Brief Review
Glaucoma and Blood Pressure
Marc Leeman, Philippe Kestelyn
• Online Data Supplement
A rterial hypertension and glaucoma are age-related con-
ditions, and their prevalence is expected to rise in the
coming years. Because these conditions are common and age-
related, with race playing a major risk factor, they can often
coexist.1 There are complex interactions between blood pres-
sure (BP), intraocular pressure (IOP), and ocular perfusion
pressure (OPP), which is the difference between mean BP and
IOP. This brief review focuses on the role of BP, whether high
or low, in the prevalence and in the progression of glaucoma.
We searched the databases of MEDLINE and EMBASE,
as well as the reference lists of the retrieved articles, up to
2018. Key words were “glaucoma,” blood pressure,” “noc-
turnal pressure,” “ocular perfusion pressure,” “antihyperten-
sive.” We privileged systematic reviews, meta-analysis, and
the most recent articles.
Glaucoma: Pathophysiology and Treatment
Glaucoma is a leading cause of blindness, and visual im-
pairment and the leading cause of irreversible blindness
worldwide, with >60 million people affected.2 The com-
mon denominator of glaucomatous optic neuropathy is the
loss of axonal nerve fibers and the death of retinal ganglion
cells in the inner nuclear layer. Primary open-angle glaucoma
Downloaded from http://ahajournals.org by on May 13, 2022
(POAG), the most common type of glaucoma, is a chronic,
progressive optic neuropathy with characteristic morpholog-
ical changes at the optic nerve head and retinal nerve fiber
layer in the absence of other ocular disease or congenital
anomalies. Progressive retinal ganglion cell death and visual
field (VF) loss are associated with these changes.3 The axons
of the retinal ganglion cells form the nerve fiber layer and
leave the eye through the cribriform plate in the sclera form-
ing the optic disc. The central portion of the disc contains no
axonal nerve fibers and is called the cup or the excavation.
The rim of neuroretinal tissue around the cup contains the
axons. Comparing the size of the cup to the overall diameter
of the disc (cup-to-disc ratio) allows the observer to quantify
the amount of excavation (Figure 1). Deepening and widen-
ing of the cup (pathological excavation) is the characteristic
morphological change in POAG. It is the result of the loss of
retinal ganglion cell axons and of deformation and remodel-
ing of connective tissue. Because loss of the retinal ganglion
cell is associated with thinning of the retinal nerve fiber layer,
measurement of the thickness of this layer by means of optical
coherence tomography is one of the most common methods
From the Hypertension Clinic, Erasme University Hospital, Université Libre de Bruxelles, Belgium; on behalf of the Belgian Society of Hypertension
(M.L.); and Department of Ophthalmology, Ghent University, Belgium; on behalf of the Belgian Glaucoma Society (P.K.).
The online-only Data Supplement is available with this article at https://www.ahajournals.org/doi/suppl/10.1161/HYPERTENSIONAHA.118.11507.
Correspondence to Marc Leeman, Hypertension Clinic, Erasme University Hospital, route de Lennik 808, B-1070 Brussels, Belgium. Email marc.
leeman@erasme.ulb.ac.be
(Hypertension. 2019;73:944-950. DOI: 10.1161/HYPERTENSIONAHA.118.11507.)
© 2019 American Heart Association, Inc.
Hypertension is available at https://www.ahajournals.org/journal/hyp
944
to diagnose structural glaucomatous damage (Figure 2). The
characteristic functional defects in glaucoma are detected by
measuring light sensitivity in the central 24° to 30° of the VF
by means of standard automated perimetry: static computer-
ized threshold perimetry of the central VF performed with
white stimuli on a dimmer white background (Figure 3). The
diagnosis of POAG is based on the presence of characteristic
structural or functional defects. The definition of POAG does
not include IOP because the disease occurs as well in patients
with elevated IOP, the so-called high-pressure glaucoma, as
in patients with IOP within the normal range, the so-called
normal-tension glaucoma (NTG). Nowadays, elevated IOP is
defined as a major risk factor for the development and the pro-
gression of glaucomatous optic neuropathy and not as a diag-
nostic biomarker as was done several decades ago.
Once the diagnosis is established, comparison of repeat
examinations of retinal nerve fiber layer thickness and VFs
with the baseline values will indicate whether the disease is
stable or progressive. If progressive, plotting nerve fiber thin-
ning and loss of visual sensitivity against time will give an
idea of the speed at which the glaucomatous process advances,
the so-called rate of progression. Rate of progression has im-
portant implications: patients who are rapid progressors espe-
cially those with a long life expectancy need more aggressive
therapy as they are more likely to become functionally im-
paired within their lifetime than slow progressors.
The cause of POAG is unknown, but genetic factors play
a role because first degree relatives of a patient with confirmed
POAG are at a higher risk of having the disease.4 The disease is
unusual under the age of 50 years but has a prevalence of 1.4% in
white people at age 60 years and 5.3% at age 80 years. Ethnicity
plays a role as the prevalence is several times higher in Americans
of African ancestry and Afro-Caribbeans than in whites. The prev-
alence in Latinos at age 60 years is 2.7%, intermediate between
whites and Afro-Caribbeans, but rises to 12.7% at age 80 years.5
In parallel, black populations exhibit a greater preva-
lence of systemic hypertension, develop symptoms of hyper-
tension at a younger age, and experience more severe organ
damage compared to other races and ethnicities. Systemic
hypertension is higher among non-Hispanic black (40.3 %)
than non-Hispanic white (27.8 %), non-Hispanic Asian (25.0
%), or Hispanic (27.8 %) adults.6 Overall, the percentage of
cardiovascular events attributable to hypertension is 36 % in
black and 21 % in white populations.7 Hence, projects are
DOI: 10.1161/HYPERTENSIONAHA.118.11507
 Leeman and Kestelyn   Glaucoma and Blood Pressure   945

Figure 1.  Normal and glaucomatous optic

discs. Left, A normal disc with a physiological
excavation surrounded by a healthy
neuroretinal rim. Right, A completely excavated
disc with no neuroretinal rim left as seen in end-
stage glaucoma.

developed to improve BP control, for example in the high-
risk Caribbean region.8
The pathogenesis of glaucoma is incompletely under-
stood, but the death of axons grouped together at the optic
disc implies that this anatomic area is primarily involved.
The typical excavation is the result of deformation and
Downloaded from http://ahajournals.org by on May 13, 2022
remodeling of the connective tissue of the optic nerve head.
Axonal injury at this site results in interruption of axonal
transport and subsequent death of the ganglion cells in the
inner nuclear layer of the retina. Initial ganglion cell death
promotes a toxic environment leading to secondary retinal
ganglion cell ganglion loss.9,10 The mechanical theory focuses

Figure 2. Optical coherence tomography (OCT) scans in a healthy subject and in a subject with glaucoma. Left, A circular OCT of the retina surrounding the
optic nerves of right and left eye in a healthy person. The green circle in the upper part of the outprint indicates the anatomic site of the measurement. Below is
a linear projection of the actual retinal scan. The retinal nerve fiber layer is the area between the green and the red lines. Below the scan is a linear presentation
from the temporal to the nasal side of the thickness of the retinal nerve fiber layer (represented by a bold black line) compared with a normal database: the
green area includes normal values, the yellow area is borderline and the red is outside normal limits. A more familiar circular presentation is provided in the
lower part of the outprint. Right, The thinning of the nerve fiber layer illustrates the structural damage observed in advanced glaucoma. Note the advanced
cupping in the more affected left eye. OCT indicates optical coherence tomography; OD, oculus dexter (right eye); and OS, oculus sinister (left eye).
 946  Hypertension  May 2019
Figure 3. Functional damage is demonstrated by the automated visual fields. Left, Normal visual fields in a healthy person. Right, Visual fields in a patient
with advanced glaucoma showing deep scotomata in the superior hemifields and typical glaucomatous field defects in the lower hemifields in both eyes. CO
indicates corrected; MD, mean defect; MS, mean sensitivity; OD, oculus dexter (right eye); OS, oculus sinister (left eye); and sLV, square root of loss variance.
on the role of elevated IOP as the direct or indirect cause of
nerve fiber damage at the level of the optic nerve head. The
vascular theory emphasizes the importance of vascular per-
fusion of the optic nerve head and considers glaucomatous
optic neuropathy to be the result of unstable blood supply
of the optic nerve head due either to vascular dysregulation
or to increased IOP, as will be discussed later.11 Both patho-
genic pathways probably contribute to cause glaucomatous
damage in the same patient, but it seems plausible that me-
chanical damage is preponderant in patients with high pres-
sure, whereas vascular dysregulation may be the key culprit
in normal pressure glaucoma.
The diagnosis of POAG is based on the detection of char-
acteristic structural (excavation of the optic disc and thin-
Downloaded from http://ahajournals.org by on May 13, 2022
ning of the retinal never fiber layer) and functional defects
(glaucomatous VF defects). Once the diagnosis is estab-
lished, the only therapeutic option is IOP reduction both in
patients with elevated IOP and in patients with IOP within
the normal range. A target pressure is calculated taking into
account IOP and severity of glaucoma at presentation, life
expectancy, and if available, rate of progression of the glau-
comatous process. Target IOP is the upper limit of the IOP
estimated to be compatible with a rate of progression suf-
ficiently slow to maintain vision-related quality of life in
the expected lifetime of the patient.12 Therapeutic modali-
ties include IOP-lowering eye drops (commonly used top-
ical medications include β-blockers, prostaglandin analogs,
α-2 agonists, carbonic anhydrase inhibitors, and cholinergic
agonists), laser treatment of the trabecular meshwork to
increase the outflow (laser-trabeculoplasty), and surgical
procedures (filtering procedures). As a last resort, reduction
of aqueous humor production can be obtained by destruc-
tion of the ciliary processes either by external laser or by
endo-photocoagulation.
Several randomized clinical trials have clearly demon-
strated the efficacy of IOP reduction in POAG.
• Lowering IOP reduces the rate of progression both in
patients with early13 and advanced glaucoma.14
• Lowering IOP reduces the rate of progression also in pa-
tients with NTG.15
• Lowering IOP also reduces the incidence of POAG in
patients who do not yet have structural or functional de-
fects but who are particularly at risk for POAG because
of high IOP values, so-called ocular hypertensives.16
These trials have provided an evidence-based founda-
tion for the treatment of POAG by means of IOP reduction.
However, it is a common clinical experience that in many
patients, the glaucomatous damage progresses despite good
IOP control, and this clinical wisdom was also confirmed
by the randomized trials. For instance, in the Collaborative
NTG Study,15 progression of glaucomatous damage occurred
in 12% of the treated eyes. Glaucomatous optic neuropathy
probably has a multifactorial cause, and factors other than
IOP should be considered. If we look into the risk factors for
POAG, the only one we can readily modify is IOP. Most oth-
ers are beyond our control: age, family history of glaucoma,
race/ethnicity, pseudo-exfoliation, central corneal thickness,
and myopia.10
BP, IOP, OPP, and Glaucoma
There are complex interactions between BP, IOP, and OPP,
which can influence glaucoma development and evolution.
High BP could increase IOP by increased production of
aqueous humor by means of elevated ciliary blood flow and
capillary pressure and decrease of aqueous outflow as a re-
sult of increased episcleral venous pressure.17,18 However, low
BP, whether spontaneous or secondary to antihypertensive
therapy, can reduce OPP, leading to ischemic damage of the
optic nerve.1,18–21 This may explain why patients can develop
NTG, that is, glaucoma despite IOP within the normal range,
and why glaucomatous patients can deteriorate their VF de-
spite well-controlled IOP.
Ambulatory BP monitoring provides the average of BP
readings over a defined period, usually 24 hours. Compared
with office BP, it is a better predictor of hypertension-medi-
ated organ damage and of cardiovascular events, such as
stroke or coronary artery disease.22 Normally, BP decreases
during the night. Both nondippers (usually defined as a <10
% decrease in nighttime BP compared to daytime BP) and ex-
treme dippers (usually defined as a ≥20 % nocturnal dip) have
an increased cardiovascular risk, although data are less con-
vincing for extreme dippers.22,23 There are also variations in
the IOP, mainly driven by body position. An increase in IOP
is observed in the supine position, which is the sleeping posi-
tion during the night.19 Consequently, OPP decreases during
sleep. In addition to the effect of the normal circadian varia-
tion for BP and of the body position for IOP, antihypertensive
 Leeman and Kestelyn   Glaucoma and Blood Pressure   947
medications and antiglaucoma medications also can influ-
ence OPP.19
Functional vascular dysregulation could play a role in the
pathogenesis of glaucomatous optic neuropathy. Fluctuations
in OPP from high or low BP can lead to unstable ocular blood
flow and oxygen supply and to oxidative stress which may be
relevant in the pathogenesis of glaucoma.11 Some glaucoma
patients have altered autoregulation of their ocular blood flow,
but also present with features of a more generalized vascular
dysfunction, such as cold extremities, a syndrome known
as primary vascular dysregulation. The Flammer syndrome,
which is associated with an increased prevalence of NTG,
describes a phenotype of subjects with a variety of symptoms
and signs and altered vascular response to stimuli such as
cold, physical, chemical, or emotional stress.24
BP and Glaucoma Prevalence
Zhao et al17 performed a systematic review and meta-analysis
of the association between BP levels and arterial hypertension
with POAG and IOP as endpoints. They identified 60 studies,
including 7 longitudinal cohort studies from different parts of
the world. The number of studies incorporated in the meta-
analysis was 29 for POAG and 18 for IOP. Virtually all studies
showed a positive association between systolic BP, diastolic
BP, and IOP. The pooled average increase in IOP associated
with a 10 mm Hg increase in systolic BP was 0.26 mm Hg,
the average increase associated with a 5 mm Hg increase in
diastolic BP was 0.17 mm Hg. The association between BP
and IOP was considered robust and consistent despite het-
Downloaded from http://ahajournals.org by on May 13, 2022
erogeneity across studies. The association between arterial
hypertension and POAG was only significant for cross-sec-
tional studies with a pooled relative risk of 1.24 (95% CI,
1.06–1.44).17
A recent retrospective study with a prolonged survey pe-
riod (11 years) performed in Korea included hypertensive
patients and a matched normotensive comparison cohort.25
Occurrence of POAG was 2 % (n=1961) in hypertensive
patients, and 1.7 % (n=1692) in control subjects (P<0.001).
Hypertension was associated with an increased incidence of
POAG with an adjusted hazard ratio of 1.16 (95 % CI, 1.09–
1.24). Patients with higher systolic BP (≥140 mm Hg) were
more likely to have POAG compared with subjects with a sys-
tolic BP <120 mm Hg.25
An important recent study suggests that antihypertensive
treatment may have a preventive effect on the development
of glaucoma. Using the National Danish Registry, 41 235
patients with arterial hypertension and glaucoma were iden-
tified between 1996 and 2012.26 Definition of both diseases
was based on redeemed prescriptions. Although the number
of redeemed prescription for glaucoma therapy increased with
time, initiation of antihypertensive treatment reduced the rate
of prescriptions for glaucoma, suggesting that starting anti-
hypertensive therapy could postpone the onset of glaucoma.
Of note, after 2 years, the rate of onset of glaucoma therapy
returned to the initial tendency.26
These studies suggest that arterial hypertension slightly
but significantly increases the risk of POAG. However, other
studies show that low BP could be associated with an increased
prevalence of POAG.
In their meta-analysis, Zhao et al17 examined the dose-
response relationship from 10 studies that used ≥3 categories
of BP or that reported BP as a continuous variable. A J-shaped
curve was obtained, implying that both low BP and high BP
are associated with increased risk of POAG.
A recent study aimed to determine which BP parameters
are associated with an increased risk of glaucoma. Of 185
eyes evaluated (93 subjects), 19 had signs of glaucomatous
optic neuropathy. Multivariate analysis showed that extreme
dipping, but not 24-hour, daytime, or nighttime BP, was asso-
ciated with an increased risk of glaucomatous damage.27 The
nighttime period is particularly critical for OPP because IOP
increases in the supine position and BP most often decreases
during the night.19
BP and Glaucoma and IOP Progression
As stated above, OPP decreases during sleep. Studies relating
BP and glaucoma progression mainly focused on the 24-hour
variations in BP and, especially, on nocturnal BP.
A meta-analysis included 5 studies (286 patients) with
well-described 24-hour ambulatory BP monitoring method,
clear report of daytime BP, nighttime BP and nocturnal dip-
ping, and assessment of VF over an observation period of
at least 2 years. Patients with POAG and NTG, and with or
without arterial hypertension, were included. Although sys-
tolic and diastolic diurnal and nocturnal BP between patients
with or without progressive VF loss were not different, noc-
turnal dips over 10 % in systolic or diastolic BP were signifi-
cantly associated with deterioration of the VF.28
In a cross-sectional study including 314 consecutive
patients with POAG or NTG (202 hypertensive and 112 nor-
motensive), extreme dippers with daytime systemic normo-
tension had more VF loss than extreme dippers with daytime
systemic hypertension.29 Based on these results, a Dresden
safety range was defined as a mean nocturnal BP between 65
and 90 mm Hg, provided IOP is well controlled (12 mm Hg in
this study). The authors suggest that patients within this range
are expected not to progress or to have a slower glaucoma
progression compared to patients outside this range. However,
given the cross-sectional design of the study, no follow-up
data are provided.29
In a multivariable analysis in 65 patients with NTG, who
had baseline 24-h IOP and BP monitoring, low nocturnal di-
astolic OPP at baseline was a significant predictive risk factor
for VF progression at 5 years.30
A retrospective study performed in Korea included 72
NTG patients who had regular VF examinations and 24-hour
ambulatory BP monitoring and who had a follow-up period of
at least 20 years.31 Hypertensive patients were excluded. In the
multivariate model, low OPP was associated with glaucoma-
tous VF progression. The dipping pattern was also associated
with VF deterioration, a more pronounced dipping being asso-
ciated with a more VF worsening.31
Comparable results were obtained in another Korean pro-
spective case-control study. In 349 consecutive patients with
NTG with a minimal follow-up of 3 years (25 % hypertensive,
all treated), extreme dipping was a significant risk factor for
optic disk hemorrhage, and VF deterioration compared with
nondipping and physiological dipping.32
 948  Hypertension  May 2019
In a prospective longitudinal study, 85 consecutive patients
with NTG (32 % hypertensive, most treated) underwent reg-
ular VF examination and had 48-hour BP monitoring at base-
line and during follow-up. After 1 year, the magnitude and
duration of nighttime BP below 10 % of daytime BP identified
patients with VF deterioration.33
A study examined the timing of antihypertensive drugs
administration (in the morning or in the morning and the eve-
ning) on several visual characteristics and ambulatory BP.34
After a first evaluation, patients with POAG and controlled
arterial hypertension were randomized into 2 groups, one tak-
ing antihypertensive treatment only in the morning (n=43) and
the other taking antihypertensive treatment in the morning and
in the evening (n=45). A second evaluation was performed 6
months later. Although 24-hour systolic BP and diastolic BP
were similar in the 2 groups, patients taking antihypertensive
drugs in the evening had lower nocturnal BP and more pro-
nounced dipping, lower nocturnal OPP, greater VF loss, and
more pronounced alteration in visual evoked potentials and
in the flow in ocular and orbital vessels examined by Doppler
ultrasound.34
However, studies suggest that high BP could adversely
affect the natural tendency of IOP to decrease with age in cer-
tain ethnic groups. In 3188 Malay and Indian adults without
glaucoma living in Singapore, with IOP and BP measurements
at baseline and during 6-year follow-up examination, the age-
related decrease in IOP was blunted in individuals who had an
increase in BP, that is, the higher the BP increase, the lower
the IOP decrease over the 6-year observation period. Data on
Downloaded from http://ahajournals.org by on May 13, 2022
VF or glaucomatous optic neuropathy are unfortunately not
provided.35
Effect of Antihypertensive Drugs on IOP
and Glaucoma
Some large-scale population-based studies have examined the
relation between antihypertensive drugs and IOP. The EPIC
(European Prospective Investigation into Cancer)-Norfolk Eye
Study included 7093 participants who had their IOP measured
and medications recorded by a research nurse during a health
examination.36 Patients treated for glaucoma were excluded.
Mean IOP ranged from 14.87 to 16.57 mm Hg. Analysis using
a multivariable linear regression model showed that the use of
β-blockers and nitrates was associated with a lower IOP (re-
spectively by 0.92 and 0.63 mm Hg). There was no significant
association between other antihypertensive drugs and IOP.36
The prospective Gutenberg Health Study enrolled 13 527
subjects taking cardiovascular medications and had IOP mea-
surements. Patients with topical IOP-lowering medications or
previous ocular surgery, thus most glaucoma patients, were
excluded. Only systemic β-blockers were associated with a
negligible reduction in IOP, in these nonglaucoma subjects.37
The Singapore Epidemiology of Eye Diseases Study
examined 8063 subjects without glaucoma who had inter-
viewer-administered questionnaire to collect data on medica-
tions.38 Mean IOP was 15.1 mm Hg. The use of β-blockers was
independently associated with a lower IOP (by 0.45 mm Hg),
whereas the use of angiotensin-converting enzyme inhibi-
tors and angiotensin receptor blockers was associated with
a higher IOP (respectively, 0.33 and 0.40 mm Hg). Although
statistically significant, these associations were considered
modest. The use of other antihypertensive drugs was not re-
lated to significant differences in IOP.38
Using the National Danish Registry, 41 235 patients treated
with glaucoma medications and antihypertensive agents were
identified. All antihypertensive drugs, except vasodilators,
such as hydralazine, delayed the development of glaucoma.26
A study examined the association between systemic medi-
cations, not specifically antihypertensive drugs, and POAG
using the United States insurance claims data.39 Prescription
drug use was calculated for a 5-year period before a POAG
procedure (cases, n=6130) or cataract surgery (controls,
n=30 650). Logistic regression showed that the use of calcium
channel blockers (odds ratio, 1.26; 95 % CI, 1.18–1.35) and
angiotensin II antagonists (odds ratio, 1.19; 95 % CI, 1.10–
1.28) was associated with an increased risk of POAG, whereas
the use of β-blockers was associated with a reduced risk (odds
ratio, 0.77; 95 % CI, 0.72–0.83).39
Concerns From Glaucoma Specialists
Regarding the 2017 American College of
Cardiology/American Heart Association
Guidelines
There is no doubt that treatment of arterial hypertension
reduces the incidence of major complications, such as cardi-
ovascular death, myocardial infarction, and stroke. The land-
mark SPRINT study (Systolic Blood Pressure Intervention
Trial) shows that a systolic BP target of <120 mm Hg is more
protective than the conservative systolic BP target of <140
mm Hg.40 In 2017, the American College of Cardiology/
American Heart Association Task Force on Clinical Practice
Guidelines recommended a target BP of <130 mm Hg (sys-
tolic) and <80 mm Hg (diastolic) for most hypertensive
patients.7 Consequently, the number of over-dippers and of
patients with glaucoma progression could potentially in-
crease in the next decades in treated hypertensive patients.1
Unfortunately, to our knowledge, neither the SPRINT trial
nor other studies comparing outcomes with different BP
targets did include assessment of glaucoma incidence or
progression.
In Summary
• Both high BP and low BP are associated with an in-
creased risk of glaucoma.
• There is mounting evidence that low nighttime BP or
excessive dipping could adversely affect glaucoma
progression.
• If any, systemic antihypertensive drugs have minimal ef-
fect on IOP.
What Could Be Recommended
• Patients with high BP should be screened for glaucoma,
and patients with glaucoma should be screened for arte-
rial hypertension.
• Patients with coexisting glaucoma and high BP should
undergo closer ophthalmologic examinations.1
• Ambulatory BP monitoring should be performed in
glaucoma patients with unexplained deterioration of
their VF, and perhaps in all patients with coexisting arte-
rial hypertension and glaucoma.1,18
 Leeman and Kestelyn   Glaucoma and Blood Pressure   949
• Identification of a low nocturnal BP or over-dipping
should prompt discussion between glaucoma and hy-
pertension specialists in charge of the patient. However,
to date, no specific recommendation can be proposed to
limit over-dipping. Importantly, the nocturnal BP fall
has prognostic implications, reduced and reverse dip-
ping being associated with a significantly higher rate of
cardiovascular events.23
• In such an uncomfortable situation (glaucoma progres-
sion and over-dipping), there may be room for precision
medicine and tailored management, always prioritizing
BP control for optimal cardiovascular protection, taking
into account that one size does not fit all.
Glaucoma and hypertension scientific societies should join
their efforts to stimulate and raise funding for research and
studies to determine the best treatment strategy for systemic
hypertensive patients with concomitant glaucoma. In partic-
ular, the role of 24-hour ambulatory BP monitoring should
further be studied, as it shows promise as a useful tool for
identifying those patients at highest risk for glaucoma pro-
gression.18 Although not referred in the most recent American
or European hypertension guidelines,7,22 future recommenda-
tion should at least raise awareness on the delicate balance
between BP and IOP in these patients.
Sources of Funding
None.
Disclosures
None.
Downloaded from http://ahajournals.org by on May 13, 2022
References
1. De Moraes CG, Cioffi GA, Weinreb RN, Liebmann JM. New recom-
mendations for the treatment of systemic hypertension and their potential
implications for glaucoma management. J Glaucoma. 2018;27:567–571.
doi: 10.1097/IJG.0000000000000981
2. Tham YC, Li X, Wong TY, Quigley HA, Aung T, Cheng CY. Global prev-
alence of glaucoma and projections of glaucoma burden through 2040:
a systematic review and meta-analysis. Ophthalmology. 2014;121:2081–
2090. doi: 10.1016/j.ophtha.2014.05.013
3. European Glaucoma Society. Terminology and Guidelines for Glaucoma.
4th ed. Savona, Italy: Publicomm srl; 2014:84.
4. Nguyen RL, Raja SC, Traboulsi EI. Screening relatives of patients
with familial chronic open angle glaucoma. Ophthalmology. 2000;107:
1294–1297.
5. Kapetanakis VV, Chan MP, Foster PJ, Cook DG, Owen CG, Rudnicka
AR. Global variations and time trends in the prevalence of primary open
angle glaucoma (POAG): a systematic review and meta-analysis. Br J
Ophthalmol. 2016;100:86–93. doi: 10.1136/bjophthalmol-2015-307223
6. Fryar CD, Ostchega Y, Hales CM, Zhang G, Kruszon-Moran D.
Hypertension prevalence and control among adults: United States, 2015–
2016. NCHS Data Brief. 2017;289:1–8.
7. Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/
ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the
prevention, detection, evaluation, and management of high blood pres-
sure in adults: executive summary: a report of the American College of
Cardiology/American Heart Association Task Force on clinical prac-
tice guidelines. Hypertension. 2018;71:1269–1324. doi: 10.1161/HYP.
0000000000000066
8. Colgrove P, Connell KL, Lackland DT, Ordunez P, DiPette DJ. Controlling
hypertension and reducing its associated morbidity and mortality in
the Caribbean: implications of race and ethnicity. J Clin Hypertens
(Greenwich). 2017;19:1010–1014. doi: 10.1111/jch.13056
9. Quigley HA. Glaucoma. Lancet. 2011;377:1367–1377. doi: 10.1016/
S0140-6736(10)61423-7
10. Jonas JB, Aung T, Bourne RR, Bron AM, Ritch R, Panda-Jonas S. Glaucoma.
Lancet. 2017;390:2183–2193. doi: 10.1016/S0140-6736(17)31469-1
11. Flammer J, Konieczka K, Bruno RM, Virdis A, Flammer AJ, Taddei S.
The eye and the heart. Eur Heart J. 2013;34:1270–1278. doi: 10.1093/
eurheartj/eht023
12. European Glaucoma Society. Terminology and Guidelines for Glaucoma.
4th ed. Savona, Italy: Publicomm srl; 2014:134.
13. Heijl A, Leske MC, Bengtsson B, Hyman L, Bengtsson B, Hussein M;
Early Manifest Glaucoma Trial Group. Reduction of intraocular pressure
and glaucoma progression: results from the Early Manifest Glaucoma
Trial. Arch Ophthalmol. 2002;120:1268–1279. doi: 10.1001/archopht.
120.10.1268
14. The AGIS Investigators. The Advanced Glaucoma Intervention Study
(AGIS):7. The relationship between control of intraocular pressure and
visual field deterioration. Am J Ophthalmol 2000;130:429–440. doi:
10.1016/S0002-9394(00)00538-9
15. Collaborative Normal-Tension Glaucoma Study Group. Comparison of
glaucomatous progression between untreated patients with normal-tension
glaucoma and patients with therapeutically reduced intraocular pressures.
Am J Ophthalmol. 1998;126:487–497. doi: 10.1016/S0002-9394(98)00223-2
16. Kass MA, Heuer DK, Higginbotham EJ, Johnson CA, Keltner JL, Miller
JP, Parrish RK 2, Wilson MR, Gordon MO. The Ocular Hypertension
Treatment Study: a randomized trial determines that topical ocular hy-
potensive medication delays or prevents the onset of primary open-angle
glaucoma. Arch Ophthalmol. 2002;120:701–713; discussion 829.
17. Zhao D, Cho J, Kim MH, Guallar E. The association of blood pressure
and primary open-angle glaucoma: a meta-analysis. Am J Ophthalmol.
2014;158:615.e9–27.e9. doi: 10.1016/j.ajo.2014.05.029
18. Levine RM, Yang A, Brahma V, Martone JF. Management of blood pres-
sure in patients with glaucoma. Curr Cardiol Rep. 2017;19:109. doi:
10.1007/s11886-017-0927-x
19. Costa VP, Harris A, Anderson D, Stodtmeister R, Cremasco F, Kergoat H,
Lovasik J, Stalmans I, Zeitz O, Lanzl I, Gugleta K, Schmetterer L. Ocular
perfusion pressure in glaucoma. Acta Ophthalmol. 2014;92:e252–e266.
doi: 10.1111/aos.12298
20. Schmidl D, Garhofer G, Schmetterer L. The complex interaction between
ocular perfusion pressure and ocular blood flow - relevance for glaucoma.
Exp Eye Res. 2011;93:141–155. doi: 10.1016/j.exer.2010.09.002
21. Leske MC. Ocular perfusion pressure and glaucoma: clinical trial and
epidemiologic findings. Curr Opin Ophthalmol. 2009;20:73–78. doi:
10.1097/ICU.0b013e32831eef82
22. Williams B, Mancia G, Spiering W, et al; Authors/Task Force Members.
2018 ESC/ESH Guidelines for the management of arterial hyper-
tension: the Task Force for the management of arterial hypertension
of the European Society of Cardiology and the European Society of
Hypertension: the Task Force for the management of arterial hyperten-
sion of the European Society of Cardiology and the European Society
of Hypertension. J Hypertens. 2018;36:1953–2041. doi: 10.1097/HJH.
0000000000001940
23. Salles GF, Reboldi G, Fagard RH, Cardoso CR, Pierdomenico SD,
Verdecchia P, Eguchi K, Kario K, Hoshide S, Polonia J, de la Sierra A,
Hermida RC, Dolan E, O’Brien E, Roush GC; ABC-H Investigators.
Prognostic effect of the nocturnal blood pressure fall in hypertensive
patients: the Ambulatory Blood Pressure Collaboration in Patients With
Hypertension (ABC-H) meta-analysis. Hypertension. 2016;67:693–700.
doi: 10.1161/HYPERTENSIONAHA.115.06981
24. Flammer J, Konieczka K. The discovery of the Flammer syndrome:
a historical and personal perspective. EPMA J. 2017;8:75–97. doi:
10.1007/s13167-017-0090-x
25. Rim TH, Lee SY, Kim SH, Kim SS, Kim CY. Increased incidence of
open-angle glaucoma among hypertensive patients: an 11-year nation-
wide retrospective cohort study. J Hypertens. 2017;35:729–736. doi:
10.1097/HJH.0000000000001225
26. Horwitz A, Klemp M, Jeppesen J, Tsai JC, Torp-Pedersen C, Kolko
M. Antihypertensive medication postpones the onset of glaucoma: evi-
dence from a Nationwide Study. Hypertension. 2017;69:202–210. doi:
10.1161/HYPERTENSIONAHA.116.08068
27. Melgarejo JD, Lee JH, Petitto M, et al. Glaucomatous optic neurop-
athy associated with nocturnal dip in blood pressure: findings from
the Maracaibo Aging Study. Ophthalmology. 2018;125:807–814. doi:
10.1016/j.ophtha.2017.11.029
28. Bowe A, Grünig M, Schubert J, Demir M, Hoffmann V, Kütting F, Pelc
A, Steffen HM. Circadian variation in arterial blood pressure and glauco-
matous optic neuropathy–A systematic review and meta-analysis. Am J
Hypertens. 2015;28:1077–1082. doi: 10.1093/ajh/hpv016
29. Pillunat KR, Spoerl E, Jasper C, Furashova O, Hermann C, Borrmann
A, Passauer J, Middeke M, Pillunat LE. Nocturnal blood pressure in
 950  Hypertension  May 2019
primary open-angle glaucoma. Acta Ophthalmol. 2015;93:e621–e626.
doi: 10.1111/aos.12740
30. Raman P, Suliman NB, Zahari M, Kook M, Ramli N. Low nocturnal di-
astolic ocular perfusion pressure as a risk factor for NTG progression: a
5-year prospective study. Eye (Lond). 2018;32:1183–1189.
31. Jin SW, Noh SY. Long-term clinical course of normal-tension glau-
coma: 20 years of experience. J Ophthalmol. 2017;2017:2651645. doi:
10.1155/2017/2651645
32. Kwon J, Lee J, Choi J, Jeong D, Kook MS. Association between noc-
turnal blood pressure dips and optic disc hemorrhage in patients with
normal-tension glaucoma. Am J Ophthalmol. 2017;176:87–101. doi:
10.1016/j.ajo.2017.01.002
33. Charlson ME, de Moraes CG, Link A, Wells MT, Harmon G, Peterson
JC, Ritch R, Liebmann JM. Nocturnal systemic hypotension increases the
risk of glaucoma progression. Ophthalmology. 2014;121:2004–2012. doi:
10.1016/j.ophtha.2014.04.016
34. Krasińska B, Karolczak-Kulesza M, Krasiński Z, Pawlaczyk-Gabriel K,
Lopatka P, Głuszek J, Tykarski A. Effects of the time of antihyperten-
sive drugs administration on the stage of primary open-angle glaucoma in
patients with arterial hypertension. Blood Press. 2012;21:240–248. doi:
10.3109/08037051.2012.666423
35. Chua J, Chee ML, Chin CWL, Tham YC, Tan N, Lim SH, Aung T,
Cheng CY, Wong TY, Schmetterer L. Inter-relationship between ageing,
Downloaded from http://ahajournals.org by on May 13, 2022
body mass index, diabetes, systemic blood pressure and intraocular pres-
sure in Asians: 6-year longitudinal study. Br J Ophthalmol. 2018;103:
196–202.
36. Khawaja AP, Chan MP, Broadway DC, Garway-Heath DF, Luben R, Yip
JL, Hayat S, Wareham NJ, Khaw KT, Foster PJ. Systemic medication and
intraocular pressure in a British population: the EPIC-Norfolk Eye Study.
Ophthalmology. 2014;121:1501–1507. doi: 10.1016/j.ophtha.2014.02.009
37. Höhn R, Mirshahi A, Nickels S, Schulz A, Wild PS, Blettner M, Pfeiffer
N. Cardiovascular medication and intraocular pressure: results from the
Gutenberg Health Study. Br J Ophthalmol. 2017;101:1633–1637. doi:
10.1136/bjophthalmol-2016-309993
38. Ho H, Shi Y, Chua J, Tham YC, Lim SH, Aung T, Wong TY, Cheng
CY. Association of systemic medication use with intraocular pres-
sure in a multiethnic Asian population: the Singapore Epidemiology
of Eye Diseases Study. JAMA Ophthalmol. 2017;135:196–202. doi:
10.1001/jamaophthalmol.2016.5318
39. Zheng W, Dryja TP, Wei Z, Song D, Tian H, Kahler KH, Khawaja AP.
Systemic medication associations with presumed advanced or uncon-
trolled primary open-angle glaucoma. Ophthalmology. 2018;125:984–
993. doi: 10.1016/j.ophtha.2018.01.007
40. Wright JT, Williamson JD, Whelton PK, et al; SPRINT Research Group.
A randomized trial of intensive versus standard blood pressure control.
N Engl J Med. 2015;373:2103–2116. doi: 10.1056/NEJMoa1511939