Myocardial Infarction

Cardiovascular Effects
The first report about a case of pulmonary embolism as adverse effect of contraception occurred in 1961 (1).

Myocardial Infarction

In the last years, the incidence of myocardial infarction(MI) was estimated of 2 to5 fold for hormonal contraceptive (HC)-users compared with nonusers ( 2,3).

The risk results dose-related, and increased also for women using low-dose pill.

Coagulation factors, especially factors VII and fibrinogen, have been established as important cardiovascular risk factors in men.  Some studies have shown the levels of   factors   VII   and   fibrinogen to be   elevated in   HC users. 

These procoagulant   alterations   are   also   observed   in   women   receiving   estrogen substitution,  but unlike HC users,  such women appear to be protected by age-related increases in the level of antitrombin III (4,5)

Smoking is an important influence-factor on the fibrinogen level,  which probably explains part of the increased   risk   of   MI   among   HC   users.

Both, smoking   and   hypertension substantially increase the risk among HC users and some data suggest an increased risk among women with diabetes, hypercholesterolaemia or a history of pre-eclampsia or hypertension-pregnancy related. 

The role of the different types of progestagens used in HCs is still controversial (6,7,8)

Clinical trials on myocardial infarction have found inconsistent results,  possibly because of differences in the prevalence of risk factors,  particularly smoking and elevated blood pressure, in the populations studied.

In the absence of a history of smoking and other conventional risk factors,  current users of modern COCs probably do not have an increased risk of myocardial infarction.  Neither are former users at risk (9)

Evidence for important differences in the risk of myocardial infarction between formulations is weak and contradictory.

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