4 research outputs found
Tumor Necrosis Factor - alpha in Clinical Manifestation of Paroxysmal Atrial Fibrillation
ΠΡΠ²Π΅Π΄Π΅Π½ΠΈΠ΅: ΠΡΠ΅Π΄ΡΡΡΠ΄Π½ΠΎΡΠΎ ΠΌΡΠΆΠ΄Π΅Π½Π΅ (ΠΠ) Π΅ Π½Π°ΠΉ-ΡΠ΅ΡΡΠ°ΡΠ° Π°ΡΠΈΡΠΌΠΈΡ Π² ΠΊΠ»ΠΈΠ½ΠΈΡΠ½Π°ΡΠ° ΠΏΡΠ°ΠΊΡΠΈΠΊΠ°. ΠΡΠ΅ ΠΏΠΎΠ²Π΅ΡΠ΅ Π΄Π°Π½Π½ΠΈ ΡΠ΅ Π½Π°ΡΡΡΠΏΠ²Π°Ρ Π·Π° ΡΡΠ°ΡΡΠΈΠ΅ΡΠΎ Π½Π° ΡΠΈΡΠΎΠΊΠΈΠ½ΠΈΡΠ΅ Π² ΠΏΠ°ΡΠΎΠ³Π΅Π½Π΅Π·Π°ΡΠ° Π½Π° Π°ΡΠΈΡΠΌΠΈΡΡΠ°, ΠΊΠ°ΡΠΎ ΠΎΠ±Π΅ΠΊΡ Π½Π° ΠΈΠ·ΡΠ»Π΅Π΄Π²Π°Π½Π΅ Π΄ΠΎ ΠΌΠΎΠΌΠ΅Π½ΡΠ° ΡΠ° ΠΏΡΠ΅Π΄ΠΈ ΠΏΠ΅ΡΡΠΈΡΡΠΈΡΠ°ΡΠ°ΡΠ° ΠΈ ΠΏΠ΅ΡΠΌΠ°Π½Π΅Π½ΡΠ½Π°ΡΠ° ΡΠΎΡΠΌΠ° Π½Π° ΡΠΈΡΡΠΌΠ½ΠΎΡΠΎ Π½Π°ΡΡΡΠ΅Π½ΠΈΠ΅.Π¦Π΅Π»: ΠΠ° ΡΠ΅ ΠΏΠΎΡΡΡΡΡΡ ΠΏΡΠΎΠΌΠ΅Π½ΠΈ Π² ΠΏΠ»Π°Π·ΠΌΠ΅Π½ΠΈΡΠ΅ ΠΊΠΎΠ½ΡΠ΅Π½ΡΡΠ°ΡΠΈΠΈ Π½Π° TNF-Ξ±, ΡΠ²ΡΡΠ·Π°Π½ΠΈ Ρ ΠΈΠ·ΡΠ²Π°ΡΠ° Π½Π° ΠΏΠ°ΡΠΎΠΊΡΠΈΠ·ΠΌΠ°Π»Π½ΠΎΡΠΎ ΠΏΡΠ΅Π΄ΡΡΡΠ΄Π½ΠΎ ΠΌΡΠΆΠ΄Π΅Π½Π΅ (ΠΠΠ).ΠΠ°ΡΠ΅ΡΠΈΠ°Π» ΠΈ ΠΌΠ΅ΡΠΎΠ΄ΠΈ: ΠΠ»Π°Π·ΠΌΠ΅Π½ΠΈΡΠ΅ ΠΊΠΎΠ½ΡΠ΅Π½ΡΡΠ°ΡΠΈΠΈ Π½Π° TNF-Ξ± Π±ΡΡ
Π° ΠΈΠ·ΠΌΠ΅ΡΠ΅Π½ΠΈ ΡΡΠΈΠΊΡΠ°ΡΠ½ΠΎ ΠΏΡΠΈ 51 ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΈ (26 ΠΌΡΠΆΠ΅ ΠΈ 25 ΠΆΠ΅Π½ΠΈ; ΡΡΠ΅Π΄Π½Π° Π²ΡΠ·ΡΠ°ΡΡ 59.84 1.60 Π³) Ρ ΠΠΠ, a ΠΈΠΌΠ΅Π½Π½ΠΎ: Π½Π΅Π·Π°Π±Π°Π²Π½ΠΎ ΡΠ»Π΅Π΄ Ρ
ΠΎΡΠΏΠΈΡΠ°Π»ΠΈΠ·Π°ΡΠΈΡΡΠ° ΠΈΠΌ (Ρ.Π΅. ΠΏΠΎ Π²ΡΠ΅ΠΌΠ΅ Π½Π° ΡΠΈΡΡΠΌΠ½ΠΎΡΠΎ Π½Π°ΡΡΡΠ΅Π½ΠΈΠ΅), 24 ΡΠ°ΡΠ° ΠΈ 28 Π΄Π½ΠΈ ΡΠ»Π΅Π΄ Π²ΡΠ·ΡΡΠ°Π½ΠΎΠ²ΡΠ²Π°Π½Π΅ Π½Π° ΡΠΈΠ½ΡΡΠΎΠ² ΡΠΈΡΡΠΌ. ΠΠΎΠΊΠ°Π·Π°ΡΠ΅Π»ΡΡ Π±Π΅ΡΠ΅ ΠΈΠ·ΠΌΠ΅ΡΠ΅Π½ Π΅Π΄Π½ΠΎΠΊΡΠ°ΡΠ½ΠΎ ΠΏΡΠΈ 52 ΠΊΠΎΠ½ΡΡΠΎΠ»ΠΈ (26 ΠΌΡΠΆΠ΅ ΠΈ 26 ΠΆΠ΅Π½ΠΈ; ΡΡΠ΅Π΄Π½Π° Π²ΡΠ·ΡΠ°ΡΡ 59.50 1.46 Π³.) Π±Π΅Π· Π°Π½Π°ΠΌΠ½Π΅ΡΡΠΈΡΠ½ΠΈ ΠΈΠ»ΠΈ Π΅Π»Π΅ΠΊΡΡΠΎΠΊΠ°ΡΠ΄ΠΈΠΎΠ³ΡΠ°ΡΡΠΊΠΈ Π΄Π°Π½Π½ΠΈ Π·Π° ΠΠ Π΄ΠΎ ΠΌΠΎΠΌΠ΅Π½ΡΠ°. ΠΠ»Π°Π·ΠΌΠ΅Π½ΠΈΡΠ΅ ΠΊΠΎΠ½ΡΠ΅Π½ΡΡΠ°ΡΠΈΠΈ Π½Π° TNF-Ξ± Π±ΡΡ
Π° ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈ Ρ ELISA ΠΊΠΈΡ (Elabscience Biotechnology Co., Ltd, China). Π‘ΠΈΠ½ΡΡΠΎΠ² ΡΠΈΡΡΠΌ Π±Π΅ Π²ΡΠ·ΡΡΠ°Π½ΠΎΠ²Π΅Π½ ΠΌΠ΅Π΄ΠΈΠΊΠ°ΠΌΠ΅Π½ΡΠΎΠ·Π½ΠΎ Ρ propafenone.Π Π΅Π·ΡΠ»ΡΠ°ΡΠΈ: ΠΡΠΈ ΠΏΠΎΡΡΡΠΏΠ²Π°Π½Π΅ Π½Π° ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΈΡΠ΅ Π² ΠΎΡΠ΄Π΅Π»Π΅Π½ΠΈΠ΅ΡΠΎ ΠΊΠΎΠ½ΡΠ΅Π½ΡΡΠ°ΡΠΈΠΈΡΠ΅ Π½Π° TNF-Ξ± Π±ΡΡ
Π° ΠΏΠΎΠ²ΠΈΡΠ΅Π½ΠΈ ΡΠΏΡΡΠΌΠΎ ΡΠ΅Π·ΠΈ Π½Π° ΠΊΠΎΠ½ΡΡΠΎΠ»ΠΈΡΠ΅ (15.06 0.81 vs 8.20 0.29 pg/mL, p<0.001). ΠΠ²Π°Π΄Π΅ΡΠ΅Ρ ΠΈ ΡΠ΅ΡΠΈΡΠΈ ΡΠ°ΡΠ° ΡΠ»Π΅Π΄ Π²ΡΠ·ΡΡΠ°Π½ΠΎΠ²ΡΠ²Π°Π½Π΅ Π½Π° ΡΠΈΠ½ΡΡΠΎΠ² ΡΠΈΡΡΠΌ ΠΏΡΠΎΠΌΠ΅Π½ΠΈΡΠ΅ ΠΏΠ΅ΡΡΠΈΡΡΠΈΡΠ°Ρ
Π° (13.09 0.70 vs 8.20 0.29 pg/mL, p<0.001). ΠΠ° Π΄Π²Π°Π΄Π΅ΡΠ΅Ρ ΠΈ ΠΎΡΠΌΠΈΡ Π΄Π΅Π½ Π»ΠΈΠΏΡΠ²Π°ΡΠ΅ Π·Π½Π°ΡΠΈΠΌΠ° ΡΠ°Π·Π»ΠΈΠΊΠ° (9.21 0.54 vs 8.20 0.29 pg/mL, p=0.10).ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅: ΠΡΠΈ ΠΠΠ ΡΠ΅ Π½Π°Π±Π»ΡΠ΄Π°Π²Π°Ρ Π΄ΠΈΠ½Π°ΠΌΠΈΡΠ½ΠΈ ΠΏΡΠΎΠΌΠ΅Π½ΠΈ Π² ΠΏΠ»Π°Π·ΠΌΠ΅Π½ΠΈΡΠ΅ ΠΊΠΎΠ½ΡΠ΅Π½ΡΡΠ°ΡΠΈΠΈ Π½Π° TNF-Ξ±. Π’Π΅ ΡΠ° Π·Π½Π°ΡΠΈΠΌΠΎ ΠΏΠΎΠ²ΠΈΡΠ΅Π½ΠΈ ΠΏΠΎ Π²ΡΠ΅ΠΌΠ΅ Π½Π° ΠΊΠ»ΠΈΠ½ΠΈΡΠ½Π°ΡΠ° ΠΈΠ·ΡΠ²Π° Π½Π° ΡΠΈΡΡΠΌΠ½ΠΎΡΠΎ Π½Π°ΡΡΡΠ΅Π½ΠΈΠ΅. Π‘Π»Π΅Π΄ Π²ΡΠ·ΡΡΠ°Π½ΠΎΠ²ΡΠ²Π°Π½Π΅ Π½Π° ΡΠΈΠ½ΡΡΠΎΠ² ΡΠΈΡΡΠΌ ΡΠ΅ ΡΠ΅ Π½ΠΎΡΠΌΠ°Π»ΠΈΠ·ΠΈΡΠ°Ρ Π±Π°Π²Π½ΠΎ Π²ΡΠ² Π²ΡΠ΅ΠΌΠ΅ΡΠΎ. Π‘ΠΏΠ΅ΡΠΈΡΠΈΡΠ½ΠΈΡΡ Ρ
Π°ΡΠ°ΠΊΡΠ΅Ρ Π½Π° ΡΡΡΠ°Π½ΠΎΠ²Π΅Π½ΠΈΡΠ΅ ΠΎΡΠΊΠ»ΠΎΠ½Π΅Π½ΠΈΡ Π΄Π°Π²Π°Ρ ΡΠ΅ΡΠΈΠΎΠ·Π½ΠΎ ΠΎΡΠ½ΠΎΠ²Π°Π½ΠΈΠ΅ Π΄Π° ΡΠ΅ ΠΏΡΠΈΠ΅ΠΌΠ΅ ΠΊΠ»ΠΈΠ½ΠΈΡΠ½Π°ΡΠ° ΠΈΠΌ Π·Π½Π°ΡΠΈΠΌΠΎΡΡ Π·Π° ΠΈΠ·ΡΠ²Π°ΡΠ° Π½Π° Π·Π°Π±ΠΎΠ»ΡΠ²Π°Π½Π΅ΡΠΎ.Introduction: Atrial fibrillation is the most common arrhythmia in clinical practice. There has been a growing body of evidence in recent years of the role of inflammatory cytokines in the pathogenesis of the rhythm disorder, although the studies have been predominantly in the field of persistent and permanent atrial fibrillation. Aim: To find changes in plasma concentrations of TNF-Ξ±, concerning the clinical manifestation of paroxysmal atrial fibrillation. Materials and Methods: Plasma concentrations of IL-6 were measured three times in 51 patients (26 men and 25 women; mean age 59.84 1.60 yrs) with paroxysmal atrial fibrillation: once immediately after hospitalization of these patients (that is, during the rhythm disorder episode at baseline), then at 24 hours and finally 28 days after restoration of sinus rhythm. The plasma concentration was measured only once in the control group of 52 control subjects (26 men, 26 women; mean age 59.50 1.46 yrs). We used ELISA kit to determine the IL-6 concentrations. The sinus rhythm was restored with propafenone for all patients. Results: Baseline plasma concentrations of IL-6 were higher than those of controls (15.06.38 0.81 vs 8.20 0.29 pg/mL, p<0.001). The difference was retained for 24 hours after sinus rhythm restoration of (13.09 0.70 vs 8.20 0.29 pg/mL, p<0.001). At 28 days there was no statistically significant difference between patients and controls (9.21 0.54 vs 8.20 0.29 pg/mL, p=0.10). Conclusion: Dynamic changes of TNF-Ξ± plasma concentrations were established in paroxysmal atrial fibrillation. The cytokine levels were significantly elevated during the clinical manifestation of the arrhythmia. They decreased slowly after restoration of sinus rhythm. The changes we found provide a strong rationale to suggest that they are most likely relevant to the clinical manifestaton of paroxysmal atrial fibrillation
Dynamics of oxidative status in patients with paroxysmal atrial fibrillation
Introduction: Studies have established oxidative disorders in persistent and permanent atrial fibrillation. Our aim was to investigate oxidative status still in the early hours of paroxysmal atrial fibrillation (PAF) and monitor its changes after sinus rhythm (SR) restoration. Material and Methods: Levels of malondialdehyde and total glutathione were determined in plasma (Pl-MDA; Pl-GSH) and erythrocytes (Er-MDA; Er-GSH) together with erythrocyte glutathione peroxidase activity (GSH-Px) in 51 patients (59.84Β±1.6 years, 26 males). Markers were investigated upon hospital admission, 24 hours and 28 days after SR restoration. They were also determined in 52 healthy subjects (59.50Β±1.46 years, 26 males). Results: Mean AF duration prior to hospitalization was 8.14Β±0.76 hours. Upon admission, Pl-MDA and Er-MDA were significantly increased (p0.05). Conclusion: Disorder of oxidative status is detected in the early hours of PAF, which persists after SR restoration. Oxidative balance is restored slowly with time. This specific dynamics of oxidative status is most likely related to AF clinical course, namely to its manifestation and recurrences
Influence of air pollution in an urban area on hospital admissions from acute myocardial infarction
It has been established that the episodes of huge atmospheric pollutions like the London fog of 1952 are responsible for an increased mortality, the larger part of which from cardiovascular events. Aim of the study is to investigate the relation between the levels of atmospheric pollutants and the frequency of hospital admissions from acute myocardial infarction (AMI) in the city of Varna. Five hundred and eighty five patients were investigated from those who were admitted to the Intensive Care Clinic of St Marina University Hospital in Varna with a diagnosis of acute myocardial infarction (AMI) in the period from December 2004 to December 2005. For the same period from October 2004 to December 2005 the relationship between the quality of the atmospheric air and the frequency of hospital admissions form AMI was investigated. For the investigated period from 1 October 2004 to 31 December 2005 a total of 585 persons were admitted for treatment at the ICC with a diagnosis of AMI, of which 393 (67.2%) were men and 192 (32.8%) were women. The mean age for them was 64.05 Β± 0.49 years (from 18 to 93 years of age). The frequency of hospital admissions from AMI show sta tis ti cally sig nif i cant correlational sub or di na tions with al most all stud ied at mo spheric pol lut ants. The atmospheric pollution in urbanised inhabited areas should be taken as a risk factor for cardio-vascular diseases. Monitoring of the quality of atmospheric air provokes multidisciplinary prophylactic interest, including the needs of cardiologic prevention.Β Scripta Scientifica Medica 2009; 41(2): 135-139
Paroxysmal Atrial Fibrillation: Dynamics of The Main Antioxidant Enzymes - Superoxide Dismutase and Catalase
INTRODUCTION: Researchers have a particularly strong interest in the mechanisms implicated in the clinical manifestation of atrial fibrillation