Abstract
Introduction: Asynchronous ventricular activation due to permanent pacing through the right ventricular apex results in functional and stmchml changes. Our aim was to examine the role of abnormal ventricular activation on the oxidative stress (serum lipid peroxidation), interleucin-6 (11-6) and hmor necrosis factor-a (TNF-a) in paced patients. Methods: We included 12 patients (7 men, aged 58&6 years) with sick sinus syndrome and first-degree atriovenhicular block, with a permanent DDDR pacemaker. All patients had a normal echocardiogram and coronary angiogram. The pacemaker was initially programmed as AA1 with a basic rate of 40 bpm. The patients were randomized to either AA1 or DDD pacing for 15 days, with a basic rate of 60 bpm, blood samples were taken and the study continued in a crossover design. During DDD pacing, the ventricular activation was fully paced. At the end of each 15.day randomization, blood samples were taken to evaluate lipid peroxides, IL-6 and TNF-a. Before randomization, the same markers were evaluated following 1 hour of AA1 and 1 hour of DDD pacing, in a random order. Results: AA1 and DDD Pacing marker values at one hour showed no significant changes (Lipid peroxides: 250&110 kmoV1, TNF-a: 2.3&0.9 pgiml, IL-6: 1.9&0.9 pg/ml in AA1 versus 267&97 kmoV1, 2.0&0.71 pgiml, 2.5&0.8 pg/ml in DDD, p:NS). However lipid peroxides and II-6 were signiiicantly lower, following the 15.day AA1 pacing period compared to the DDD pacing period (Lipid peroxides: 372&136 kmoV1, II-6: 3.6&1.2 pg/ml in AAI versus 499&110 kmoV1,4.9&1.7 pg/ml in DDD, p<O.O5). TNF-a showed no change (3.2&1,0 pg/ml in AA1 versus 3,5&0.6 pg/ml in DDD, p:NS). Conclusions: Asynchronous ventricular activation sequence caused by right ventricular apical pacing, results in increased cytokine activation and oxidative stress levels after a short-term period of continuous pacing.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call