Key result
Cardiac resynchronization therapy is a well-established treatment for chronic heart failure, but new predictors such as inflammatory markers are needed to identify potential responders.
Why the study?
Does cardiac resynchronization therapy reduce systemic inflammation in patients with chronic heart failure?
Does cardiac resynchronization therapy reduce systemic inflammation in patients with chronic heart failure?
Answers are grounded in this paper and cite their sources.
Highlights the potential of systemic inflammation reduction as a novel marker of response to cardiac resynchronization therapy in heart failure.
Chronic heart failure (CHF) is the final common pathway for various cardiac pathologies and, despite significant progress in its treatment in recent years, this complex clinical syndrome still has a poor prognosis.1,2 Cardiac resynchronization therapy (CRT) is a wellestablished option in the treatment of CHF that results in significant clinical improvements, ventricular reverse remodeling, and lower mortality in selected patients.2---4 However, based on current selection criteria, a significant proportion of patients with CHF do not respond positively to CRT. 5 It is therefore important to identify new predictors that will improve the selection of potential responders to this therapy.Although the pathophysiology of CHF is still poorly understood, neurohormonal stimulation and immune activation have been shown to be involved in the development and progression of this systemic disease.6,7 There is growing evidence that levels of various pro-inflammatory cytokines are elevated in patients with CHF, and that this inflammatory ଝ Please cite this article as: António N. Reduc ¸ão da inflamac ¸ão sistémica após terapêutica de ressincronizac ¸ão cardíaca: uma nova forma de resposta?Rev Port Cardiol.
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Natália António (2018) conducted an editorial in Chronic heart failure (CHF). Cardiac resynchronization therapy (CRT) was evaluated. Cardiac resynchronization therapy is a well-established treatment for chronic heart failure, but new predictors such as inflammatory markers are needed to identify potential responders.
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