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Effects of Blood Pressure and Retinal Arteriolar Caliber on Diabetic Retinopathy Risk – A Conceptual Paradox
- Ning Cheung, Tien Y Wong (19 September 2008)
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Statistically significant indifference
- Konrad Pesudovs (13 October 2008)
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Re: Statistically significant indifference: response from authors
- Maria E Craig, Patricia Herald Gallego and Kim C Donaghue (16 October 2008)
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Ning Cheung, Research Fellow Centre for Eye Research Australia, University of Melbourne, Royal Victorian Eye and Ear Hospital, Tien Y Wong
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Gallego et al. provide compelling evidence for a continuous relation between elevated blood pressure and risk of retinopathy in young people with type 1 diabetes.1 The underlying pathophysiological mechanisms for this relation, however, were not explained and remain unclear. It is well known that elevated blood pressure can cause adverse changes in the retinal vasculature. For example, retinal arteriolar narrowing is a classical sign of hypertension.2,3 Population-based studies have consistently shown that retinal arteriolar narrowing, which can now be reliably measured by using computer-based analysis of retinal images, is positively and monotonously associated with both past and current blood pressure levels.2,3 Prospective studies indicate that the presence of retinal arteriolar narrowing may also predict the risk of incident hypertension, independent of conventional cardiovascular risk factors.2,3 Based on these findings, it would be logical to hypothesize that retinal arteriolar narrowing could play a pathogenic role in the link between elevated blood pressure and the development of diabetic retinopathy. Nevertheless, recent studies on the association between retinal vascular caliber changes and diabetic retinopathy do not seem to support such theory. In fact, a paradoxical relation has been observed. Prospective data from two population-based studies of older people with type 2 diabetes, along with those from a sub-cohort of this study in young people with type 1 diabetes, show that retinal arteriolar dilation, instead of narrowing, is an independent predictor for diabetic retinopathy risk.4-6 This finding fits well with an intriguing hypothesis that retinal arteriolar dilation may, according to the laws of Laplace and Starling, increase downstream capillary pressure.4 The resultant capillary wall dilation, leakage and rupture can correspondingly lead to the development of diabetic retinopathy signs, including microaneurysms, exudates, hemorrhages and macular edema. What do all these findings mean? The answer is not obvious. Although we are now more certain that elevated blood pressure is a risk factor for the development of diabetic retinopathy in patients with either type 1 or 2 diabetes, our understanding of the mechanistic pathways occurring in the retinal circulation is far from complete. (1) Gallego PH, Craig ME, Hing S, Donaghue KC. Role of blood pressure in development of early retinopathy in adolescents with type 1 diabetes: prospective cohort study. BMJ 2008;337:a918. doi: 10.1136/bmj.a918. (2) Wong TY, Mitchell P. Hypertensive retinopathy. N Engl J Med 2004;351:2310-7. (3) Wong TY, Mitchell P. The eye in hypertension. Lancet 2007;369:425-35. (4) Cheung N, Tikellis G, Wang JJ. Diabetic retinopathy. Ophthalmology 2007;114:2098-9 (5) Rogers SL, Tikellis G, Cheung N, Tapp R, Shaw J, Zimmet PZ, Mitchell P, Wang JJ, Wong TY. Retinal arteriolar caliber predicts incident retinopathy: the Australian Diabetes, Obesity and Lifestyle (AusDiab) study. Diabetes Care 2008;31:761-3. (6) Cheung N, Rogers SL, Donaghue KC, Jenkins AJ, Tikellis G, Wong TY. Retinal arteriolar dilation predicts retinopathy in adolescents with type 1 diabetes. Diabetes Care 2008;31:1842-6. Competing interests: None declared |
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Konrad Pesudovs, Associate Professor of Ophthalmology Flinders Medical Centre, Bedford Park, SA 5042, Australia
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Gallego et al appear to over-estimate the risk of retinopathy associated with higher blood pressure by 10 fold. In the discussion they state: “In the longitudinal cohort, a 10mmHg higher systolic blood pressure was associated with a 3-20% higher risk of retinopathy; a 10 mm Hg higher diastolic blood pressure increased the risk for retinopathy by 2 -30%”. However, the odds ratios presented in table 3 are: systolic blood pressure (mm Hg) 1.01 (1.003 to 1.02) and diastolic blood pressure (mm Hg) 1.01 (1.002 to 1.03). These represent a 0.3-2% and a 0.2-3% increase in risk. This may well be a statistically significant difference, but it is also very close to no difference at all. The authors interpretation of a difference in risk of the order of 1% as an indication for “lowering blood pressure, even in patients without hypertension” to “improve retinal outcomes” does not seem justified. Competing interests: None declared |
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Maria E Craig, Paediatric Endocrinologist The Children's Hospital at Westmead, Locked Bag 4001, Westmead NSW 2145, Australia, Patricia Herald Gallego and Kim C Donaghue
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Assoc Prof Konrad Pesudovs raises an important issue with regard to effect size but he has misunderstood our results. We have not overestimated the effect of blood pressure on retinopathy by tenfold. In table 3 the odds ratios were determined using blood pressure as a continuous variable (i.e. in 1 mmHg increments). We recognised, however, that a 1 mmHg change in blood pressure is a small clinical change. Therefore we reported the effect size using 10 mmHg increments in the discussion. This also reflects the more common practice of reporting blood pressure in the clinical setting. Rather than stating a 1 mmHg increase in systolic blood pressure increases the risk of retinopathy by 0.3-2%; we report that a 10 mmHg increase in SBP increases the risk of retinopathy by 3-20%. Competing interests: None declared |
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