Sympathetic activation and endothelial dysfunction in polycystic ovary syndrome are not explained by either obesity or insulin resistance.
OBJECTIVE
Polycystic ovary syndrome (PCOS) is a common endocrine condition underpinned by insulin resistance and associated with increased risk of obesity, type 2 diabetes and adverse cardiovascular risk profile. Previous data suggest autonomic imbalance [elevated sympathetic nervous system (SNS) activity and decreased heart rate variability (HRV)] as well as endothelial dysfunction in PCOS. However, it is not clear whether these abnormalities are driven by obesity and metabolic disturbance or whether they are independently related to PCOS.


METHODS
We examined multiunit and single-unit muscle SNS activity (by microneurography), HRV (time and frequency domain analysis) and endothelial function [ischaemic reactive hyperaemia index (RHI) using the EndoPAT device] in 19 overweight/obese women with PCOS (BMI: 31·3 ± 1·5 kg/m(2), age: 31·3 ± 1·6 years) and compared them with 21 control overweight/obese women (BMI: 33·0 ± 1·4 kg/m(2), age: 28·2 ± 1·6 years) presenting a similar metabolic profile (fasting total, HDL and LDL cholesterol, glucose, triglycerides, insulin sensitivity and blood pressure).


RESULTS
Women with PCOS had elevated multiunit muscle SNS activity (41 ± 2 vs 33 ± 3 bursts per 100 heartbeats, P < 0·05). Single-unit analysis showed that vasoconstrictor neurons were characterized by elevated firing rate and probability and incidence of multiple spikes (P < 0·01 for all parameters). Women with PCOS also had impaired endothelial function (RHI: 1·77 ± 0·14 vs 2·18 ± 0·14, P < 0·05). HRV did not differ between the groups.


CONCLUSIONS
Women with PCOS have increased sympathetic drive and impaired endothelial function independent of obesity and metabolic disturbances. Sympathetic activation and endothelial dysfunction may confer greater cardiovascular risk in women with PCOS.
Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Vic., Australia.|Department of Physiology, Monash University, Clayton, Vic., Australia.
Elisabeth A
EA
Lambert
Monash Centre for Health Research and Implementation, Monash University and Monash Health, Clayton, Vic., Australia.
Helena
H
Teede
Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Vic., Australia.
Carolina Ika
CI
Sari
Monash Centre for Health Research and Implementation, Monash University and Monash Health, Clayton, Vic., Australia.
Eveline
E
Jona
Monash Centre for Health Research and Implementation, Monash University and Monash Health, Clayton, Vic., Australia.
Soulmaz
S
Shorakae
Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Vic., Australia.
Kiri
K
Woodington
Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Vic., Australia.
Robyn
R
Hemmes
Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Vic., Australia.
Nina
N
Eikelis
Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Vic., Australia.
Nora E
NE
Straznicky
Monash Centre for Health Research and Implementation, Monash University and Monash Health, Clayton, Vic., Australia.
Barbora
B
De Courten
Clinical Obesity Research laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Vic., Australia.
John B
JB
Dixon
Hypertension & Kidney Disease Laboratories, Baker IDI Heart & Diabetes Institute, Melbourne, Vic., Australia.|Primary Health Care and the Department of Cardiovascular Medicine, Alfred Hospital, Prahran, Vic., Australia.
Markus P
MP
Schlaich
Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Vic., Australia.|Faculty of Medicine, Nursing and Health Sciences, Monash University, Clayton, Vic., Australia.
Gavin W
GW
Lambert
D000328:Adult; D002318:Cardiovascular Diseases / Q000097:blood; D005260:Female; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D009765:Obesity / Q000503:physiopathology*; D011085:Polycystic Ovary Syndrome / Q000097:blood / Q000209:etiology* / Q000503:physiopathology*; D012307:Risk Factors; D013564:Sympathetic Nervous System / Q000503:physiopathology*