I read with interest the article by Man et al.
1 in which the authors measured posterior pole capillary flow in diabetic eyes of different axial lengths using the Heidelberg Retinal Flowmeter. They hypothesized that the decreased retinopathy seen in longer axial length eyes could be explained by a decreased capillary flow in the longer axial length eyes. They expected this because of previous studies demonstrating a decrease in total retinal flow in myopic eyes. Their results showed there to be no decrease in capillary flow in the longer axial length diabetic eyes using the Heidelberg device. Benavente-Perez et al.
2 also found there to be no difference in capillary flow with increasing axial length in normals using a similar device.
Some authors have noted retinal flow (presumably capillary flow is a reflection of retinal flow) to be decreased in myopia, but this phenomenon is most notable in the higher myopes.
3,4 Retinal arterial diameter is a proxy for retinal flow (by the Murray law) and Patton et al.
5 noted a nonstatistically significant trend towards decreased retinal arterial diameters with increasing axial length. However, Wong et al.
6 noted that retinal arterial diameter is constant in a group of eyes ranging from +4 to −6 diopters (D). We had similar results to those of Wong et al.
6 over this range of refractive errors.
7 When the eye's refractive error exceeds −6 D to become more myopic, then these eyes would be considered as being in the malignant myopic group with an associated loss of retinal tissue and consequent need for less retinal flow. We would not have expected retinal flow or retinal capillary flow to be decreased in the range of axial lengths presumably studied by the authors.
However, our original article linking protective factors in diabetic retinopathy to a common pathophysiologic mechanism refers specifically to pressure
7 and not flow (although the two often are linked). High pressure in the capillaries will promote leakage and rupture (Starling principle and Laplace law). The longer arterial tree in axial myopia will result in an attenuation of the intraluminal arteriolar pressure over the course of its increased length; hence, presenting to the capillary bed a lower hydrostatic pressure. We calculated this to be an additional 0.6 mm Hg for every 1 mm increase in axial length from the origin of the central retinal artery at the optic nerve to arterioles of 40 μL in size. Presumably, this decrease in pressure would be even greater by the time the capillary bed was reached, but we were unable to calculate the additional attenuation in these very small vessels. So a decreased capillary flow would not be necessary to explain less retinopathy because pressure in the capillaries would be lowered because of the increased frictional pressure loss induced by the longer vascular tree in the myopes.
The elucidation of the mechanism of capillary microangiopathy in diabetes is critical for prevention and treatments. Perhaps the authors can devise a means to measure for intraluminal pressure. To date, we have not been able to do this.