Why the study?
To clarify how cardiac and peripheral impairments to oxygen delivery and utilization contribute to exercise intolerance and adverse events, and relate to pathophysiologic trait diversity and multiplicity.
How do cardiac and peripheral impairments to oxygen delivery and utilization contribute to exercise intolerance and adverse events in HFpEF, and how does this relate to clinical phenogroup multiplicity?
Population
643 patients with HFpEF and 219 non-cardiac dyspnoea controls
Comparison
HFpEF patients across descriptive clinical trait phenogroups vs non-cardiac dyspnoea controls
Design
Cohort study with invasive cardiopulmonary exercise testing and clinical follow-up
Key result
Increasing clinical phenogroup multiplicity (≥2 vs 0-1 traits) in HFpEF patients was associated with a greater risk for heart failure hospitalization or death (HR 1.74; 95% CI 1.08-2.79).
Authors
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May support phenogroup-based risk stratification in HFpEF; leaves open whether targeting multiple traits improves outcomes.
Cohort (n=862)
How do cardiac and peripheral impairments to oxygen delivery and utilization contribute to exercise intolerance and adverse events in HFpEF, and how does this relate to clinical phenogroup multiplicity?
Effect estimate: HR 1.74 (95% CI 1.08-2.79)
In patients with HFpEF, greater multiplicity of clinical phenogroup traits is associated with worse exercise haemodynamics, poorer exercise capacity, and increased risk of heart failure hospitalization or death.
Larson et al. (2023) conducted a cohort in Heart failure with preserved ejection fraction (HFpEF) (n=862). Presence of multiple (≥2) clinical phenogroup traits vs. 0-1 clinical phenogroup traits was evaluated on Heart failure hospitalization or death (HR 1.74, 95% CI 1.08-2.79). Increasing clinical phenogroup multiplicity (≥2 vs 0-1 traits) in HFpEF patients was associated with a greater risk for heart failure hospitalization or death (HR 1.74; 95% CI 1.08-2.79).