Cardiovascular Risk in PCOS Women

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PCOS is considered a pathological condition at high risk for CVDs. This is not only due to the presence of androgen excess, insulin resistance, obesity, DM2, and dyslipidemia, but also because of many other risk factors (120) (Table 2). These cardiovascular risk factors are often evident at an early age, suggesting that women with PCOS represent a large population at increased risk for developing

Table 1

Prevalence of Impaired Glucose Tolerance (IGT) and Type 2 Diabetes Mellitus (DM2) in Women with PCOS Living in Different Geographical Areas in the World

Table 1

Prevalence of Impaired Glucose Tolerance (IGT) and Type 2 Diabetes Mellitus (DM2) in Women with PCOS Living in Different Geographical Areas in the World

Reference

Ethnicity

IGT

T2D

Age range (years)

Legro et al. 1999 (115)

Hispanic-American

31.1%

7.5%

14-44

Ehrmann et al. 1999 (116)

Hispanic-American

35%

10%

13.5-40

Weerakiet et al. 2001 (117)

Asian Thai

22.8%

17.7%

15-40

Gambineri et al. 2004 (88)

Italian

15.7%

2.5%

Classic and Newer Risk Factors for Cardiovascular Diseases in PCOS

• Insulin resistance

Metabolic syndrome (glucose, lipid, ABP disorders)

• Impaired glucose tolerance and type 2 diabetes mellitus

• Decreased cardiac systolic flow velocity and diastolic dysfunction

• Endothelial dysfunction

• Increased vascular stiffness

• Low-grade chronic inflammation

• Increased oxidative stress

• Altered circulating divalent cations

• Altered hemostasis including impaired fibrinolysis

• Increased tissue plasminogen activator antigen

• Homocysteine

• Left ventricular hypertrophy

• Increased endothelin 1

• Impaired arterial viscoelastic properties

• Increased intima media thickness

• Others early-onset CVD, even if this has not yet been confirmed in prospective studies (121). The risk of CHD and myocardial infarction has been reported to be increased in patients with PCOS compared with regularly cycling women (122), although, to date, no prospective study of cardiovascular mortality in PCOS has been performed (123). On the other hand, several studies reported alterations in intermediate end-points for CVD in this population (120). In fact, endothelial (124) and diastolic (125) dysfunction have been demonstrated in PCOS subjects and have been associated with both elevated androgen levels and insulin resistance. Elevated homocysteine and left ventricular hypertrophy have recently been shown to be independently associated with an increased risk of CVD (126). Other biochemical, morphological, and functional markers of early CVD have been evaluated to correctly identify the cardiovascular morbidity of this syndrome. One of the early signs of CVD is endothelial injury. Precocious anatomical and functional arterial changes have also been reported in PCOS women (120, 121). In this case too, insulin resistance is likely the major risk factor for the occurrence of CVD in PCOS women and could play a key role in the development of endothelial damage, which is an early sign of atherosclerosis.

Data on endothelial dysfunction in PCOS patients are poor and conflicting. An association between PCOS and early carotid atherosclerosis was demonstrated in several studies (120,121). Some authors (127) reported no difference in flow mediated dilation, which is a measure of reactive vascular hyperemia, between PCOS patients and controls. Conversely, others (124) showed markedly diminished endothelium-dependent and insulin-mediated flow responses in the femoral artery of women with PCOS. Furthermore, endothelin-1, a marker of vasculopathy and of endothelial dysfunction, has been reported to be increased in PCOS women (128). In addition, some authors (129) have reported impaired carotid viscoelastic properties in PCOS women, providing additional evidence of vascular dysfunction in women with this syndrome.

A recent study (130) reported increased vascular stiffness and a functional defect in the vascular action of insulin in PCOS patients. In young, normal weight women with PCOS who had normal lipids and blood pressure, endothelial function was altered and intima media thickness was increased, suggesting early functional and structural preatherosclerotic vascular impairment (131). Furthermore, some studies have shown that a 6-month course of metformin improved endothelial structure and function in these young, normal-weight PCOS women (132), further supporting a role for insulin resistance in the pathogenesis of these abnormalities. Intriguingly, some authors have even hypothesized a cardioprotective effect of androgens on the vascular wall in women with PCOS (133). Impaired fibrinolysis, one of the more important cofactors in the development of fatal ischemic heart disease in women (134), has also been demonstrated in women with PCOS. Specifically, a significant increase in serum PAI-1 activity has been reported. This increase was again positively related to insulin resistance but independent of obesity (120). Recently, several data have demonstrated a correlative and causative relationship between insulin resistance and low-grade inflammation (135), which are both important predictors of CVD. Increased levels of CRP have been demonstrated in PCOS women, as well as an increased leukocyte count, specifically in lymphocytes and monocytes (136). Several studies have also shown increased circulating levels of TNF-a and IL-6 (137), although the direct impact of obesity per se, particularly the abdominal phenotype, has been questioned. Other proinflammatory cytokines, such as IL-18, were reported to be increased in PCOS (138). Collectively, the above findings indicate that low-grade chronic inflammation could be a novel mechanism contributing to the increased risk of CHD in PCOS.

Preliminary studies suggested a slight increase in CVD events in women with PCOS. However, the small size and number of these epidemiological studies have been inadequate for conditions as common as PCOS and CVD in women. Larger prospective trials with long-term follow-up are therefore needed to better define the incidence of CVD in PCOS.

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