Polycystic ovary syndrome or Stein-Leventhal syndrome is the most common endocrine-metabolic disorder of reproductive-aged women that implies various severe consequences to female health, including alarming rates of infertility. Great efforts have been made in the last 2 decades to define the syndrome. The exact prevalence of PCOS varies depending on which criteria are used to make the diagnosis, but is as high as 15%–20% when the European Society for Human Reproduction and Embryology criteria are used. Clinical manifestations include oligomenorrhea or amenorrhea, hyperandrogenism, and frequently infertility. Although its exact etiology remains elusive, it is known to feature several hormonal disturbances, including hyperandrogenemia, insulin resistance, and hyperinsulinemia. Insulin appears to disrupt all components of the hypothalamus-hypophysis-ovary axis, and ovarian tissue insulin resistance results in impaired metabolic signaling but intact mitogenic and steroidogenic activity, favoring hyperandrogenemia. Many clinical studies have underlined the connection between PCOS and the cardiovascular risk profile of such female patients, due to a lipid/glucose altered metabolism, hypertension, and systemic inflammatory condition. Apart from well-known cardiovascular risk factors, the recent studies underline interesting common features among these patients such as “non dipping” pattern of blood pressure and increased serum levels of homocysteine. Therefore, PCOS could be considered as a real cardiovascular risk factor which affects the quality of life seriously. Given these severe implications, it is important to thoroughly understand the pathophysiologic interconnections underlying PCOS, in order to provide superior therapeutic strategies and warrant improved quality of life to women with this syndrome.