Among women taking combined hormonal contraceptives (COCs),  arterial accidents rarely occur, and isolated cases are reported also, in women taking only-progestin   preparations   (POP). 

In   the   meantime,  the   lowering   of   the ethinylestradiol dose of hormonal contraceptives (HCs), accompanied by a steady decline in   venous accidents, clearly   did   not   reduce the   risk of   arterial accidents ⁽³¹⁾. 

Furthermore,  arterial thrombosis seems to be unrelated to the duration of use or past use of COCs ^(2,26). 

Several studies have indicated that smoking and age with hypertension, diabetes and, hypercholesterolemia are most important risk factors as well as thrombophilia ^{(6,37,39,43,45)}.

The mortality from arterial diseases is 3.5 times higher than the number of deaths from venous diseases in women under 30 years taking COC s and 8.5 times higher in those 30-44 years old.

Moreover,COCs with second generation of progestagens seem to confer a smaller increase in the risk of venous diseases and a higher risk of arterial complications,compared   with   COCs   containing   third   generation progestagens ^(46,47). 

In addition,  epidemiologic studies suggest that arterial disease   risk   in   young   women   decreases   within   5-10   years   of   smoking cessation ⁽⁴⁸⁾.

Nevetheless,  it is believed that COC use,  per se,  does not cause arterial disease, it can synergize with subclinical endothelial damage to promote arterial occlusion.  The prothrombotic effect of the hormonal contraceptive estrogen intervenes in a cycle of endothelial damage and repair which would otherwise remain clinically silent, or would ultimately progress because of presence of smoking, hypertension or other factors,  to atherosclerosis ^(47,48).

Therefore,  the risk of arterial diseases does not seem to increase in healthy non smoker women under 35 years ⁽⁴⁹⁾. However, a study performed on 152 women with peripheral arterial disease (PAD)  and 925 control women (age 18-49 years) affirmed that all types of COC s were associated with an increase of PAD ⁽⁵⁰⁾.

The same results were obtained from a rigorous meta-analysis of the Literature from 1980 to 2002 ⁽³³⁾.

The effects of COCs on the haemostasis and inflammation variables, resulting in an increased thrombosis risk,show large differences in the women’s response and the polymorphism in the estrogen receptor-1 (ER1) gene may explain part of this inter-individual response.