Abstract
Right heart failure is characterized by morphological and functional changes. We wish to advance the concept that the RV afterload by itself is insufficient as an explanation of the mechanism of RV failure and that RVF prevention and preservation of RV function are important treatment goals for patients with severe PAH. We also take the position that RVF is potentially reversible. This has been shown experimentally in the Su/Hx rat model of severe RVF, where carvedilol treatment has reversed RVF without reducing the RV afterload.[10] This “proof of principle” investigation has stimulated the search for mechanisms and molecular targets of RVF reversibility (Table 2). Mitochondrial energy metabolism is compromised during RVF and β-adrenergic receptor blockade[43] and perhaps diet or excersie may improve cardiac mitochondrial function.[48,49] Both the positive and negative impact of neuroendocrine factors[3,50] on a right ventricle “under pressure” deserve detailed studies.
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CITATION STYLE
Voelkel, N. F., Gomez-Arroyo, J., Abbate, A., & Bogaard, H. J. (2013). Mechanisms of right heart failure—A work in progress and a plea for failure prevention. Pulmonary Circulation, 3(1), 137–143. https://doi.org/10.4103/2045-8932.109957
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