Findings from this study suggest physicians should be hesitant to attribute abnormalities in optic nerve structural measures to hypertension. Photo: Getty Images.

Participants from the Atherosclerosis Risk in Communities study and nested Eye Determinants of Cognition study were observed over 30 years to gain long-term insight into their eye health. Specifically, black and white individuals had their BP measured six different times from 1987 to 2017 and were subsequently categorized into five BP patterns: sustained normotension; midlife normotension, late-life hypertension; sustained hypertension; midlife normotension, late-life hypotension and midlife hypertension, late-life hypotension.

The researchers used a model to predict associations of BP patterns with late-life OCT ganglion cell complex (GCC) and peripapillary retinal nerve fiber layer thickness (RNFL). Of the 931 eyes included from 931 patients, mean GCC and RNFL thickness measurements were 90.8μm ± 10.3μm and 89.9μm ± 11.2μm, respectively, in the sustained normotension pattern. The sustained hypertension pattern was not much different, with GCC and RNFL measurements of 89.4μm ± 11.9μm and 90.1μm ± 12.2μm, respectively.

Based on these averages, the researchers of the study note that no significant differences were found in GCC or RNFL thickness for any anomalous BP patterns. As such, they posit that the results “support prior studies that found no relationship between hypertension or antihypertensive treatment and glaucoma, suggesting that BP is not a significant risk factor for optic nerve damage in the general population.”

The researchers of the study do note that their definition of a clinically meaningful difference in GCC or RNFL thickness was classified as a difference of greater than or equal to 8μm, since a prior study indicated a mean decrease of 8μm was associated with initial visual field loss in RNFL thickness compared to healthy subjects. As such, they realize this threshold may not be generalizable to GCC thickness.

They also relay their inclusion of antihypertensive medication in defining hypertension, since those with nonhypertensive BP on this kind of medication presents biological differences from nonhypertensive patients not on the medication. As one previous study outlines, these biological differences were noted in disc rim area and cup area between patients with normal DBP resultant of the medication and those with normal DBP but not due to treatment.

Finally, the authors of the study compare their findings to similar ones previously conducted. They outline that one study found lower MAP and DBP to be associated with greater RNFL loss rates. However, no such findings were observed in hypotensive BP patterns in this study. The authors relay that this difference may be due to the discrepancy of participants who were glaucoma suspect, being 57% in the previous study, while only 5% in this study had glaucomatous optic nerve damage. They suspect that the results of this study may be more applicable to the general population, explaining that retinal structure measures could be different in a disease setting.

As their findings relate to clinical application, the authors of the study caution that “when caring for patients, practitioners should be hesitant in attributing abnormalities in optic nerve structural measures to hypertension, hypertensive treatment or hypotension.”