Why the study?
Does targeting nitric oxide and PDE5 inhibition improve outcomes in patients with heart failure with preserved ejection fraction?
Does targeting nitric oxide and PDE5 inhibition improve outcomes in patients with heart failure with preserved ejection fraction?
Despite promising preclinical data showing reduced LV stiffness, clinical trials of NO and PDE-5 inhibitors in HFpEF have been neutral, prompting a reevaluation of this therapeutic target.
There has been considerable focus on the potential role of nitric oxide (NO) and phosphodiesterase (PDE)-5 inhibition in treating heart failure with preserved ejection fraction (HFpEF). However, the results from studies have been conflicting. In a preclinical study, pre-treatment of diabetic rats with a PDE-5 inhibitor, vardenafil, resulted in a significant decrease in left ventricle stiffness. However, the results from clinical trials have been neutral. In this perspective piece, the authors discuss whether or not it is time to move on from targeting NO and PDE5 for the treatment of HFpEF.
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Cruz et al. (2017) studied this question.
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