Inflammation plays a key role in adverse right ventricular remodeling in pulmonary hypertension, suggesting anti-inflammatory strategies may serve as potential therapeutic targets.
Hypothesis-generating for anti-inflammatory strategies in pulmonary hypertension right ventricular remodeling; prospective human trials needed before clinical consideration.
Adverse right ventricular (RV) remodeling leads to ventricular dysfunction and failure that represents an important determinant of outcome in patients with pulmonary hypertension (PH). Recent evidence indicates that inflammatory activation contributes to the pathogenesis of adverse RV remodeling and dysfunction. It has been shown that accumulation of inflammatory cells such as macrophages and mast cells in the right ventricle is associated with maladaptive RV remodeling. In addition, inhibition of inflammation in animal models of RV failure ameliorated RV structural and functional impairment. Furthermore, a number of circulating inflammatory mediators have been demonstrated to be associated with RV performance. This work reviews the role of inflammation in RV remodeling and dysfunction and discusses anti-inflammatory strategies that may attenuate adverse structural alterations while promoting improvement of RV function.
No takes yet. Share an insight, caveat, or question.
Sydykov et al. (2018) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: