Principles of Clinical and Engineering Integration in Hemocompatibility - Biomaterials Science: An Integrated Clinical and Engineering Approach - page 15

Hypercoagulability of pregnancy is caused by modifications in the plasma
levels of many clotting factors. Fibrinogen can be increased up to 3 times
the normal value while protein S, a physiological anticoagulant, decreases.
Thrombin also increases. Protein C and antithrombin III are not predisposed
to change. An impairment in fibrinolysis due to an increase in plasminogen
activator inhibitor-1 (PAI-1) and the placenta-synthesized PAI-2 is observed.
These changes have been suggested to be a preparation for the prevention of
bleeding during labor [33, 35, 36, 38-41].
Other etiologies for hypercoagulability of pregnancy have also been
pointed out. Venous stasis can be a culprit, and may occur at the end of the
first trimester, from enhanced distensibility of the vessel walls by hormonal
effect as well as prolonged bed rest. Acquired etiologies include antiphos-
pholipid antibodies, as in systemic lupus erythematosis, which can exist
before pregnancy. Congenital etiologies that can cause hypercoagulability in
pregnancy and in the general population include factor V Leiden mutation,
prothrombin mutation, protein C and S deficiencies, and antithrombin III
deficiency [2, 33-41].
Pregnant women with prosthetic valves have an increased incidence of
thromboembolic complications. An important consideration is adequate
and effective antithrombotic therapy. Among other important consideration
to take into account here is the ability of a therapeutic agent to cross the
placenta and cause harm to the fetus. Warfarin, for example, is known to
cross the placenta. Since warfarin use in the first trimester of pregnancy is
associated with a substantial risk of embryopathy and fetal death, warfarin
is typically stopped when a patient is trying to become pregnant or when
pregnancy is detected. Typically, heparin, particularly low-molecular-weight
heparin, is used alternatively and does not typically cross the placenta. This
treatment may be continued until delivery [33-41].
When assessing biomaterials, it is important to take into consideration such
hypercoagulable states and their underlying physiological mechanisms, as
many patients can have these concomitant conditions. Suggestions would
include using models with these coagulation changes to assess these condi-
tions, especially where a specific need for a particular medical device during
this condition should arise. Furthermore, altering the coagulation concentra-
tions in order to define a pregnancy-related model may introduce interesting
and insightful information as a whole for innovative surface modifications of
biomaterials [1, 2, 33-41].
Autoimmune States
There are many autoimmune states in which the body produces antibod-
ies against a variety of antigens. One of the problems that may be faced
in these states is hypercoagulability. One particularly noteworthy state is
the antiphospholipid syndrome (APS), which is the most common acquired
thrombophilia, characterized by venous and arterial thrombosis, recurrent