These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Changes in central arterial pressure waveforms during the normal menstrual cycle.
    Author: Ounis-Skali N, Mitchell GF, Solomon CG, Solomon SD, Seely EW.
    Journal: J Investig Med; 2006 Sep; 54(6):321-6. PubMed ID: 17134615.
    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.
    [Abstract] [Full Text] [Related] [New Search]