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Updated: Aug 6, 2026

Echocardiographic Assessment Using Subxiphoid-Only Examination for Hypotensive Patients
Published on: April 18, 2025
Subclinical hypotension in acute decompensated heart failure: prognosis and treatment implementation
Giulio Savonitto1, Davide Stolfo2, Mattia Emanuele Biber3
1Department of Medicine (DAME), University of Udine, Udine, Italy; Department of Medicine Clinical Science and Education, Södersjukhuset Karolinska Institutet, Stockholm, Sweden.
Aims:
Patients with subclinical hypotension are common but underrepresented in acute decompensated heart failure (ADHF) clinical studies. Whether low baseline systolic blood pressure (SBP) impacts long-term prognosis or limits guideline-directed medical therapy (GDMT) remains uncertain.
Methods And Results:
We analyzed 2105 ADHF admissions from the TRI-AHF registry; after excluding patients on inotropes/vasopressors or mechanical support, 1590 were included (96 hypotensive, SBP ≤100 mmHg; 1494 normotensive). Propensity score-matching yielded 92 hypotensive and 216 normotensive patients (effective ratio ≈1:2.35). The primary endpoint was 1-year all-cause mortality or first HF hospitalization; secondary analyses were at 5 years. GDMT prescription and uptitration (RAASi/ARNI, beta-blockers, MRAs) were assessed, in the HFrEF population, at discharge and 1 year. In the matched cohort, admission hypotension was associated with higher 1-year risk (HR 2.16, 95% CI 1.47-3.17) and persisted at 5 years (HR 1.80, 95% CI 1.32-2.46); the association was stronger in women (p-interaction=0.032). Spline analysis showed a non-linear risk increase below ∼100 mmHg. In HFrEF, admission hypotension was not independently associated with reduced GDMT prescription or uptitration at discharge or 1 year; optimization was more strongly influenced by renal dysfunction, absence of prior therapy, and older age, with secular increases in MRA use/composite optimization and a modest decline in RAASi/ARNI ≥50% at discharge.
Conclusion:
Subclinical hypotension at ADHF admission identifies a fragile, high-risk phenotype with adverse outcomes, without clear evidence of independently impaired GDMT implementation. Recognition of this profile should prompt individualized, physiology-guided strategies to safely optimize therapy.
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