Heart failure places a heavy social and economic burden in modern societies. Despite therapeutic advances, its prognosis is still worse than that of most cancers suggesting that important pathophysiological mechanisms remain unidentified. Inflammation contributes to the development and progression of heart failure, regardless of etiologies. Inflammatory response perpetuation may result either from excessive activation of proinflammatory cascades or disturbances in the resolution of inflammation. Although cardiovascular research has extensively investigated the proinflammmatory processes involved in heart failure pathophysiology, the mechanisms responsible for inflammation resolution in this syndrome remain largely disregarded.
In the latest years, several classes of lipid mediators of resolution of inflammation, such as lipoxins, resolvins, protectins and maresins, have emerged and there is increasing evidence that they exert cardiovascular, metabolic and renoprotective effects that might delay the onset and progression of heart failure. Some of these mediators or their synthetic analogues are under evaluation in clinical trials for several inflammatory conditions, including cardiovascular disease. There are also some drugs already used in general clinical practice (e.g low-dose aspirin, statins, ticagrelor) that can induce the synthesis of proresolving mediators, as well as therapies that may hinder inflammation resolution. There is a notable lack of studies regarding the effects on inflammation resolution of standard drugs used for heart failure treatment, such as beta-blockers, angiotensin converting enzyme inhibitors and diuretics, as well as the effects of their combination with other drugs used in the management of heart failure comorbidities. Higher severity of human chronic heart failure was recently shown to be associated with decreased levels of proresolving lipid mediators thus suggesting that current heart failure polytherapy does not effectively stimulate the resolution of inflammation. Thus, it is imperative to evaluate the impact of heart failure patient medication on inflammation resolution pathways in order to improve therapeutic effectiveness and disease prognosis.
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Reference: Reina-Couto, M.; et al. (2016). Resolving Inflammation in Heart Failure: Novel Protective Lipid Mediators, Curr. Drug Targets., DOI: 10.2174/1389450117666160101121135