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Published on: October 22, 2014
Retinal microcirculation as a window to coronary artery disease
Weronika Kowalczyk1, Mikołaj Basza2, Joanna Przybek-Skrzypecka1
1Department of Ophthalmology, Medical University of Warsaw, Poland; SPKSO Ophthalmic University Hospital in Warsaw, Poland.
Insights
Retinal imaging offers accessible biomarkers for coronary artery disease (CAD) risk, reflecting both epicardial atherosclerosis and microvascular dysfunction. This approach aids in differentiating CAD endotypes and improving patient risk assessment.
Area of Science:
- Ophthalmology and Cardiology
- Biomarkers and Diagnostic Imaging
- Vascular Biology
Background:
- Coronary artery disease (CAD) encompasses epicardial stenosis and ischemia due to microvascular dysfunction.
- Current coronary artery disease screening methods are invasive and costly.
- Retinal imaging offers accessible biomarkers reflecting both epicardial atherosclerosis and coronary microvascular dysfunction.
Purpose of the Study:
- To summarize the links between retinal measures and coronary anatomy, physiology, and clinical phenotypes.
- To inform risk assessment strategies for coronary artery disease.
- To explore the potential of retinal imaging in differentiating CAD endotypes.
Main Methods:
- Narrative synthesis of studies.
- Linking retinal structure and perfusion metrics (fundus, OCT/OCTA, FAZ, choroidal indices) with coronary angiography, functional ischemia indices (CFR, IMR, MFR), and clinical phenotypes (obstructive CAD, INOCA, slow coronary flow).
Main Results:
- Retinal microvascular alterations (narrower arterioles, wider venules, lower arteriovenous ratio) predict CAD, MI, stroke, and mortality.
- OCT angiography shows reduced vessel density and enlarged FAZ correlating with CAD severity and risk profiles.
- Retinal findings in coronary microvascular dysfunction (CMD)/Ischemia with Non-Obstructive Coronary Arteries (INOCA) show generalized microvascular dysfunction, including sex-specific differences and links to slow coronary flow.
Conclusions:
- Retinal imaging provides accessible biomarkers for systemic vascular alterations in CAD.
- Retinal imaging may assist in risk stratification and endotype differentiation for CAD.
- Clinical translation requires standardized studies, AI analytics, and integration with quantitative coronary physiology to overcome current limitations.
Abstract:
Coronary artery disease includes obstructive epicardial stenosis and ischemia with non-obstructive coronary arteries driven by microvascular dysfunction. Population screening is limited by the invasiveness and cost of current coronary tests. Retinal imaging provides accessible biomarkers that reflect both epicardial atherosclerosis and coronary microvascular dysfunction, thereby supporting risk stratification and endotype differentiation in coronary artery disease. The aim was to summarize links between retinal measures and coronary anatomy, physiology, and clinical phenotypes to inform risk assessment in cardiology. Narrative synthesis of studies linking retinal structure and perfusion (fundus metrics, OCT/OCTA vessel density in superficial/deep plexuses, foveal avascular zone, choroidal indices) with angiographic burden, functional indices of ischemia (CFR, IMR, PET-derived myocardial flow reserve), and clinical endotypes (obstructive CAD, INOCA, slow coronary flow). Retinal microvascular alterations-narrower arterioles, wider venules, and lower arteriovenous ratio-predict CAD, myocardial infarction, stroke, and cardiovascular mortality; OCT angiography frequently demonstrates reduced vessel density and enlarged FAZ correlating with stenosis burden, multivessel disease, and systemic risk profiles. In CMD/INOCA, patterns consistent with generalized microvascular dysfunction are observed, including sex-specific differences (e.g., venular calibre changes in women with microvascular angina) and associations between retinal metrics and myocardial flow abnormalities such as slow coronary flow. Retinal imaging yields accessible biomarkers reflecting systemic vascular alterations associated with both epicardial coronary atherosclerosis and coronary microvascular dysfunction and may assist risk stratification and endotype differentiation in CAD; however, clinical translation is constrained by device/segmentation heterogeneity, comorbidity confounding, small cross-sectional designs, and limited integration with quantitative coronary physiology. Standardized, multicentre longitudinal studies and AI-enhanced analytics are needed to establish prognostic value and clinical utility.
