Greater Arterial Stiffness in Polycystic Ovary Syndrome (PCOS) Is an Obesity- But Not a PCOS-Associated Phenomenon
Context: Polycystic ovary syndrome (PCOS) and obesity are associated with cardiovascular disease, but it is unclear to what extent they contribute independently. Arterial stiffness might link obesity and PCOS to cardiovascular diseases. Objective: Our objective was to investigate whether PCOS in the...
Saved in:
Published in: | The journal of clinical endocrinology and metabolism Vol. 95; no. 10; pp. 4566 - 4575 |
---|---|
Main Authors: | , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Bethesda, MD
Endocrine Society
01-10-2010
|
Subjects: | |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | Context: Polycystic ovary syndrome (PCOS) and obesity are associated with cardiovascular disease, but it is unclear to what extent they contribute independently. Arterial stiffness might link obesity and PCOS to cardiovascular diseases.
Objective: Our objective was to investigate whether PCOS in the presence or absence of obesity is linked with arterial stiffness.
Design and Setting: We conducted a cross-sectional study, including 31 obese (18 with PCOS) and 39 lean (22 with PCOS) women.
Interventions and Main Outcome Measures: Estimates of arterial stiffness were obtained by ultrasonography (distensibility and compliance of carotid, femoral, and brachial arteries; carotid elastic modulus; and intima-media thickness) and pulse wave transit time analyses (carotid-femoral pulse wave velocity and aortic augmentation index).
Results: Obese women, with or without PCOS, had stiffer arteries than lean women. After adjustment for 24-h mean arterial pressure and age, obesity was inversely associated with the femoral, brachial, and carotid distensibility coefficients [β (95% confidence interval), −0.354 (−0.614 to −0.094), −0.354 (−0.547 to −0.161), and −0.248 (−0.370 to −0.126) 10−3/kPA, respectively] and with the femoral and carotid compliance coefficients [−0.296 (−0.563 to −0.029) and −0.190 (−0.377 to −0.003) mm2/kPA, respectively] but not with the brachial compliance coefficient [−0.018 (−0.052–0.015) mm2/kPA], Young’s elastic modulus [0.049 (−0.005–0.103) kPA], aortic pulse wave velocity and aortic augmentation index [0.050 msec (−0.959–1.058 msec) and −1.831% (−8.196–4.534%), respectively]. Analyses with waist circumference as key independent variable gave broadly similar results. In contrast, PCOS was not associated with arterial stiffness estimates after adjustment for the presence of obesity.
Conclusions: In young obese women with PCOS, (central) obesity, rather than PCOS itself, is associated with increased arterial stiffness. These data emphasize that, from the perspective of cardiovascular risk reduction, the focus should be on central fat mass reduction in obese women with PCOS.
Arterial stiffness might link obesity and PCOS to cardiovascular diseases; data showed that obesity, rather than PCOS itself, is associated with increased arterial stiffness. |
---|---|
Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0021-972X 1945-7197 |
DOI: | 10.1210/jc.2010-0868 |