Key result
Low birth weight is associated with retinal arteriolar narrowing, suggesting these microvascular changes may be an intermediate pathway linking early life exposures to cardiovascular disease.
Retinal arteriolar narrowing may serve as a microvascular marker linking low birth weight and early life exposures to the later development of hypertension and cardiovascular disease.
Retinal arteriolar assessment may refine CVD risk stratification in low birth weight adults; leaves open causal pathways for prospective trials.
Low birth weight is an indicator of exposure to unfavorable fetal environment and has been associated with the development of hypertension and cardiovascular disease in adulthood. There is now growing evidence suggesting that alterations in the microcirculation associated with exposure to a suboptimal in utero environment play a key role in the development of cardiovascular disease. Proposed hypothetical mechanisms include: fetal circulatory redistribution, impaired synthesis of elastin, and endothelial dysfunction in response to antenatal and postnatal environment. More recent studies have shown associations of low birth weight with capillary rarefaction and narrowing retinal arteriolar caliber in both children and adults. This suggests that vascular adaptations in utero persist into maladaptive circulatory changes in adulthood, which may reflect an increased susceptibility to hypertension and cardiovascular disease later in life. Therefore, the association between low birth weight and narrower retinal arteriolar caliber, together with associations between narrower retinal arteriolar caliber and risk of hypertension and cardiovascular disease, suggest that retinal arteriolar narrowing may be a marker on the microvascular pathway and mechanisms linking early life exposures and subsequent cardiovascular disease.
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Sasongko et al. (2010) conducted a review in Cardiovascular disease and hypertension. Low birth weight was evaluated. Low birth weight is associated with retinal arteriolar narrowing, suggesting these microvascular changes may be an intermediate pathway linking early life exposures to cardiovascular disease.
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