Myocardial inflammation in experimental acute right ventricular failure: Effects of prostacyclin therapy

Challenges and opportunities in treating inflammation associated with pulmonary hypertension

“…In this group of patients, it is presently unclear whether a smoldering inflammation harbored in the small lung vessels contributes to the lung vascular disease or whether the inflammation is an obligatory accompaniment of lung vascular injury. Steroid- or aspirin treatment have been without impact on PAH (24), and long-term treatment with prostacyclin, which has anti-inflammatory properties (36,41,42), does not reverse established PAH.…”

“…Experimentally, over-expression of various cytokines has been demonstrated in heart failure models. While data derived from heart tissue of PAH patients are presently lacking, it is not farfetched to postulate that effective treatment of patients with severe PAH decreases the activity of inflammatory cells in the myocardium and the activation of cardiomyocytes and fibroblasts (36, 158). Alternatively, a reduction of the degree of systemic inflammation may also reduce the inflammatory response in the stressed heart.…”

The Roles of Immunity in the Prevention and Evolution of Pulmonary Arterial Hypertension

“…Both right and left ventricular blood flow reserve is compromised in severe PAH (114), and we wonder to what extent systemic and myocardial inflammation (115), and not only the pressure-overloaded right ventricle, limits heart function. The "sick lung circulation" (115) is one source of inflammatory mediators, and it is possible that ischemic or otherwise stressed myocardium produces its own performancelimiting factors (116). There is thus a strong rationale to explore, in various forms of PH, antiinflammatory and immune-modulating treatment options, very much in analogy to the options reviewed by Dinarello in the article "An Expanding Role for Interleukin-1 Blockade from Gout to Cancer" (64).…”

Epigenetics, inflammation and metabolism in right heart failure associated with pulmonary hypertension

“… 171 Dewatche et al. 174 observed that persistent RVF following PAB was associated with increased myocardial expression of IL-1β, IL-6, monocyte chemoattractant protein 1, pro-inflammatory IL-6/IL-10, concomitantly with neutrophil and macrophage infiltration; expression of IL-33 decreased, whereas macrophage inflammatory protein-1α expression remained unchanged. Thereby, they concluded that an acute afterload-induced RVF is associated with the activation of inflammatory processes.…”