WHAT YOU NEED TO KNOW
- Researchers analyzed retinal images from more than 90,000 people in the AlzEye and U.K. Biobank studies.
- People who later developed AFib had thinner mGCIPL retinal layers an average of 4 years before hospital presentation.
- About 62% of people with AFib did not know they had the condition before diagnosis in a recent study.
- Experts said more research is needed before retinal imaging can become a practical AFib screening tool.
Atrial fibrillation can remain hidden because it may cause no noticeable symptoms or produce symptoms that resemble other common problems. A new study suggests subtle changes in the retina could help identify the heart rhythm condition as early as 4 years before diagnosis.
About 52.55 million people worldwide are estimated to be living with atrial fibrillation, also known as AFib. The condition occurs when the upper and lower chambers of the heart beat out of sync, resulting in a fluttering or racing heartbeat.
People with AFib face an increased risk of stroke, heart failure, heart attack, and dementia. Yet the condition frequently goes undetected until it becomes a problem, and one recent study found that about 62% of people with AFib did not know they had it before diagnosis.
The new research, published in PLOS Digital Health, examined whether retinal imaging might reveal signs associated with AFib. Researchers analyzed optical coherence tomography scans and color retinal photographs from more than 90,000 people participating in the AlzEye and U.K. Biobank cohort studies.
Optical coherence tomography, commonly called OCT, allows clinicians to examine layers within the retina, the light sensitive tissue at the back of the eye. Fundus photographs provide additional images of the retina and its visible blood vessels.
“The retina is the only place in the body where blood vessels and nerve fiber tissue can be analyzed noninvasively with commonly available eye tests like OCT scans or fundus photographs,” said lead study author Josef Huemer, MD.
Huemer is a consultant ophthalmologist at Moorfields Eye Hospital and an honorary senior research fellow at the Institute of Ophthalmology University College London. He said previous research had identified retinal signals associated with ocular events among people with AFib.
At the end of the study, researchers found that participants with AFib consistently had a thinner macular ganglion cell and inner plexiform layer, known as the mGCIPL. This measurement combines two retinal layers involved in processing and relaying visual information to the brain.
The ganglion cell layer carries visual information from the retina toward the brain. The inner plexiform layer is involved in transmitting information about visual signals such as motion and changes between light and darkness.
“Thinning of the mGCIPL is a sign of retrograde, or past, degeneration, and is therefore not disease specific,” Huemer explained. He said the change was most likely caused by mini strokes in the brain, which are a common finding among people with AFib.
Researchers observed the finding in both study cohorts, including hospital patients and healthy volunteers. Huemer said this consistency gave the team confidence in the results, although the retinal change itself is not exclusive to AFib.
The researchers also detected thinning of the inner nuclear layer. Huemer said this layer is not affected by retrograde degeneration, and the team’s hypothesis is that cardiovascular disease may cause the thinning because the area is vulnerable to micro strokes in the eye.
Among participants who did not have AFib when their retinal images were collected, those who later developed the condition had thinner mGCIPL layers an average of 4 years before presenting to a hospital with AFib. The finding raises the possibility that routine retinal imaging could contribute to earlier risk assessment.
Huemer said OCT scans can quantify this thinning and are widely available in primary care ophthalmology, including high street optometrists in the U.K. The next step is to determine whether the finding can improve risk calculations and help identify people who should receive long term electrocardiogram monitoring.
The research team is conducting further OCT image analysis involving cardiovascular disease in large scale datasets. Huemer said the researchers have also expanded their dataset to support more research into oculomics, the study of links between eye features and wider health.
Benjamin Bert, MD, a board certified ophthalmologist at MemorialCare Orange Coast Medical Center, was not involved in the study. He said researchers hypothesize that silent ischemia, involving small episodes of poor blood flow, could damage retinal tissue and cause the observed thinning.
Bert added that mild damage to the brain could potentially lead to cellular atrophy in the retina. These proposed explanations remain hypotheses rather than established mechanisms connecting AFib with retinal changes.
Cheng-Han Chen, MD, a board certified interventional cardiologist and medical director of the Structural Heart Program at MemorialCare Saddleback Medical Center, was also not involved. He said routine eye imaging could potentially broaden clinicians’ ability to recognize AFib risk and identify people who might benefit from closer cardiovascular monitoring.
“The underlying mechanism linking AFib with changes in the cells or blood vessels of the eye is not yet well understood,” Chen explained. He said future research must determine which eye changes are associated with AFib, whether they reliably predict the condition, and how retinal imaging performs across different populations.
Chen described the findings as promising but emphasized that they represent an early step toward understanding a possible connection between the heart and eye. Researchers must still establish whether the technique could ultimately become a practical screening tool.
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