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Rev Neurol Dis. 2011 ; 8(1-2): 19.
Hypertension-related eye abnormalities and the risk of stroke

Amanda D. Henderson, M.D.(1), Beau B. Bruce, M.D., M.S.(1),(2), Nancy J. Newman, MD(1),(2),
and Valrie Biousse, MD(1),(2)
(1)Department of Ophthalmology, Emory University School of Medicine, Atlanta, Georgia
(3),
(2)Department
of Neurology, Emory University School of Medicine, Atlanta, Georgia
(3)Department
of Neurological Surgery, Emory University School of Medicine, Atlanta, Georgia
Abstract
Many studies have shown that hypertensive ocular funduscopic abnormalities are clearly related to
stroke, even after controlling for level of blood pressure and other vascular risk factors. Retinal
abnormalities indicative of a breakdown of the blood-retina barrier confer a greater increase in risk
for stroke than sclerotic retinal changes. Similar retinal changes also have a positive relationship
with stroke mortality. Hypertensive ocular fundus abnormalities are also reported to be associated
with an increased risk for cognitive impairment, cerebral atrophy, progression of MRI-defined
white matter lesions, and subclinical infarction. Recent advances in fundus photography allow for
improved accuracy and consistency in interpretation of funduscopic lesions, and improve the
feasibility of screening for these abnormalities in at-risk patient populations. Evaluating the ocular
fundus for signs of hypertensive retinopathy, in combination with an assessment of the presence or
absence of other known vascular risk factors, may allow clinicians to further individualize a risk
profile for stroke to each individual patient, thus permitting more accurate risk stratification and,
potentially, guiding treatment strategies.
Introduction
Hypertension causes microvascular damage in both the cerebral and retinal circulations (1
3). Because the retinal and cerebral vessels share embryological and anatomical
characteristics, they also may show similar patterns of damage from diseases such as
hypertension (3). Thus, it has long been suggested that examination of the ocular fundus
could provide a noninvasive view of intracranial vascular pathology (2). Large populationbased studies have confirmed that standardized assessment of ocular fundus photographs
provides reliable evaluation of retinal hypertensive abnormalities that have been correlated
with a higher risk of cerebrovascular disease (Tables 1 and 2) (2,46). The retinal vessel
pathology serves as an important marker for stratification of patients risk for having or
developing cerebrovascular disease (2,46). Incorporation of these markers into risk
stratification algorithms should enhance the ability to ensure appropriate clinical follow-up
and treatment plans for each individual patient. To evaluate the potential value of retinal
imaging as a tool to predict stroke risk, we describe the ocular effect of hypertension and
review the reported associations between the ocular effects of hypertension and
cerebrovascular disease.
Address correspondence to Dr. Valrie Biousse, Neuro-Ophthalmology Unit, Emory Eye Center, 1365-B Clifton Rd. NE, Atlanta, GA
30322. Phone: (404)778-5360. Fax: (404)778-4849. vbiouss@emory.edu.
None of the authors have any conflict of interest.
Henderson et al.
Page 2
Ocular effects of systemic hypertension

Hypertension causes both acute and chronic ocular abnormalities. These changes affect
different areas of the eye, producing three categories of hypertensive ocular change:
choroidopathy, retinopathy, and optic neuropathy (Figures 1,2,3) (1,710).
Hypertensive choroidopathy occurs as a result of choroidal ischemia, which develops

because the choroidal vasculature does not possess the autoregulatory capacity of the retinal
vasculature (1,710). Hypertensive choroidopathy can be divided into three phases. During
the acute ischemic phase, choroidal arterioles constrict, leading to necrosis of the
choriocapillaris and retinal pigment epithelium and the accumulation of exudates in the
subretinal space. The clinical fundus findings during this phase include white areas (a
manifestation of retinal pigment epithelium necrosis), and focal serous retinal detachment
most often involving the macula and peripapillary region. Retinal fluorescein angiography
shows patches of hypoperfused choriocapillaris, particularly in the central region of the
macula. The chronic occlusive phase is characterized by extreme narrowing or occlusion of
the choroidal capillaries and yellowing and leakage of the retinal pigment epithelium
overlying the occluded regions. Retinal detachment also may occur in this phase.
Degenerative retinal pigment epithelium lesions develop in the macula and peripheral retina
and gradually become more extensive. Finally, during the chronic reparative phase of
hypertensive choroidopathy, the occluded choroidal arteries, arterioles, and choriocapillaris
are recanalized, the retinal pigment epithelium heals, and the retina reattaches. Chronic
Elschnig spots, appearing as hyperpigmented areas with surrounding atrophy, or nonspecific
areas of mottling, often remain. During this phase, fluorescein angiography shows
underlying choroidal fluorescence (Figure 1).
Hypertensive retinopathy describes a spectrum of microvascular abnormalities in people

with elevated blood pressure and may be divided into several phases, which do not
necessarily occur in the order described (1,710). In the vasoconstrictive phase, an acute rise
in blood pressure causes the retinal vessels to increase their vascular tone, which manifests
clinically as generalized retinal arteriolar narrowing. Alternatively, in vessels with
significant arteriosclerosis, which prevents certain vascular segments from narrowing, more
focal arteriolar narrowing occurs. The sclerotic phase of hypertensive retinopathy occurs in
the presence of chronically elevated blood pressure and is characterized by hyperplasia of
the tunica media, hyaline degeneration of the arteriolar wall, and intimal thickening, which
manifest clinically as vessel attenuation, increased arteriolar light reflex, arteriovenous
nicking, and increased tortuosity of arterioles. Arteriovenous nicking describes narrowing of
a venule as an arteriole crosses over it. Increased arteriolar light reflex refers to an increased
light reflex from the central portion of the retinal arteriolar surface (Figures 1 and 2).
Sclerotic changes may lead to long-term complications, including macroaneurysms,
microaneurysms, central retinal artery or vein occlusion, epiretinal membrane formation,
cystoid macular edema, and vascular remodeling. Severely elevated BP may lead to the
exudative phase, causing endothelial damage and disruption of the blood-retina barrier, with
leakage of plasma and blood products into the vessel wall. This causes vessel dilation and
eventual failure of autoregulation (Figure 3). The effects of this phase lead to many of the
classic retinal signs associated with hypertensive retinopathy, including flame-shaped
hemorrhages in the nerve fiber layer of the retina, dot and blot hemorrhages, boat-shaped
hemorrhages, microaneurysms, hard exudates from the leakage of lipids, and cotton wool
spots that represent infarctions of the nerve fiber layer (Figure 2). The most widely used
scale for grading hypertensive retinopathy is the Keith, Wagener, and Barker classification,
which grades retinopathy from I to IV based on its severity (Table 3) (11).
Henderson et al.
Page 3
Hypertensive optic neuropathy results from severely elevated blood pressure, and can also
be divided into three phases (Figure 3) (1,710). During the acute ischemic phase,
vasoconstriction in the prelaminar optic nerve leads to axonal hydropic swelling, axolemma
disruption, and glial swelling. Vasoconstriction is more severe in the retrolaminar region and
leads to endothelial swelling, degeneration of pericytes, and, eventually, vacuolated axons
and glial swelling. This pathologic process occurs secondary to optic nerve ischemia,
although raised intracranial pressure is also posited to play a role. Axonal swelling in the
prelaminar optic nerve is decreased during the resolution phase. In the retrolaminar optic
nerve, disintegrated myelinated axons and lipid-laden microglial cells are present.
Degeneration of endothelial cells and pericytes is evident. In the atrophic phase, axons of the
prelaminar optic nerve are replaced by proliferated glial cells, and myelinated axons largely
disappear from the retrolaminar optic nerve. Additionally, lipid-laden microglia are absent at
this stage. Some blood vessels lose their endothelial cells and pericytes and only retain a
basement membrane. Clinically, chronic optic nerve swelling is progressively replaced by
optic atrophy (Figure 3).
Evaluating the ocular effects of hypertension with retinal photography

To evaluate hypertensive funduscopic damage, the retinal vasculature must be visualized

either via funduscopy or photography. With the advent of digital fundus cameras, highresolution digital images are easily acquired and quality assessed instantly. Computerassisted image analysis techniques can be used to make quantitative measurements and to
characterize abnormalities of the retinal microvasculature (12,13). Several studies show that
the use of fundus photography results in more accurate documentation of the signs of
retinopathy in the general population, when compared with clinical ophthalmoscopy (14
17). Depending on the camera used, fundus photography may require pharmacologic
pupillary dilation or not. Non-mydriatic photography is advantageous because it avoids
pupillary dilation, and is therefore less time consuming. However, dilated fundus
photography may produce higher quality photographs in some patients. When evaluating
non-mydriatic fundus photography for the Atherosclerosis Risk in Communities (ARIC)
study, 81% of fundus photographs were deemed adequate for a retinal examination (18). Our
group recently reported similar findings, with 83% of patients who had bilateral nonmydriatic fundus photography having a high quality photograph in at least one eye, and only
3% of patients having no photographs of diagnostic value (19). The percentage of patients
with a quality dilated fundus photograph in at least one eye ranged from 92% to 98% in the
Blue Mountains Eye Study (BMES), depending on the specific fundus abnormality being
evaluated (20). The use of fundus photography for the acquisition of retinal images is a
valuable tool for the evaluation of hypertensive ocular changes in patients at risk for
cerebrovascular disease (14).
Ocular effects of systemic hypertension and stroke

Diverse study types provide evidence for the association between ocular fundus changes and
cerebrovascular disease. Histologic studies showed that fibrous or fibro-hyalinoid
thickenings of the retinal arteries near the optic disc reflect intracerebral arterial
abnormalities, and are associated with an increased risk of both cerebral hemorrhage and
cerebral infarction (3). Functional studies of the retinal vasculature show that prolonged
retinal arteriovenous passage time is associated with lacunar infarction, confirmed by CT
scan (21). Additionally, lower central retinal artery end-diastolic and mean velocities and
higher central retinal artery resistive indices and pulsatility have been associated with
cerebral small vessel disease (22).
Henderson et al.
Page 4
The strongest evidence supporting the use of hypertensive funduscopic findings in the
stratification of patients at risk for cerebrovascular disease comes from longitudinal studies
that evaluated the relationships between these ocular findings and cerebrovascular disease
(Table 2). The initial studies examining these relationships, published in Japan during the
1970s through 1990s, reported associations between hypertensive funduscopic findings and
subclinical and clinical stroke. However, many of these studies did not control for blood
pressure, which may have influenced the results (2).
More recent large population-based studies (Table 1), using photographs to define
retinopathy signs, have provided further support for some of the earlier findings that,
hypertensive ocular abnormalities predict stroke risk, even after controlling for blood
pressure and other vascular risk factors (Table 2). In the ARIC study, hypertensive
retinopathy increased the risk of stroke two- to three-fold (23). The BMES demonstrated a
higher risk of combined stroke events (defined as incident stroke, transient ischemic attack
or cerebrovascular death), in patients with hypertensive retinopathy (20). Significant,
although generally weaker, relationships between other microvascular funduscopic findings
and stroke have also been reported in the ARIC study (15,18), the Cardiovascular Health
Study (CHS) (16,24,25), and the Rotterdam Eye Study (17,26,27). Arteriovenous nicking,
focal arteriolar narrowing, microaneurysms, soft exudates, blot hemorrhages, flame-shaped
hemorrhages, decreased arteriovenous ratio, and larger retinal venular caliber have been
shown to be associated with increased risk for stroke (4,2331).
In addition to subclinical and clinical stroke, stroke mortality may be related to retinal
hypertensive abnormalities. The BMES and BDES reported a relationship between
retinopathy and cerebrovascular death in patients without diabetes. However, these studies
did not detect any relationship between retinal arteriolar diameter or focal arteriolar
narrowing and cerebrovascular death (4,20,28,32).
Several studies have focused on the relationship between hypertensive retinopathy and
abnormalities detected on brain imaging. Retinopathy, arteriovenous nicking, retinal
arteriolar sclerosis, and focal arteriolar narrowing have been associated with cerebral white
matter lesions, even after controlling for blood pressure (3235). Interestingly, in the
Rotterdam Eye Study, retinal vessel diameter was not related to the severity of cerebral
small vessel disease; however, larger retinal venular diameter was associated with marked
progression of periventricular white matter lesions and subcortical white matter lesions over
time, after adjusting for vascular risk factors (27). These findings are consistent with the
idea that retinal microvasculature abnormalities likely precede and are harbingers of the
development of cerebral white matter lesions. Not only are cerebral white matter lesions
related to retinal hypertensive abnormalities, but they are also related to stroke. The presence
of MRI-defined white matter lesions has been shown to be associated with an increased risk
of incident clinical stroke, and, importantly, the presence of both retinopathy and cerebral
white matter lesions has shown a multiplicative effect on the risk for clinical stroke (33,34).
This interaction between retinopathy and white matter lesions may have two possible
explanations: microvascular pathology may be more severe in patients with both retinopathy
and white matter lesions, or retinopathy may be a marker for a more malignant form of
cerebral white matter lesions. Regardless of the reason, this relationship suggests that
funduscopic examination or retinal photography is useful for risk stratification in patients
with evidence of cerebral white matter lesions on MRI (34).
Conclusion and future perspectives

The presence of hypertensive funduscopic abnormalities is clearly related to stroke, even
after controlling for level of blood pressure and other vascular risk factors. Retinal changes
Henderson et al.
Page 5
indicative of a breakdown of the blood-retina barrier (such as retinal hemorrhages,

microaneurysms and cotton wool spots) seem to confer a greater increase in stroke risk than
sclerotic retinal changes (such as generalized and focal retinal arteriolar narrowing and
arteriovenous nicking). Evaluating for these retinal signs, along with the assessment of the
presence or absence of other known vascular risk factors, may allow clinicians to further
individualize a risk profile for stroke for each patient. This would permit more accurate risk
stratification and, potentially, play a role in guiding treatment strategies.
With continuing improvement in retinal photographic techniques and retinal image analysis,
evaluation of retinal microvascular signs of hypertension from retinal photographs may
begin to move from predominately the research arena to clinical practice. The use of nonmydriatic fundus photography, in particular, allows for easy screening for funduscopic
abnormalities in the neurologists office.
Acknowledgments
This study was supported in part by a departmental grant (Department of Ophthalmology) from Research to Prevent
Blindness, Inc., core grant P30-EY06360 (Department of Ophthalmology), KL2- RR025009 (BBB), UL1RR025008 (BBB/VB), K23-EY019341 (BBB), and the Knights Templar Eye Foundation (BBB/VB). Dr. Bruce
received the American Academy of Neurology Practice Research Fellowship. Dr. Newman is a recipient of the
Research to Prevent Blindness Lew R. Wasserman Merit Award.
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Only very few relevant articles to this review were selected in the list below (there are
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14. Wong TY. Is retinal photography useful in the measurement of stroke risk? Lancet Neurol. 2004;
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[PubMed: 21268749]
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23. Wong TY, Klein R, Couper DJ, et al. Retinal microvascular abnormalities and incident stroke: the
Atherosclerosis Risk in Communities Study. Lancet. 2001; 358:11341140. [PubMed: 11597667]
24. Longstreth W Jr, Larsen EK, Klein R, et al. Associations between findings on cranial magnetic
resonance imaging and retinal photography in the elderly: the Cardiovascular Health Study. Am J
Epidemiol. 2007; 165:7884. [PubMed: 17041135]
25. Wong TY, Kamineni A, Klein R, et al. Quantitative retinal venular caliber and risk of
cardiovascular disease in older persons: the cardiovascular health study. Arch Intern Med. 2006;
166:23882394. [PubMed: 17130394]
26. Ikram MK, de Jong FJ, Bos MJ, et al. Retinal vessel diameters and risk of stroke: the Rotterdam
Study. Neurology. 2006; 66:13391343. [PubMed: 16682664]
27. Ikram MK, De Jong FJ, Van Dijk EJ, et al. Retinal vessel diameters and cerebral small vessel
disease: the Rotterdam Scan Study. Brain. 2006; 129:182188. [PubMed: 16317022]
28. Wong TY, Klein R, Nieto FJ, et al. Retinal microvascular abnormalities and 10-year
cardiovascular mortality: a population-based case-control study. Ophthalmology. 2003; 110:933
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29. Witt N, Wong TY, Hughes AD, et al. Abnormalities of retinal microvascular structure and risk of
mortality from ischemic heart disease and stroke. Hypertension. 2006; 47:975981. [PubMed:
16585415]
30. Hirai FE, Moss SE, Knudtson MD, et al. Retinopathy and survival in a population without
diabetes: The Beaver Dam Eye Study. Am J Epidemiol. 2007; 166:724730. [PubMed: 17591594]
31. Wang JJ, Liew G, Klein R, et al. Retinal vessel diameter and cardiovascular mortality: pooled data
analysis from two older populations. Eur Heart J. 2007; 28:19841992. [PubMed: 17626032]
32. Kwa VI, van der Sande JJ, Stam J, et al. Retinal arterial changes correlate with cerebral smallvessel disease. Neurology. 2002; 59:15361540. [PubMed: 12451193]
33. Kobayashi S, Okada K, Koide H, et al. Subcortical silent brain infarction as a risk factor for
clinical stroke. Stroke. 1997; 28:19321939. [PubMed: 9341698]
34. Wong TY, Klein R, Sharrett AR, et al. Cerebral white matter lesions, retinopathy, and incident
clinical stroke. Jama. 2002; 288:6774. [PubMed: 12090864]
35. Kwon HM, Kim BJ, Oh JY, et al. Retinopathy as an indicator of silent brain infarction in
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Henderson et al.
Page 7
Main points
The presence of hypertensive funduscopic abnormalities is clearly related to

stroke, even after controlling for level of blood pressure and other vascular risk
factors.
Retinal changes indicative of a breakdown of the blood-retina barrier (such as

retinal hemorrhages, microaneurysms and cotton wool spots) seem to confer a
greater increase in stroke risk than sclerotic retinal changes (such as generalized
and focal retinal arteriolar narrowing and arteriovenous nicking).
With continuing improvement in retinal photographic techniques and automated

retinal image analysis, evaluation of retinal microvascular signs of hypertension
from retinal photographs may begin to move from predominately the research
arena to clinical practice.
Evaluation for signs of hypertensive retinopathy, along with the assessment of

the presence or absence of other known vascular risk factors, may allow
clinicians to further individualize a risk profile for stroke for each patient, thus
permitting more accurate risk stratification and, potentially, guiding treatment
strategies.

Henderson et al.
Page 8

Figure 1.
Evolution of severe bilateral hypertensive retinopathy and choroidopathy over time (the
right eye is on the left and the left eye is on the right).
Top row of photographs: Acutely, the patient complains of mild bilateral visual loss and
blood pressure is 224/68 mmHg. Note the attenuation of retinal arteries, dilation of the
veins, cotton wool spots (soft exudates) (white circle), flame shaped hemorrhages (white
arrowheads), hard exudates (white arrow), and Elschnig spots (star). There is macular edema
bilaterally, which explains the decreased visual acuity.
Second row of photographs: Retinal fluorescein angiography showing hyperfluorescence at
the level of the Elschnig spots (star), and microaneurysms (white arrows).
Third row of photographs: Retinal appearance two weeks later (after normalization of blood
pressure). Note the improvement of macular edema and the increased hard exudates.
Henderson et al.
Page 9
Bottom row of photographs: Three months later, the cotton wool spots and retinal
hemorrhages have resolved. The arterial attenuation persists, and the veins are less dilated.
Both optic nerves have become slightly pale.

Henderson et al.
Page 10

Figure 2.
Stage III/IV hypertensive retinopathy (the right eye is on the left and the left eye is on the
right). There is mild bilateral optic nerve edema. Note the arteriovenous nicking (white
arrows), the flame hemorrhage (white arrowhead), the boat-shaped hemorrhage (star), and
the arteriolar narrowing (black arrows).

Henderson et al.
Page 11

Figure 3.
Severe stage IV hypertensive retinopathy with bilateral optic nerve head edema in the setting
of malignant hypertension (the right eye is on the left and the left eye is on the right).
Top row of photographs: Acutely, there is severe bilateral optic nerve head edema with
dilated and tortuous veins and exudates.
Bottom row of photographs: Three months after treatment of hypertension, the optic nerve
edema has resolved, but the patient has developed severe bilateral optic nerve atrophy.


Number of
5888
15,792
4926
3654
14,926
Study name or
Cardiovascular Health Study

(CHS)
Atherosclerosis Risk in
Communities (ARIC) study
Beaver Dam Eye Study (BDES)
Blue Mountains Eye Study

(BMES)
Rotterdam Eye Study
>45
4997
4384
4564
6597
Age
range in
years
Prospective cohort study ongoing since 1990 in the city of Rotterdam in The Netherlands. As of 2008, 14,926 subjects aged 45 years or
over comprise the Rotterdam Study cohort.
Population-based survey of vision and eye disease in an urban population aged 49 years or older, resident in two postcode areas in the
Blue Mountains region, west of Sydney, Australia.
A private census of the population of Beaver Dam, Wisconsin (US) was performed from September 15, 1987 to May 4, 1988 to identify
all residents in the city or township of Beaver Dam, Wisconsin, who were 43 to 84 years of age. Of the 5924 eligible individuals, 4926
participated in the baseline examination between March 1, 1988 and September 14, 1990. 3684 of those surviving (81.1%) participated
in the 5-year follow- up examination between March 1, 1993 and June 14, 1995.
Population samples were selected by probability sampling methods in 19871989 from 4 US communities: Forsyth County, North
Carolina (n = 4,035); Jackson, Mississippi (blacks only; n = 3,728); the northwestern suburbs of Minneapolis, Minnesota (n = 4,009);
and Washington County, Maryland (n = 4,020).
Prospective cohort study based on sampling from Medicare eligibility lists, non- institutionalized, ambulatory men and women age 65
and older were enrolled, including 5201 at 4 US field centers (Forsyth County, North Carolina; Sacramento County, California;
Washington County, Maryland; and Allegheny County, Pennsylvania) in 198990, and an additional 687 African-American participants
in 199293 at 3 of the 4 sites.
Recent large population-based studies evaluating the relationships between ocular effects of hypertension and cerebrovascular disease
Table 1
Henderson et al.
Page 12
Henderson et al.
Page 13
Table 2
Association of hypertensive retinal microvascular changes and neurologic and cardiovascular complications in
recent large population-based studies
Retinal microvascular changes
Associations
Strength of association*
Retinal hemorrhages
Current blood pressure
+++
Microaneurysms
Carotid artery disease
+++
Cotton wool spots
Incident clinical stroke
+++
Subclinical cerebral disease (MRI)
+++
Cognitive impairment
+++
Cardiovascular mortality
+++
Renal dysfunction
+++
+++
Past blood pressure
+++
++
Subclinical cerebral disease (MRI)
++
Renal dysfunction
Metabolic syndrome
+++
Incident hypertension
Metabolic syndrome
+++
Past blood pressure
+++
Incident hypertension
++
Carotid atherosclerosis
++
Incident heart disease
++
Metabolic syndrome
Larger retinal venular caliber

++
Severity of hypertensive retinopathy (See Table 3)
Associations
Strength of association*
Grade I/II hypertensive retinopathy
Stroke
+/++
Ischemic heart disease
+/++
Stroke
+++
Cognitive impairment
+++
+++
Renal dysfunction
+++
Mortality
+++
Arterio-venous nicking
Focal arteriolar narrowing
Generalized arteriolar narrowing
Grade III hypertensive retinopathy
Grade IV hypertensive retinopathy
Henderson et al.
Page 14
Strength of association: +++ (relative risk/odds ratio >2.0); ++ (relative risk/odds ratio 1.52.0); + (relative risk/odds ratio <1.5)

Henderson et al.
Page 15
Table 3
Keith, Wagener, and Barker classification of hypertensive retinopathy, which grades retinopathy from I to IV
based on its severity (11)
Grade I
Slight or modest narrowing of the retinal arterioles, with an arteriovenous ratio of 1:2
Grade II
Modest to severe narrowing of retinal arterioles with an arteriovenous ratio <1:2 or arteriovenous nicking
Grade III
Soft exudates or flame-shaped hemorrhages
Grade IV
Bilateral optic nerve edema


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Published in final edited form as:

Hypertension-related eye abnormalities and the risk of stroke

of Neurology, Emory University School of Medicine, Atlanta, Georgia

of Neurological Surgery, Emory University School of Medicine, Atlanta, Georgia

NIH-PA Author Manuscript

NIH-PA Author Manuscript

Ocular effects of systemic hypertension

NIH-PA Author Manuscript

Hypertensive choroidopathy occurs as a result of choroidal ischemia, which develops

NIH-PA Author Manuscript

Hypertensive retinopathy describes a spectrum of microvascular abnormalities in people

NIH-PA Author Manuscript

Evaluating the ocular effects of hypertension with retinal photography

NIH-PA Author Manuscript

To evaluate hypertensive funduscopic damage, the retinal vasculature must be visualized

Ocular effects of systemic hypertension and stroke

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Conclusion and future perspectives

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indicative of a breakdown of the blood-retina barrier (such as retinal hemorrhages,

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The presence of hypertensive funduscopic abnormalities is clearly related to

Retinal changes indicative of a breakdown of the blood-retina barrier (such as

With continuing improvement in retinal photographic techniques and automated

Evaluation for signs of hypertensive retinopathy, along with the assessment of

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Cardiovascular Health Study

Beaver Dam Eye Study (BDES)

Blue Mountains Eye Study

Rotterdam Eye Study

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Current blood pressure

Carotid artery disease

Cotton wool spots

Incident clinical stroke

Subclinical cerebral disease (MRI)

Current blood pressure

Past blood pressure

Incident clinical stroke

Subclinical cerebral disease (MRI)

Current blood pressure

Current blood pressure

Past blood pressure

Incident clinical stroke

Incident heart disease

Larger retinal venular caliber