In this study, we investigated the retinal vessel
caliber, choroidal thickness, and OPP in patients with
low cardiac output. Our results showed that choroidal
thickness, retinal vascular caliber, and foveal thickness
were similar among patients with chronic systolic
heart failure and healthy individuals. Additionally, no
significant correlation was observed between EF and
retinal-choroidal vessel thickness, and OPP did not
significantly affect the RAC, RVC, or SFCT.
Retinal vessel diameter provides information about
the microcirculation and can reflect the vascular
effects of some systemic diseases.[7-10] A narrower
RAC is associated with systemic arterial hypertension
and coronary heart disease, whereas a wider one is
associated with diabetes mellitus, lipid abnormalities,
and smoking.[7-10] In our study, we found that low
cardiac output was associated with neither RVC nor
RAC alterations. These outcomes may suggest that
the inner retina receives enough blood flow to function
properly even with low cardiac output.
Choroidal thickness measurements have become
popular, since the development of enhanced depth
OCT, and among the various results reported in
researches, systemic diseases have been shown to
influence choroidal thickness.[11-14] The choroidal
thickness increases with diabetes mellitus,
hypercholesterolemia, and acromegaly, yet decreases
with systemic sclerosis.[11-14] In our study, however,
low EF did not significantly affect the choroidal
thickness. In another study, Altinkaynak et al.[5]
found that SFCT was lower in patients with chronic
heart failure, resulting possibly from different patient
characteristics or systemic medications used. The
aforementioned study included patients who had EF
lower than 55%, whereas our study included those
with EF lower than 40%.
Several systemic diseases such as diabetes mellitus
and arterial hypertension are known to be associated
with a thicker macula.[15,16] We found that chronic
heart failure did not cause any significant increase or
decrease in the macular thickness, and the similarity
of visual acuity values in the study and control groups
might confirm those outcomes regarding the macular
thickness. The IOP values were also found to be
similar in both groups. In contrast to our results,
Meira-Freitas et al.[17] reported that chronic heart
failure was associated with lower IOP, whereas similar to our results, Altinkaynak et al.[5] found no significant
difference in the IOP measurements between the heart
failure patients and healthy controls.
Furthermore, several peripheral vascular
compensatory mechanisms may contribute to low
cardiac EF due to chronic heart failure.[18] Choi et
al.[19] reported that cerebral blood flow decreased
with chronic heart failure and their results might be
generalized for ocular blood flow, as well. However,
the authors found that cerebral blood flow was
not associated with EF.[19] Although alterations in
the RAC, RVC, and SFCT concurred with the
peripheral vascular effects of chronic heart failure,
the differences were not statistically significant in our
study. According to our results, gross pathological
ocular vascular alterations in chronic heart failure are
unlikely, since patients with such conditions usually
do not have visual or ocular problems, as assessed by
routine ophthalmological examinations.
Regarding the clinical relevance, our study showed
that potential ocular alterations related to low amounts
of ocular blood flow in chronic heart failure did not
include choroidal thickness or retinal vessel caliber.
By contrast, ocular ischemia occurred when a stenosis
of 90% of the common or internal carotid arteries
was present and retinal-choroidal vascular thickness
decreased as a result of low ocular blood flow.[20,21] The
choroid nourishes the outer retinal layers, and retinal
vessels supply blood to the inner retinal layers. The
proper functioning of both structures is essential for
normal vision, and their anatomy does not change with
low cardiac output.
Nonetheless, there are some limitations
to this study. First, having fundus fluorescein
and indocyanine green angiographies to show
additional chorioretinal vascular parameters such
as hypoperfusion would have been helpful. Second,
the sample size could have been larger, despite
the difficulty of identifying low cardiac output
patients without any associated systemic diseases.
Third, we included patients with heart failure due
to low EF in this study. However, EF patients with
normal/preserved heart failure are also present.
Hence, if an EF with normal/preserved heart failure
patient group was available, it might have resulted in
a more accurate comparison. Fourth, the EF of the
patient group in the study ranged from 30 to 40%.
If patients with lower EFs (such as 20 to 30% versus
10 to 20%) were included, interesting results could have been obtained. Finally, the patients included
in the study were those with non-ICPM. If ICMP
patients were included, more robust results might
have been attained.
In conclusion, low ejection fraction due to chronic
systolic heart failure does not significantly alter the
retinal vessel or choroidal thickness measurements.
Additionally, this condition exerts no significant effect
on intraocular pressure, ocular perfusion pressure, or
foveal thickness. We, thus, suggest that there is no need
to measure cardiac ejection fraction for the evaluation
of subfoveal choroidal thickness and retinal vessel
caliber. Nevertheless, future studies investigating the
effects of coexistent systemic disorders in addition to
heart failure would likely clarify the hemodynamic
autoregulation of the posterior pole.
Declaration of conflicting interests
The authors declared no conflicts of interest with respect
to the authorship and/or publication of this article.
Funding
The authors received no financial support for the research
and/or authorship of this article.