Evolving use of natriuretic peptide receptor type-C as part of strategies for the treatment of pulmonary hypertension due to left ventricle heart failure. (15th April 2019)

• Record Type: Journal Article
• Authors: Egom, Emmanuel E.; Maher, Vincent; El Hiani, Yassine
• Is Part Of: International journal of cardiology. Volume 281(2019)
• Page Start: 172
• Page End: 178
• Publication Date: 2019-04-15
• Subjects: PH, pulmonary hypertension -- LV-HF, left ventricular heart failure -- NPR-C, natriuretic peptides clearance receptor (type C); Cardiology -- Periodicals; Electronic journals; 616.12
• DOI: 10.1016/j.ijcard.2018.06.001
• Languages: English
• ISSNs: 0167-5273

Abstract

Abstract: Pulmonary hypertension (PH) due to left ventricular heart failure (LV-HF) is a disabling and life-threatening disease for which there is currently no single marketed pharmacological agent approved. Despite recent advances in the pathophysiological understanding, there is as yet no prospect of cure, and the majority of patients continue to progress to right ventricular failure and die. There is, therefore an urgent unmet need to identify novel pharmacological agents that will prevent or reverse the increase in pulmonary artery pressures while enhancing cardiac performance in PH due to LV-HF. In the present article, we first focused on the Natriuretic Peptide Receptor type C (NPR-C) based therapeutic strategies aimed at lowering pulmonary artery pressure. Second, we reviewed potential NPR-C therapeutic strategies to reverse or least halt the detrimental effects of diastolic dysfunction and impaired nitic oxide signalling pathways, as well as possibilities for neurohumoral modulation. Highlights: PH due to LV-HF is a disabling and life-threatening disease for which there is currently no single marketed pharmacological agent approved. The failure of to date therapeutic strategies suggests that important pathogenic mechanisms have neither been identified nor therapeutically targeted. NPR-C based therapeutic strategies may lower pulmonary artery pressure and have a positive impact on myocardial oxygen delivery and consumption for energy metabolism. Evidence also suggests NPR-C therapeutic strategies may reverse or at least halt the detrimental effects of diastolic dysfunction and impaired NO signaling. NPR-C should now be considered as a critical protective receptor in the heart rather than just being a clearance receptor.