Abstract
Background: Most trials testing phosphodiesterase 5 inhibitors (PDE5I) in heart failure with preserved ejection fraction (HFpEF) yielded a neutral outcome possibly because of low myocardial cyclic guanosine monophosphate (cGMP) content, which reduces effectiveness of PDE5I. Angiotensin converting enzyme inhibitors (ACEI), angiotensin II receptor blockers (ARB) and statins (STAT) increase myocardial cGMP content through upregulated endothelial nitric oxide synthase. The acute and chronic effects on cardiac remodeling and dysfunction of PDE5I after optimized ACEI-ARB-STAT therapy were therefore evaluated.
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