Key result
Endothelium-dependent vasodilation was significantly lower during the active phase compared to the placebo phase in women using very low dose OCPs (5.33% vs. 7.23%; P=0.024).
Why the study?
Does the active phase of levonorgestrel/ethinyl estradiol oral contraceptive pills alter endothelial function compared to the placebo phase in healthy young women?
Observational (n=17)
Does the active phase of levonorgestrel/ethinyl estradiol oral contraceptive pills alter endothelial function compared to the placebo phase in healthy young women?
Absolute Event Rate: 5.33% vs 7.23%
p-value: p=0.024
Very low dose ethinyl estradiol combined with levonorgestrel impairs endothelium-dependent vasodilation during the active phase, suggesting levonorgestrel may antagonize the vascular effects of ethinyl estradiol.
Active-phase very low-dose OCPs were associated with impaired endothelial function; hypothesis-generating and should not yet change prescribing.
Oral contraceptive pills (OCPs) are a popular contraception method. Currently, lower-dose ethinyl estradiol formulations are most commonly prescribed, although they have been linked to increased arterial vascular risk. The aim of this study was to investigate endothelial function in healthy young women using lower-dose ethinyl estradiol OCPs. We examined flow-mediated, endothelium-dependent and nitroglycerin-mediated, endothelium-independent vasodilation of the brachial artery, comparing two doses of ethinyl estradiol/levonorgestrel OCPs in 15 healthy young women on two study days: once during the active phase and once during the placebo phase of an OCP cycle. Group low dose (LD) (n=7) active pills contained 150 microg levonorgestrel/30 microg ethinyl estradiol versus Group very low dose (VLD) (n=8) with 100 microg levonorgestrel/20 microg ethinyl estradiol. Endothelium-dependent vasodilation was lower during the active phase in Group VLD (5.33 +/- 1.77% vs. 7.23 +/- 2.60%; P=0.024). This phase difference was not observed in Group LD (8.00 +/- 0.970% vs. 7.61 +/- 1.07%; P=0.647). Endothelium-independent vasodilation did not differ between phases in either group. Finally, we measured endothelium-dependent vasodilation in two additional women who received 10 microg of unopposed ethinyl estradiol. Endothelium-dependent vasodilation was increased by unopposed ethinyl estradiol compared with the placebo phase (10.88 +/- 2.34% vs. 6.97 +/- 1.83%). These results suggest that levonorgestrel may antagonize the activity of ethinyl estradiol. Thus both the progestin type and estradiol dose need to be considered when assessing arterial vascular risk of OCP use in women.
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Torgrimson et al. (2007) conducted an observational in Healthy (n=17). Active phase of oral contraceptive cycle vs. Placebo phase of oral contraceptive cycle was evaluated on Endothelium-dependent vasodilation in Group VLD (100 microg levonorgestrel/20 microg ethinyl estradiol) (p=0.024). Endothelium-dependent vasodilation was significantly lower during the active phase compared to the placebo phase in women using very low dose OCPs (5.33% vs. 7.23%; P=0.024).
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