports the first action potential (AP) voltage-clamp comparison between wild-type (WT) and V307L KCNQ1 (co-expressed with KCNE1 to recapitulate IKs) and identifies an effective pharmacological inhibitor of recombinant 'IKs' channels incorporating the V307L KCNQ1 mutation. Perforated-patch voltage-clamp recordings at 37°C of whole-cell current carried by co-expressed KCNQ1 and KCNE1 showed a marked (-36 mV) shift in half-maximal activation for V307L compared to WT KCNQ1; a significant slowing of current deactivation was also observed. Under AP clamp, peak repolarising current was significantly augmented for V307L KCNQ1 compared to WT KCNQ1 for both ventricular and atrial AP commands, consistent with an ability of the V307L mutation to increase repolarising IKs in both regions. The quinoline agent mefloquine inhibited WT KCNQ1+KCNE1 with an IC50 of 3.4 µM compared to 3.3 µM for V307L KCNQ1+KCNE1 (P >0.05). This establishes mefloquine as an effective inhibitor of recombinant 'IKs' channels incorporating this SQT2 KCNQ1 mutation.

6

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The influence of experimental hyperlipidemia on the time course of contractility during simulated ischaemia and reperfusion and responsiveness to phenylephrine of rat heart papillary muscle

80%

Kocic I., Dworakowska D., Konstanski Z., Dworakowski R.

Journal of Physiology and Pharmacology

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1998

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tom 49

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nr 3

Ograniczanie wyników

Human skeletal muscle-derived stem/progenitor cells modified with connexin-43 prevent arrhythmia in rat post-infarction hearts and influence gene expression in the myocardium

Pathophysiological mechanism of cardiac arrhytmias as a key for optimal nonpharmacological treatment

Diameter of the cavo-sinus-tricuspid area in relation to type I atrial flutter

Cardiac ion channel gene mutations in Greek long QT syndrome patients

Action potential clamp and mefloquine sensitivity of recombinant IKs' channels incorporating the V307L KCNQ1 mutation

The influence of experimental hyperlipidemia on the time course of contractility during simulated ischaemia and reperfusion and responsiveness to phenylephrine of rat heart papillary muscle