The present study investigates the influence of cardiovascular parameters on glaucomatous damage and progression. In the previous literature, the most recognized systemic cardiovascular factor for glaucoma progression was high systemic blood pressure, and also low blood pressure was considered a major risk factor. It was hypothesized that there is a U-shaped correlation between blood pressure and glaucoma damage. Other systemic parameters discussed are vasospastic susceptibility and migraine.
This study of Marshall et al. evaluated structural and functional parameters of glaucoma damage at baseline and during follow-up to investigate the association between cardiovascular disease and glaucoma damage in a cohort of 1314 patients (2628 eyes). The parameters tested included baseline and longitudinal SD OCT imaging of the macular ganglion cell/interplexiform layer thickness (mGCIPL) and the peripapillary nerve fiber layer (pRNFL) as well as Humphrey visual field assessment. In their concept, retinal vascular hypoperfusion may predispose damage of retinal ganglion cells at an IOP comparable with that of the normal population. In the present study, there was a correlation between systemic hypertension and initial damage to the mGCIPL and pRNFL as well as between high BP and mGCIPL pregression and VF progression, respectively. The authors therefore assume that hypertension is particularly harmful via vascular pathways to the macula. The association between systolic blood pressure and structural progression was comparable to that observed between intraocular pressure and structural progression. In addition, there might be an association between antihypertensive therapy and glaucoma progression due to the overtreatment at nighttime, resulting in nocturnal hypotension. The association between mGCIPL progression and blood pressure, but not IOP, suggests that vascular pathways may be particularly important in glaucomatous damage of the macula. The authors also found that a higher systolic blood pressure was associated with an increased risk of visual field progression and mGCIPL progression. The observed relationship between blood pressure and IOP implies that the effects of hypertension on glaucomatous progression may be mediated partly by IOP pathways. One challenge of interpretation of GCIPL damage is a possible overlap with age-related macula degeneration (AMD) which is frequent in the age group of glaucoma patients.
In hypercholinesterolemia a similar bimodal influence can be assumed: Sequelae from arteriosclerosis would impair the microvasculature of the mGCIPL complex and the pRNFL, but statins ‐ a frequent therapeutic approach ‐ might be also neuroprotective. In the present study, statin use was predictive of baseline mGCIPL defects, whereas no correlation was found between cholesterol parameters and structure.
Myocardial infarction was found to be associated with a higher baseline damage of the mGCIPL, although the authors suggest further elucidation of this correlation.
Considering that the ganglion cell body (as measured in the macula area) and the nerve fiber, (being the axon of the same GC body and measured at the peripapillary retina) are the same neuron, a separate degeneration of one or the other does not seem plausible. Hence it is not clear from the data presented why pRNFL should behave differently from mGCIPL.
However, taking the findings as a whole and probably not as a specific proof for damage of one specific location by cardiovascular disease, the results of this paper are of great importance to the concept of mutual impact of IOP and vascular factors for glaucoma damage and progression.