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- AVA, asynchronous ventricular activation
- IL-6, interleukin-6
- LP, lipid peroxides
- RAVP, right apical ventricular pacing
- TNFα, tumour necrosis factor α
Asynchronous ventricular activation (AVA), caused by right apical ventricular pacing (RAVP), results in the deterioration of both systolic and diastolic function.1,2 Chronic RAVP under DDDR pacing mode in patients with sick sinus syndrome revealed a detrimental effect on left ventricular fractional shortening, left atrium dilation, and myocardial blood flow.3,4
Furthermore, although the mechanism has not been fully elucidated, pro-inflammatory cytokines and oxidative stress have been shown, in both experimental and clinical studies, to affect the myocardium, compromising ventricular systolic performance.5
We hypothesised that these two latter factors are implicated in the functional and metabolic abnormalities in patients with AVA caused by RAVP. With this in mind we studied the concentrations of interleukin-6 (IL-6), tumour necrosis factor α (TNFα), and lipid peroxides (LP) in patients with sick sinus syndrome and a permanent dual chamber pacemaker during physiological and RAVP, as produced by AAIR and DDDR permanent pacing, respectively.
We enrolled consecutive patients with sick sinus syndrome, first degree atrioventricular block (PR interval ⩾ 200 ms), and normal intraventricular conduction, who required a dual chamber pacemaker implantation.
The pacemaker was initially programmed as AAIR with a basic rate of 40 bpm for a three month period and then the patients were randomised …
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