Editor—Sattar and Greer discuss the probability that complications in pregnancy may predispose women to vascular and metabolic disease in later life.1 The link between pregnancy complications and coronary heart disease remains unexplained. We believe that during pregnancy the hormonal and other stresses provoke cardiovascular and metabolic abnormalities in susceptible individuals, which may recur and become permanent as the patient ages. Many of these are coronary risk factors; disturbances in glucose metabolism, which underlie the development of gestational diabetes, are a good example.
An uncomplicated pregnancy is characterised by obvious changes in lipid metabolism early in pregnancy.2 These include the formation of small, dense subfractions of low density lipoprotein, an important risk factor for atherosclerosis.3 These are retained in the arterial intima, are more easily oxidised, and once oxidised are rapidly taken up into macrophages, creating foam cells and atherosclerotic plaques. The additional effect of pregnancy on lipid metabolism in people with diabetes and those at increased risk of developing diabetes may markedly increase cardiovascular risk in these women.
We recently studied three groups of pregnant women: healthy controls (n=17, mean age 29.2 (SD 1.1 years)), women with type 2 diabetes (n=12, mean age 32.5 (1.6) years), and women with gestational diabetes mellitus (n=12, mean age 32.8 (1.5) years). Venous blood was taken during each trimester (first, 1-13 weeks; second, 14-27 weeks; and third, 28 weeks to term). Samples were analysed for subfractions of low density lipoprotein (polyacrylamide gel electrophoresis) and triglycerides. A score for low density lipoprotein was calculated from the area under the curve for each subfraction; the higher the score the smaller, denser and more atherogenic the low density lipoprotein particles.4
Triglyceride concentrations increased throughout pregnancy in all groups. This was most obvious during the second trimester in women with gestational diabetes (figure). Low density lipoprotein score progressively increased throughout pregnancy, implying the formation of potentially atherogenic lipoproteins. These changes were exaggerated in women with type 2 diabetes but more particularly in those with gestational diabetes (figure).
We found that pregnancy and diabetes have an additive effect on the development of an atherogenic lipid profile. Importantly, this is exaggerated earlier in pregnancy in gestational diabetes. This finding may identify women who are particularly susceptible to the premature development of atherosclerosis. We agree with Sattar and Greer that women with gestational diabetes should be targeted during and after pregnancy with advice on diet and lifestyle to try to modify this excess cardiovascular risk.
Figure.
Triglyceride concentrations and low density lipoprotein score during pregnancy in normal controls and women with type 2 or gestational diabetes. *P<0.05, **P<0.01 compared with normal pregnancy
References
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