Previous observations suggest that cardiac resynchronization therapy (CRT) may exert an anti-inflammatory effect. The objective of this study was to evaluate the effect of temporary interruption of long-term CRT on plasma concentrations of proinflammatory cytokines and brain natriuretic peptide (BNP). The study group consisted of 54 patients (32 male and 22 female, mean age 64 years) with chronic heart failure (HF) treated with CRT. BNP, high-sensitivity C-reactive protein (hs-CRP), interleukin 6 (IL-6), and neopterin were measured three times: after 26-28 weeks of continuous CRT (CRT-on), 48 h after its cessation (CRT-off), and 48 h after switching the CRT-on again. CRT interruption resulted in a significant worsening of left ventricular systolic function: reduction of cardiac output (CO), dP/dt, and left ventricular ejection fraction (LVEF), as well as deterioration of mitral regurgitation in the CRT responder group. A significant increase in serum concentrations of hs-CRP, neopterin, IL-6, and BNP was noted in this subpopulation. In CRT nonresponders, no significant changes were observed. In responders the changes in serum concentrations of hs-CRP, IL-6, neopterin, and BNP, following CRT interruption, significantly correlated with the respective changes in thoracic fluid content (TFC) and inversely correlated with LVEF changes. Even short (48 h) interruption of long-term CRT led to a significant increase of proinflammatory cytokines and BNP concentrations in responders. The changes in hs-CRP, IL-6, neopterin, and BNP concentrations correlated with the change in TFC-marker of pulmonary congestion and inversely correlated with the change in LVEF.
PurposeInteratrial block (IAB) frequently coexists with sinus node disease and is considered a risk factor of left atrial dysfunction, atrial arrhythmias, and heart failure development. Conventional right atrial appendage (RAA) pacing impairs intra- and interatrial conductions and consequently prolongs P wave duration. Biatrial (BiA) pacing helps correct IAB, but its advantageous influence remains controversial. The aim of the study was to compare the effects of BiA and RAA pacing on cardiac hemodynamics and serum concentrations of inflammatory markers and neuropeptides.MethodsTwenty-eight patients with IAB and preserved atrio-ventricular conduction treated with BiA pacing were studied. Standard invasive hemodynamic measurements were performed during BiA and RAA pacings. Furthermore, the influence of 1 week of BiA and RAA pacing on neuropeptides: atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) and markers of inflammation: high sensitivity C-reactive protein (hs-CRP), interleukin 6 (IL-6), and neopterin was examined.ResultsBiA pacing resulted in significant increase of cardiac output (CO) and reduction of pulmonary capillary wedge pressure. We demonstrated significantly lower concentrations of ANP, hs-CRP, IL-6, and neopterin after 1 week of BiA in comparison to RAA pacing. BNP levels remained unchanged.ConclusionsBiA pacing in comparison to RAA pacing improves hemodynamic performance in patients with IAB and preserved atrio-ventricular conduction. BiA pacing is associated with reduction of ANP and markers of inflammation (hs-CRP, IL-6, and neopterin).
Introduction: Immune system activation and oxidative stress are involved in the pathogenesis of heart failure (HF). We aimed to test the hypothesis that upgrading from right ventricular pacing (RVp) to biventricular pacing (BiVp) can counteract these phenomena. Methods: 28 HF patients, with BiVp were switched to RVp for one week, and then returned to BiVp. Immediately prior to, and 48 h after the return to BiVp, left ventricular (LV) systolic function was evaluated by echocardiography, and serum N-terminal pro-brain natriuretic peptide (NTproBNP), C-reactive protein (CRP), tumor necrosis factor alpha (TNF-a), interleukin 6 (IL6), nitric oxide metabolites (NO x ) and malondialdehyde (MDA) were assayed. Results: LV systolic function significantly improved 48 h after switching from RVp to BiVp: Ao-VTI ( p < 0.001), SV ( p < 0.001) and CO ( p < 0.001), and mitral regurgitation significantly decreased ( p = 0.003). At the same time, indices of peripheral immune activation decreased: TNF-a ( p = 0.02) and IL6 ( p < 0.001). MDA decreased ( p < 0.001), whereas NO x increased ( p = 0.04). NTproBNP and CRP did not change. In addition, in ''responders'' (i.e. CO increase > 10% during BiVp vs. RVp) NTproBNP decreased and NO x increased. However, during BiVp, the decreases in TNF-a, IL6, and MDA occurred both in responders and in non-responders and were accompanied by a reduction in mitral regurgitation. Conclusion: The beneficial effect of BiVp compared to RVp extends beyond improving cardiac haemodynamics and comprises a decrease in immune activation accompanied by an increase in serum NO x and decrease in serum MDA.
The aim of the study was to compare the bidirectional transoesophageal DC cardioversion (BOC) with unidirectional transoesophageal DC cardioversion (UOC) and to evaluate, if the reversion of the polarity of electrodes alters the effectiveness and the amount of energy during BOC. UOC was attempted in 300 patients (pts) with atrial fibrillation (AF) and BOC in 241 pts with AF. In UOC mode shocks were delivered between the 4-ring oesophageal electrode (cathode) and the chest pad (anode) positioned in the precordial region. In BOC shocks were delivered between the same oesophageal electrode and two chest pads joined with each other, positioned on both sides of the sternum. First 147 pts were cardioverted with the oesophageal electrode as a cathode, next 94 with an anode in oesophageal position. The effectiveness of both modes (UOC and BOC) was very high, however in pts with chronic AF success rate was better in BOC approach (82% vs 100%). BOC, compared with UOC, allowed to decrease the threshold defibrillation significantly: in pts with recent onset of AF from 61.5 J to 33.3 J and in pts with chronic AF from 99.8 J to 75.2 J. In pts with long standing AF the reduction of the defibrillation threshold was statistically not significant (from 68.6 J to 50.6 J). The effectiveness of BOC was also very high independently of the polarity of electrodes. The change of the polarity did not affect the minimal and total successful energy of shocks, too. In pts with oesophageal electrode as a cathode defibrillation threshold was 48.4 J and in pts with the anodal electrode 43.7 J. In conclusions we found BOC as a very effective method in pts with AF. Defibrillation threshold in BOC is lower than in UOC and the polarity of electrodes does not influence the success rate and successful energy.
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