Background: The effect of cardiac resynchronization therapy (CRT) on systemic inflammation
and neurohormonal alterations associated with heart failure is not well characterized.
Accordingly, we aimed to assess the long term effects of CRT on systemic inflammation and
neurohormonal factors in heart failure patients.
Methods and results: In 47 HF patients (NYHA III–IV) we evaluated, at baseline and after
one year of CRT: TNF-α, TNF soluble receptors (sTNFR1 and sTNFR2), insulin-like growth
factor-1α (IGF-1α), adiponectin, norepinephrine, pro-atrial natriuretic peptide (pro-ANP),
N-terminal-pro-brain natriuretic peptide (NT-proBNP) and angiotensin II, NYHA functional
class, quality of life (the Minnesota Living with Heart Failure questionnaire), a 6-minute walk
test and an echocardiogram. Long-term CRT decreased activation of renin–angiotensin system
(RAS) only in patients with reverse remodelling. It failed to prevent a decline in adiponectin
levels, regardless of reverse remodelling. NT-proBNP remained unchanged in patients with
reverse remodelling, whereas its levels increased in those without reverse remodelling. IGF-1α
increased with CRT, whereas CRT had no effect on pro-ANP and inflammatory markers.
Conclusions: Long-term CRT is associated with decreased RAS activation and stabilization
of NT-proBNP in heart failure patients with reverse remodelling. Long-term CRT, with or
without reverse remodelling, does not affect systemic inflammation and fails to prevent
a decline in adiponectin
