Initiation of angiotensin receptor-neprilysin inhibitors or mineralocorticoid receptor antagonists decreased diastolic pulmonary artery pressure by -1.56 mm Hg and -1.15 mm Hg, respectively.
Cohort (n=292)
Does the initiation of guideline-directed medical therapies (ARNI, MRA, SGLT2i, β-blockers) reduce pulmonary artery pressure in patients with heart failure?
Initiation of ARNI and MRA, but not SGLT2 inhibitors, is associated with a rapid and significant reduction in diastolic pulmonary artery pressure within 30 days in patients with heart failure.
Effect estimate: Change of -1.56 mm Hg (ARNI) and -1.15 mm Hg (MRA) (95% CI -3.54 to -0.40 (ARNI); -1.82 to -0.47 (MRA))
BACKGROUND: While clinical benefits of guideline-directed medical therapy in patients with heart failure (HF) are well established, acute hemodynamic changes after initiation of these agents are not well described. Wireless pulmonary artery pressure (PAP) monitoring using implantable sensors is ideally suited to determine changes in pressure following medication titration. METHODS: We compared PAP from 7 days pre-initiation to the 7-day period following 30 days of newly initiated treatment with core HF therapies: angiotensin receptor-neprilysin inhibitors, mineralocorticoid receptor antagonists, sodium-glucose co-transporter-2 inhibitors, and β-blockers in patients implanted with a PAP sensor (CardioMEMS, Abbott) as part of the GUIDE-HF study (Hemodynamic-Guided Management of HF). Patients with changes in loop diuretics or other core HF therapies during the 30-day interval were excluded from the analysis. RESULTS: Of 2358 patients in the study, 50 patients had new angiotensin receptor-neprilysin inhibitor initiation, 97 patients had new sodium-glucose co-transporter-2 inhibitor initiation, 112 patients had new mineralocorticoid receptor antagonist initiation, and 33 had new β-blocker initiation at least 30 days post-implant, continued to take the medication for at least 30 days, and were included in this analysis. Following angiotensin receptor-neprilysin inhibitor or mineralocorticoid receptor antagonist initiation, diastolic PAP decreased by -1.56 (95% CI, -3.54 to -0.40) and -1.15 (95% CI, -1.82 to -0.47) mm Hg, respectively, in the absence of changes in loop diuretics or other core HF therapies. By contrast, there was no detectable change in PAP following the new initiation of the sodium-glucose co-transporter-2 inhibitor. A trend to higher PAP was observed after β-blocker initiation though differences were not significant. CONCLUSIONS: These results may inform the selection of pharmacological therapy to manage elevated filling pressures during hemodynamic-guided therapy. REGISTRATION: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03387813.
Desai et al. (Thu,) conducted a cohort in Heart failure (n=292). Initiation of core HF therapies (ARNI, MRA, SGLT2i, or beta-blockers) vs. 7 days pre-initiation (baseline) was evaluated on Change in diastolic pulmonary artery pressure (PAP) (Change of -1.56 mm Hg (ARNI) and -1.15 mm Hg (MRA), 95% CI -3.54 to -0.40 (ARNI); -1.82 to -0.47 (MRA)). Initiation of angiotensin receptor-neprilysin inhibitors or mineralocorticoid receptor antagonists decreased diastolic pulmonary artery pressure by -1.56 mm Hg and -1.15 mm Hg, respectively.