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A study by Dantas et al (2004) , reported that male hypertensive rats present higher superoxide anion  concentration (markers of oxidative stress involved in vascular diseases) under basal condition than do females.  An AT-1-dependent overexpression of the NAD(P)H-oxidase components may account for the sexual dimorphism in oxidative stress, and may play an important role in the noted sex differences on incidence of cardiovascular disease [1].

Kain et al (2001) investigated sex differences in conventional, coagulation and fibrinolytic factors in South Asian ischemic stroke patients. Their results suggest that South Asian females have increased FVII levels and that females with a history of ischemic stroke have a decreased fibrinolytic potential in comparison with men[2].

Traditional risk factors for atherosclerosis cannot account for all patients who develop coronary heart disease or stroke and this has stimulated interest in reevaluating these factors and considering other determinants of pathogenesis[3]. Our understanding of atherogenesis has evolved from a focus on lipid deposition within the arterial wall causing obstruction to the inclusion of an inflammatory process that involves specific cellular and molecular responses to endothelial dysfunction.

Recent studies have shown that C-reactive proteins (CRP) have a role in atherothrombosis and indicate that concentrations of these substances could be used as a marker for future vascular events. Rogowski et al[4] discovered significant sex differences in hs-CRP concentrations despite perfect matching for age and body mass index (BMI), this should be reflected in guidelines that suggest hs-CRP cut-off points for the stratification of vascular risk[4]. At the present there is insufficient support for the widespread use of a CRP screening test as a strategy for determining the risk of CVD.


The risk of rupture in male patients with an abdominal aortic aneurysm ( AAA) is low. However, the four-time higher risk of rupture in female patients with AAA of the same size suggests that a lower threshold for surgery should be considered in fit women[5].


The combined oral contraceptive pill (OCP) and hormone replacement therapy (HRT) increase the risk of venous thrombosis. Women should be evaluated for other factors predisposing them to thrombosis before these drugs are prescribed.

Though the increased thrombotic risk associated with the OCP and HRT is usually attributed to estrogen, Weisberg[6] suggests that contraceptives containing the progestogens desogestrel, gestodene or norgestimate may also increase risk. However, confounding factors in these studies make interpretation difficult. The increased risks associated with HRT may be offset by its benefits in relieving menopausal symptoms.

Data from the National Hospital Discharge Survey (2003) do not support a sex bias in the diagnosis of Pulmonary Embolism (PE) or Deep Venous Thrombosis (DVT), the use of diagnostic tests, or the duration of hospitalization for PE or DVT[7].

Risk factors

The risk of developing blood clots is greater for women who have one or several of these risk factors:

  • Pregnancy: a woman’s risk of developing blood clots is six times greater when she is pregnant. During pregnancy estrogens are elevated in the blood and studies have shown that estrogen increases blood clotting.

  • Birth control pill: oral contraceptives that contain progesterone are associated with increased risk. Women who had progesterone skin implants also carry a risk of DVT and PE.

  • Hormone replacement therapy: any HRT that contains the hormone estrogen (also known as estrogen replacement therapy) or progesterone may increase the risk of blood clots.

Men and women both experience the following risk factors:

  • Varicose veins: these veins in the leg are distended, lengthened and twisted, making blood flow slower than normal.

  • Prolonged immobility: people who are immobile for a long period of time, such as bedridden patients or those on long plane flights, are at risk for developing blood clots due to stasis.

Other risk factors include clotting abnormalities, obesity, history of DVT, cancer, stroke, chronic heart or respiratory failure, and procedures such as orthopedic, pelvic and abdominal surgery. The risk of developing blood clots also increases with age.


1. Dantas AP, Franco Mdo C, Silva-Antonialli MM, Tostes RC, Fortes ZB, Nigro D, Carvalho MH, Gender differences in superoxide generation in microvessels of hypertensive rats: role of NAD(P)H-oxidase, Cardiovascular Research. 61(1):22-9, 2004

2. Kain K, Catto AJ, Carter AM, Young J, Bamford J, Bavington J, Grant PJ. Decreased fibrinolytic potential in South Asian women with ischaemic cerebrovascular disease,British Journal of Haematology, 114(1):155-61, 2001

3. Nguyen VH, McLaughlin MA., Coronary artery disease in women: a review of emerging cardiovascular risk factors, Mount Sinai Journal of Medicine. 69(5):338-49, 2002

4. Rogowski O, Zeltser D, Shapira I, Burke M, Zakut V, Mardi T, Ben-Assayag E, Serov J, Rozenblat M, Berliner S., Gender difference in C-reactive protein concentrations in individuals with atherothrombotic risk factors and apparently healthy ones, Biomarkers, 9(1):85-92, 2004

5. Brown P. M., Zelt D. T. and Sobolev B, The risk of rupture in untreated aneurysms: The impact of size, gender, and expansion rate, Journal of Vascular Surgery, 2003;37:280-4.

6. Weisberg E., Contraception, hormone replacement therapy and thrombosis, Aust Prescr 2002;25:57-9

7. Stein PD, Hull RD, Patel KC, Olson RE, Ghali WA, Alshab AK, Meyers FA, Venous thromboembolic disease: comparison of the diagnostic process in men and women Archives of Internal Medicine,2003;163(14):1689-94

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