Tricuspid regurgitation is a barrier to guideline-directed medical therapy implementation in patients with acute decompensated heart failure and reduced ejection fraction
Tricuspid regurgitation is a barrier to guideline-directed medical therapy implementation in patients with acute decompensated heart failure and reduced ejection fraction
Enrico Brollo,Daniele Cocianni,11 Authors,D. Stolfo
TLDR
The severity of TR in ADHF is a determinant of poor implementation of RASi/ARNi and beta-blockers therapy at 1-year follow-up; however, the lower mortality associated with treatment optimization was not influenced by TR severity.
Abstract
Guideline-directed medical therapy (GDMT) reduces mortality in heart failure with reduced ejection fraction (HFrEF), but multiple barriers prevent the correct implementation of recommended treatments.
We sought to evaluate the role of tricuspid regurgitation (TR) as an obstacle for GDMT implementation in a cohort of HFrEF patients after an episode of acute decompensated heart failure (ADHF).
We enrolled patients hospitalized for ADHF with left ventricular ejection fraction (LVEF) ≤ 40%. TR severity was categorized as moderate–severe or trivial-mild. Optimization of renin–angiotensin system inhibitors/angiotensin receptor-neprilysin inhibitors (RASi/ARNi), beta-blockers and mineralocorticoid receptor antagonists (MRA) therapy was defined when patients were prescribed these drugs at ≥50% of the target dose (TD) at 1-year follow-up.
858 patients were enrolled. At 12 months, patients receiving ≥50% TD of RASi/ARNi, beta-blockers and MRA were 51%, 29%, and 47% respectively. After adjustment for multiple confounders, moderate–severe TR was inversely associated with the likelihood of ≥50% TD up-titration of RASi/ARNi (OR = 0.572, P = .029) and of beta-blockers (OR = 0.526, P = .038), but not of MRA (OR = 0.995, P = .984). RASi/ARNi and beta-blockers optimization was associated with lower 1- and 5-years all-cause mortality risk regardless the severity of TR. The association between RASi/ARNi optimization and 5-years survival was more pronounced in patients with moderate–severe TR vs patients with trivial-mild TR (P for int = .039).
The severity of TR in ADHF is a determinant of poor implementation of RASi/ARNi and beta-blockers therapy at 1-year follow-up; however, the lower mortality associated with treatment optimization was not influenced by TR severity.
