Retinal artery and vein diameters during pregnancy in diabetic women

To study systemic and retinal circulatory variables and vasoactive hormones during pregnancy in women with and without diabetes.

Prospective study of 45 women with type 1 diabetes and 6 healthy pregnant women, from the first trimester of pregnancy to half a year after delivery, by using a fundus photographic method of determining retinal vessel diameters.

In diabetic women, the mean arterial blood pressure increased from 90.7 +/- 10.9 mm Hg (mean +/- SD) in the first trimester to 102.4 +/- 16.4 mm Hg in the third trimester, accompanied by retinal arteriolar constriction, from a mean diameter of 95.5 +/- 11.3 to 92.2 +/- 12.9 microm (P = 0.007), arteriolar constriction being prominent in nonsmokers, from 96.6 +/- 11.1 to 92.3 +/- 13.0 microm (P < 0.001; n = 38), but absent in smokers, from 89.2 +/- 11.5 to 92.0 +/- 13.6 microm (P = 0.28). Healthy nonsmoking women demonstrated an increase in blood pressure during pregnancy comparable to that in diabetic women, but the change in mean retinal arteriolar diameter, from 88.5 +/- 10.9 microm in the first to 91.6 +/- 10.2 microm in the third trimester, did not reach statistical significance (P = 0.38). Diabetic retinopathy levels increased during pregnancy, but the change in arteriolar diameter from the first to the third trimester did not correlate with retinopathy, arterial blood pressure, HbA(1c), or atrial natriuretic peptide. Plasma angiotensin II correlated positively with the change in arteriolar diameter in women who did not smoke (P < 0.05). After delivery, retinal vessel diameters returned to the first trimester range in all subgroups.

From the first to the third trimester of pregnancy, blood pressure increased and retinal arteriolar diameter decreased in diabetic women, but the arteriolar constriction associated with pregnancy and systemic arterial blood pressure increase was remarkably absent in diabetic women who smoked tobacco before and during pregnancy. It is unknown whether smoking inhibits this vasoconstrictive response by deactivating mechanisms of physiological adaptation or by activating these mechanisms before the first trimester of pregnancy.