Abstract
BACKGROUND: The heart rate increases by 10-20 beats per minute (bpm) throughout pregnancy in women, reaching maximum heart rate in the third trimester. During pregnancy, important changes in thyroid hormones also occur, with increases of up to 50% in the levels of triiodothyronine (T(3)), the biological active thyroid hormone. In addition, T(3) has been shown to regulate cardiac electrophysiology. OBJECTIVE: Thus, in the present study the potential contribution of T(3) in pregnancy-induced increased heart rate was explored. METHODS: We compared the heart rate between nonpregnant and pregnant mice under control conditions and after altering thyroid hormone levels with T(3) and propylthiouracil (PTU, an antithyroid drug) treatments. RESULTS: Consistent with the clinical data, we found a 58% rise in T(3) levels during pregnancy in mice. Although pregnant mice had a higher baseline heart rate (607 ± 8 bpm, P = .004) and higher T(3) levels (1.9 ± 0.4 nM, P = .0005) than nonpregnant mice (heart rate: 546 ± 16 bpm; T(3) levels: 1.2 ± 0.1 nM), their heart rate responded similarly to T(3) treatment as nonpregnant mice (nonpregnant: Δ130 ± 22 bpm; pregnant: Δ126 ± 17 bpm, P = .858). Additionally, the heart rate remained significantly elevated (607 ± 11 bpm, P = .038) and comparable to untreated pregnant mice, after the use of the antithyroid drug PTU, although T(3) levels (1.3 ± 0.2 nM, P = .559) returned to nonpregnant values. CONCLUSION: Based on these results, it is unlikely that T(3) contributes significantly to the pregnancy-induced increased heart rate.