CARDIOVASCULAR JOURNAL OF AFRICA • Volume 25, No 5, September/October 2014
AFRICA
231
In support of Cuspidi
et al
.,
31
the frequency of severe
retinopathy (i.e. grade 4) appeared to be low among subjects
with LVH. The same observation was made among subjects
with CKD as well as those with stroke. While we do not have
a definitive explanation for this observation, it is possible
that hypertensive patients in our setting have a reduced life
expectancy so that severe retinopathy has no time to develop.
Hypertensive retinopathy had no association with stroke
in this study, which is at odds with reports from earlier
investigations. Indeed, many cross-sectional studies have
demonstrated a clear relationship between hypertensive ocular
fundoscopic abnormalities and both clinical and subclinical
stroke, even after adjusting for other independent vascular risk
factors.
32-34
However, definitive convincing evidence in favour of
this association has been provided by longitudinal studies.
35-39
Unlike most of these earlier studies that used ocular fundus
photography and brain imaging techniques to increase the
diagnostic accuracy, our diagnosis of stroke was clinical and
retrospective in nature. As a result, a substantial number of
patients who suffered subclinical stroke and/or hypertensive
retinopathy, identifiable using imaging techniques, may have
been unaccounted for. The cost of medical imaging modalities
such as CT scans limits the patient’s access to this sensitive
diagnostic tool. This limitation is also valid for the association
between LVH and hypertensive retinopathy.
Studies on predictors of hypertensive retinopathy have
reported conflicting results. For example, while aging, obesity
measured by BMI, and smoking have been traditionally
associated with increased risk of hypertensive retinopathy, Sharp
et al
.
40
found that age and systolic blood pressure did not
influence hypertensive retinopathy in people of African origin,
despite a higher prevalence of hypertensive retinopathy in this
group compared to people of European descent.
In the ARIC study,
35
only mean blood pressure was associated
with hypertensive retinopathy in the subset of participants of
African descent. LVHandBMI were not significant determinants,
and smoking had a marginally non-significant effect. The risk-
reducing effect of aging, smoking, and LVH on retinopathy that
we found is surprising and adds to existing inconsistencies in
results across studies. We speculated that higher mortality rates,
selectively affecting older people as a result of hypertension-
related complications, and other morbidities in our setting may
contribute to the inverse ORs observed for age and LVH.
Because arteriolar narrowing and arteriovenous nipping can
be found in the absence of hypertension, it has been argued
that these signs have little or no value in the management of
hypertension, and that clear evidence is lacking to show that
patients with mild hypertensive retinopathy need physician
referral or follow up. Conversely, landmark prospective studies
have provided evidence of the clinical value of retinal arteriolar
narrowing. For example, in the Beaver Dam Eye study,
41
the five-
year incidence of retinopathy in general and that of arteriolar
narrowing was significantly higher in patients with elevated
blood pressure, despite being on antihypertensive treatment,
relative to those with controlled blood pressure and those with
no hypertension.
The Blue Mountain Eye study
42
reported an association
between generalised retinal arteriolar narrowing at baseline
and about a three-fold increased risk of five-year incidents
of severe hypertension. These findings emphasise the clinical
value of assessing retinal arteriolar change for cardiovascular
risk prediction, and are supported by international guidelines
for hypertension management such as the US Joint National
Committee on Prevention, Detection, Evaluation and Treatment
of High Blood Pressure, the European Society of Cardiology,
the European Society of Hypertension, and the British Society
of Hypertension.
We acknowledge that this study has some limitations. The
diagnosis of hypertensive retinopathy, particularly in the
early stages, has been shown to suffer from high rates of
inter- and intra-observer variability when assessed with direct
ophthalmoscopy, as in this study. Because only one observer
made the assessment and there was no intra-observer, the results
presented herein did not account for the possible effect of low
reliability. An additional limitation that may have influenced the
results is the small number of study participants who underwent
GFR assessment and echocardiogram, which may limit the
generalisability of our findings.
Conclusion
There was no association between hypertensive retinopathy and
LVH, CKD or stroke in this series. There was a trend towards
increased risk for developing TOD among people with advanced
retinopathy. CKD emerged as the only significant predictor of
hypertensive retinopathy.
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