Key result
HFrEF is linked to ~55% lower retinal arterial vasodilation compared to HFpEF.
Why the study?
Vascular dysfunction plays a key role in heart failure and retinal vascular function partly mirrors cardiac vasculature, but the association between retinal vascular dysfunction and LVEF in heart failure was unknown.
Cohort (n=270)
No
Retinal microvascular function decreases progressively with lower LVEF in heart failure patients, while HFpEF patients exhibit greater baseline retinal arteriolar constriction, suggesting distinct underlying microvascular pathophysiologies across HF phenotypes.
Greater retinal microvascular impairment in HFrEF/HFmrEF than HFpEF may support noninvasive phenotyping; leaves open whether it reflects cardiac microvascular differences or alters management.
Background Vascular dysfunction is a key factor for the development, progression and prognosis of heart failure (HF) and a target of different therapeutic strategies. In the current guidelines diagnostic and therapeutical strategies for HF are different according to left ventricular ejection fraction (LVEF). Retinal vascular function partly mirrors the vasculature in the heart. The association of retinal vascular dysfunction and LVEF is currently unknown. Methods In this observational, single center, cohort study, HF patients of different aetiologies were prospectively enrolled and divided according to HF with preserved (HFpEF, LVEF >50%), mildly reduced (HFmrEF, LVEF 40-50%) and reduced ejection fraction (HFrEF, LVEF <40%). Retinal vascular function was quantified using a retinal vessel analyzer, measuring flicker-light induced retinal arterial vasodilation (FIDart). Additionally other vascular parameters, such as flow mediated dilatation (FMD) and pulse wave velocity (PWV) were assessed. Results 270 HF patients were included. Of this study population, 75 patients were categorised HFpEF (mean age 63.6 ± 14.1 years, 29.3% female), 37 HFmrEF (66.3 ± 11.4 years, 21.8% female) and 158 HFrEF (61.5 ± 11.8 years, 22.2% female). Retinal vascular function in patients with HFrEF and HFmrEF was significantly more impaired compared to patients with HFpEF (mean FIDart HFpEF 2.2 ± 2.2% vs. HFmrEF 1.3 ± 1.4%, p=0.04; HFpEF 2.2 ± 2.2% vs. HFrEF 1.0 ± 1.5% p<0.001, see Figure). Overall, retinal arterioles were more constricted in HFpEF compared to HFrEF (mean central retinal arteriolar equivalent [CRAE] 181.34 ± 20.3 μm vs. 190.0 ± 18.3 μm, p=0.003, respectively). There was no difference in FMD and other vascular parameters. Conclusion A gradual decrease in retinal vascular function was observed according to reduction of EF. HFpEF patients are characterised by a vasoconstrictive retinal arterial pattern at baseline. This may reflect different pathophysiological mechanisms underlying retinal vascular function in HFpEF and HFrEF.
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Piciacchia et al. (2026) conducted a cohort in Heart failure (n=270). Heart failure with reduced or mildly reduced ejection fraction (HFrEF and HFmrEF) vs. Heart failure with preserved ejection fraction (HFpEF) was evaluated on Flicker-light induced retinal arterial vasodilation (FIDart) (p=<0.001). HFrEF and HFmrEF were associated with significantly impaired retinal arterial vasodilation compared to HFpEF (mean FIDart 1.0% and 1.3% vs 2.2%; p<0.001 and p=0.04).
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