Left ventricular myocardial mass index and its correlates as an early marker of cardiovascular risk among nonobese normotensive Indian women with polycystic ovary syndrome: lessons from a cross-sectional study

Normotensive, nonobese Indian women with polycystic ovary syndrome more likely have elevated left ventricular mass than do controls matched for age and body mass index, and it positively correlates with proinflammatory markers but not with androgen excess.

Volume 113, Issue 6, Pages 1299–1307.e2


Aafia Rashid, M.Sc., M.Phil.a, Akbar Masood, M.Sc., Ph.D.d, Ishfaq A. Wani, M.Sc.a, Imran Hafeez, M.B.B.S., M.D., D.M.c, Tabasum Parvez, M.B.B.S., M.D.b, Mohd Afzal Zagar, M.Sc., Ph.D.d, Mohd Ashraf Ganie, M.B.B.S., M.D., D.M.



To quantitate left ventricular mass index (LVMI) and correlate it with inflammation, insulin resistance (IR) and serum androgen levels among nonobese normotensive women with polycystic ovary syndrome (PCOS).


Cross-sectional study


Tertiary care institute in North India


A total of 260 drug-naive women qualifying the Rotterdam 2003 criteria for diagnosis of PCOS and 250 apparently healthy women matched for age and body mass index (BMI).


Clinical, biochemical, hormonal, and inflammatory marker assessment was followed by estimation of LVM and LVMI by 2-dimensional echocardiography.

Main Outcome Measures

LVM and LVMI in nonobese, normotensive women with PCOS and its correlation with subinflammation, IR, and androgen excess.


Mean ages (28.08 ± 4.18 vs. 29.44 ± 6.33 years) and BMI (24.43 ± 4.15 vs. 23.92 ± 4.21 kg/m2) of cases vs. controls were comparable, as was blood pressure and plasma glucose (1 hour after oral glucose tolerance test [OGTT]). Women with PCOS had fewer menstrual cycles per year and higher Ferriman-Gallwey scores, plasma insulin, homeostasis model assessment of IR, total testosterone, plasma glucose (fasting and 2 hours after OGTT), serum high-sensitive C-reactive protein, tumor necrosis factor-α, and interleukin-6 than did the controls (P<.001). Significant differences were observed in LVM (101.50 ± 30.19 vs. 89.35 ± 27.57 g) and LVMI (63.60 ± 16.67 vs. 56.32 ± 10.84 g/m2) between women with PCOS and the controls (P<.001). Multivariate analysis revealed that proinflammatory markers and IR rather than hyperandrogenism correlated with LVMI.


We conclude that normotensive nonobese women with PCOS were more likely to have elevated mean LVMI than were healthy controls and it was positively correlated with proinflammatory markers and IR but not with androgen excess. Well-designed long-term follow-up studies with a larger cohort of subjects with comprehensive cardiovascular risk assessment are warranted to conclusively answer the question.

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