4 research outputs found
Paroxysmal atrial fibrillation is associated with early coagulation activity regardless of risk factors for embolism
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
Paroxysmal Atrial Fibrillation: Dynamics of The Main Antioxidant Enzymes - Superoxide Dismutase and Catalase
Abstract
INTRODUCTION: Researchers have a particularly strong interest in the mechanisms implicated in the clinical manifestation of atrial fibrillation.
OBJECTIVE: To examine dynamically the activity of the antioxidant enzymes, su-peroxide dismutase and catalase in patients with paroxysmal atrial fibrillation (duration â‹‹ 48 hours).
MATERIALS AND METHODS: The studied parameters were examined in the erythrocytes of 51 patients (59.84 ± 1.60, 26 men) immediately after their hospitalization, at 24 hours and 28 days after restoration of sinus rhythm. 52 controls (59.50 ± 1.46, 26 men) were also included, none of which had a history of arrhythmia. Propafenone was used to manage the rhythm abnormality. The enzyme activity was determined by a spectrophotometric method.
RESULTS: The average duration of atrial fibrillation episodes until the time of hospitalization was 8.14 hours (from 2 to 24 hours). During patient hospitalization the activity of superoxide dismutase and catalase was considerably higher compared to that of the controls (8.46 ± 0.26 vs 5.81 ± 0.14 U/mg Hb; 7.36 ± 0.25 vs 4.76 ± 0.12 E240/min/mg Hb; P ⋋ 0.001). This difference was maintained 24 hours after the rhythm regularization (7.19 ± 0.25 vs 5.81 ± 0.14 U/mg Hb, p ⋋ 0.001; 5.30 ± 0.21 vs 4.76 ± 0.12 E240/min/mg Hb, p ⋋ 0.05). Twenty-eight days after the restoration of sinus rhythm, the activity of catalase remained increased (5.11 ± 0.08 vs 4.76 ± 0.12 E240/min/mg Hb, p ⋋ 0.05).
CONCLUSION: The paroxysmal atrial fibrillation in our study was characterized with significantly increased activity of superoxide dismutase and catalase even in the early hours of clinical manifestation of the disorder, which then slowly decreased with the restoration of sinus rhythm. Therefore, we can conclude that changes in oxidative status are closely related to the disease and are probably a part of the intimate mechanisms related to its initiation and clinical course.</jats:p
Pacemaker associated reduction of left ventricle systolic function
In recent years, data have been accumulated on the negative effect of right ventricular (RV) stimulation, leading to left ventricular (LV) asynchrony, proarrhythmias and progressive heart failure (HF). On the other hand, biventricular pacing has been shown to affect ventricular asynchrony, reduce HF manifestations, and improve prognosis in patients with LV dysfunction and wide QRS complex. The induced asynchrony from apical right ventricular pacing is unequivocally associated with changes in myocardial perfusion, LV dysfunction, and poorer prognosis for patients over time. This has led researchers for decades to look for an alternative position for electrode placement. The incidence of pacemaker-induced cardiomyopathy (PICM) ranges from 5.9 to 39% in patients with RV pacing, depending on the given definition and the limit for the degree of pacing. Upgrading to biventricular pacing has been shown to reverse the cardiomyopathy. Recently, there has been evidence of a positive effect of His bundle pacing (HBP) in the treatment of PICM even in patients with no improvement after biventricular pacing. The question about the pathogenetic mechanisms of PICM is currently unanswered. The connection between electrical asynchrony and the negative effect on cardiac pump function is clear. There is also evidence of an established relationship between asynchrony and coronary blood flow. The predisposing individual characteristics of the patient in which these negative effects are manifested are not clear. This is an issue that requires further studies.</jats:p