Cardiometabolic risk in women with polycystic ovary syndrome: a comprehensive review.

Abstract

Introduction: Polycystic ovary syndrome (PCOS) is a common endocrine disorder affecting reproductive-aged women, which is associated with a significantly higher risk of developing cardiometabolic abnormalities. The present review is aimed to understand the different mechanism related to the cardiometabolic alteration of women with PCOS.

Evidence acquisition: A literature search was made on terms encompassing PCOS, hyperandrogenism, obesity, lipid metabolism, insulin resistance, inflammation, oxidative stress, gut microbiota, cardiovascular event, and mortality.

Evidence synthesis: Hyperandrogenism is the key signature of women with PCOS. Androgens by reducing the intracellular signal of insulin, induce an insulin resistance that is compensated by hyperinsulinemia. Hyperinsulinemia and insulin resistance are the key determinants of the metabolic syndrome and therefore of the cardiovascular risk. Obesity, oxidative stress and chronic inflammation further increase insulin resistance and represent adjunctive pejorative risk factors. Modification of gut microbiota is common in women with PCOS, and it is consequent to hyperandrogenism and obesity. Gut dysbiosis contributes to induce metabolic alterations. In women with PCOS the cardiovascular risk depends upon syndrome manifestation. The risk is maximal in hyperandrogenic obese anovulatory women, milder in hyperandrogenic non obese women, and is not increased in non-hyperandrogenic PCOS women.

Conclusions: Among PCOS women, phenotypes characterized by hyperandrogenism, anovulation and obesity are at high risk of cardiometabolic alterations. In general, a careful investigation on the presence of cardiovascular risk factors, and the use of appropriate remedies to reduce them, is useful in all PCOS women with hyperandrogenism, and in particular in those with associated anovulation and obesity.