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Changes in Central Arterial Pressure Waveforms during the Normal Menstrual Cycle
  1. Nadia Ounis-Skali,
  2. Gary F. Mitchell,
  3. Caren G. Solomon,
  4. Scott D. Solomon,
  5. Ellen W. Seely
  1. From the Endocrinology, Diabetes and Hypertension Division (N.O.-S., E.W.S.), Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; Cardiovascular Engineering (G.F.M.), Waltham, MA; Division of General Medicine (C.G.S.), Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; Cardiovascular Division (S.D.S.), Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA
  1. Address correspondence to: Dr. Ellen W. Seely, Endocrinology, Diabetes and Hypertension Division, Brigham and Women's Hospital, 221 Longwood Avenue, Boston, MA 02115; tel: 617 732 5012; fax: 617 732 5764; e-mail: eseely{at}partners.org.
  2. Supported by NIH grants K24 RR 018613 and R01 HL 67332 to EWS and GCRC MO1-RR02635.
  3. Presented in part as a poster at the American College of Cardiology Scientific Sessions, Atlanta, GA, March 2002.

Abstract

Background Changes in estradiol and progesterone during the human menstrual cycle may impact vascular and cardiac function. Renin-angiotensin-aldosterone system (RAAS) hormones increase during the luteal phase of the menstrual cycle and may antagonize the vascular effects of estradiol. This study was designed to investigate central arterial changes, cardiac function, and RAAS activity in response to gonadal steroid variations during the menstrual cycle.

Methods We studied 15 women during the follicular and midluteal phases with determination of estradiol, progesterone, hormones of the RAAS, and spot urine sodium and creatinine levels. Central pulsatile hemodynamics was evaluated using calibrated carotid tonometry and central aortic Doppler flow. Systolic ejection period (SEP) and systolic pressure time integral (SPTI) were computed from carotid pressure waveforms.

Results Levels of estradiol, progesterone, and RAAS hormones were higher in the luteal phase. SEP and SPTI were lower during the luteal phase, whereas central and peripheral blood pressures and measures of arterial stiffness were unchanged between the two phases. The urine sodium-to-creatinine ratio was similar at both phases.

Conclusion Central arterial stiffness does not differ between the follicular and midluteal phases of the menstrual cycle in healthy women, despite significant changes in estradiol and progesterone levels. Systole was shortened during the midluteal phase. RAAS activation during the luteal phase may be responsible for a lack of the expected estradiol-mediated reduction in arterial stiffness between the two phases of the menstrual cycle. Because load was unchanged, the decrease in SEP and SPTI may represent a direct effect of estrogen, progesterone, or RAAS activation on ventricular function.

Key Words
  • menstrual cycle
  • renin-angiotensin-aldosterone system
  • blood vessel

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