Biventricular versus right ventricular pacing decreases immune activation and augments nitric oxide production in patients with chronic heart failure.
BACKGROUND
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-alpha), 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-alpha (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-alpha, IL6, and MDA occurred both in responders and in non-responders and were accompanied by a reduction in mitral regurgitation.


CONCLUSIONS
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.
Rubaj
Andrzej
A
Department of Cardiology, Medical University of Lublin, Poland. arubaj@yahoo.com
Ruciński
Piotr
P
Rejdak
Konrad
K
Oleszczak
Krzysztof
K
Duma
Dariusz
D
Grieb
Paweł
P
Kutarski
Andrzej
A
D000368:Aged; D000369:Aged, 80 and over; D002303:Cardiac Output, Low / Q000276:immunology* / Q000503:physiopathology; D002304:Cardiac Pacing, Artificial / Q000009:adverse effects / Q000379:methods*; D002908:Chronic Disease; D005260:Female; D006352:Heart Ventricles / Q000294:innervation*; D006801:Humans; D007249:Inflammation; D015850:Interleukin-6 / Q000276:immunology; D008297:Male; D008315:Malondialdehyde / Q000032:analysis / Q000276:immunology; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain; D009569:Nitric Oxide / Q000096:biosynthesis / Q000276:immunology*; D010138:Pacemaker, Artificial; D013599:Systole; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology; D016277:Ventricular Function, Left / Q000276:immunology* / Q000502:physiology
D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D020097:Natriuretic Peptide, Brain; D009569:Nitric Oxide; D008315:Malondialdehyde