Impact of Polycystic Ovary Syndrome on Silent Coronary Artery Disease and Cardiovascular Events; A Long-term Population-based Cohort Study.


Journal

Archives of medical research
ISSN: 1873-5487
Titre abrégé: Arch Med Res
Pays: United States
ID NLM: 9312706

Informations de publication

Date de publication:
04 2022
Historique:
received: 22 08 2021
revised: 29 10 2021
accepted: 04 11 2021
pubmed: 27 11 2021
medline: 28 4 2022
entrez: 26 11 2021
Statut: ppublish

Résumé

The existing data regarding the impact of Polycystic Ovary Syndrome (PCOS) on the risk of developing cardiovascular disease (CVD) are conflicting. To explore the effect of PCOS status on the occurrence of silent coronary artery disease (CAD)/CVD. A total of 1591 women without CVD at baseline, aged 18-45 years, including 356 PCOS patients (defined by the Rotterdam criteria) and 1235 eumenorrheic non-hirsute women without polycystic ovarian morphology (controls), were selected from the Tehran Lipid and Glucose Study (TLGS). The median follow-up was 15.4 years, and most participants were in their late reproductive years at the end of the study. Silent CAD and CVD outcomes in PCOS and control groups were compared according to the multivariable-adjusted hazard ratios (HRs) and cumulative hazard functions. There was no difference in CVD risk factors between the PCOS and control groups. After controlling for confounders, PCOS status did not increase the risk of silent CAD (HR: 0.96, 95% CI 0.86-1.08). Regardless of PCOS status, women with a history of silent CAD showed 2.25 times higher CVD events than those without this history (95% CI 1.63-3.10). PCOS status reduced the CVD incidence by 42%, independently of silent CAD or traditional risk factors (HR: 0.58, 95% CI 0.35-0.98). Whereas silent CAD, regardless of PCOS, accelerated CVD, PCOS preserved it, most likely due to a combination of protective factors, including the endocrine pattern in the late reproductive period, environmental/social elements, and recruiting additional counseling and lifestyle modifications.

Sections du résumé

BACKGROUND
The existing data regarding the impact of Polycystic Ovary Syndrome (PCOS) on the risk of developing cardiovascular disease (CVD) are conflicting.
AIM
To explore the effect of PCOS status on the occurrence of silent coronary artery disease (CAD)/CVD.
METHODS
A total of 1591 women without CVD at baseline, aged 18-45 years, including 356 PCOS patients (defined by the Rotterdam criteria) and 1235 eumenorrheic non-hirsute women without polycystic ovarian morphology (controls), were selected from the Tehran Lipid and Glucose Study (TLGS). The median follow-up was 15.4 years, and most participants were in their late reproductive years at the end of the study. Silent CAD and CVD outcomes in PCOS and control groups were compared according to the multivariable-adjusted hazard ratios (HRs) and cumulative hazard functions.
RESULTS
There was no difference in CVD risk factors between the PCOS and control groups. After controlling for confounders, PCOS status did not increase the risk of silent CAD (HR: 0.96, 95% CI 0.86-1.08). Regardless of PCOS status, women with a history of silent CAD showed 2.25 times higher CVD events than those without this history (95% CI 1.63-3.10). PCOS status reduced the CVD incidence by 42%, independently of silent CAD or traditional risk factors (HR: 0.58, 95% CI 0.35-0.98).
CONCLUSIONS
Whereas silent CAD, regardless of PCOS, accelerated CVD, PCOS preserved it, most likely due to a combination of protective factors, including the endocrine pattern in the late reproductive period, environmental/social elements, and recruiting additional counseling and lifestyle modifications.

Identifiants

pubmed: 34823887
pii: S0188-4409(21)00221-6
doi: 10.1016/j.arcmed.2021.11.001
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

312-322

Informations de copyright

Copyright © 2021. Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Conflict of Interest The authors declare that they have no conflict of interest.

Auteurs

Fatemeh Mahboobifard (F)

Reproductive Endocrinology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Electronic address: f.mahboobifard@sbmu.ac.ir.

Maryam Rahmati (M)

Reproductive Endocrinology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Atrin Niknam (A)

Reproductive Endocrinology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Ehsan Rojhani (E)

Reproductive Endocrinology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Amir Abbas Momenan (AA)

Prevention of Metabolic Disorders Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Fereidoun Azizi (F)

Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Fahimeh Ramezani Tehrani (F)

Reproductive Endocrinology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Electronic address: ramezani@endocrine.ac.ir.

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