Pregnancy is not commonly considered a risk factor for acute myocardial infarction, however pregnancy increase the risk of acute myocardial infarction 3- to 4-fold [14, 15]. Many risk factors are unique for pregnancy-related acute myocardial infarction and several diagnostic steps are often required for the myocardial infarction confirmation (Appendix 1).
Cardiac function and hormonal milieu are unfavorably altered in pregnancy whereas cardiac output is increased in the presence of elevated levels of estrogen and progesterone [12, 13]. The hypercoagulable state of pregnancy , in the presence of increased vascular reactivity , may further magnify the risk of myocardial infarction. Progesterone excess and postpartal degeneration of the matrix in the medial and intimal sections of the coronary arteries may contribute to flow alterations and artery dissections .
Superimposed hypertension, as in the reported case may further damage blood vessels already weakened by hemodynamic stress and hormonal alterations. Overall, an increasing prevalence of cardiovascular risk factors with advanced maternal age contributes to pregnancy-associated complications [18, 19]. More than 70% of patients with ET and recurrent thrombosis have multiple cardiovascular risk factors [20, 21]. Overweight, arterial hypertension and a positive family history were present in this case, yet all were moderate and hypertension only recently developed.
In a recent retrospective review of 228 reported cases of pregnancy-related acute myocardial infarction, morphology of the coronary arteries was present in 164 cases. Atherosclerosis with or without intracoronary thrombus was found in 70 cases (43%), and definite or probable coronary thrombus without evidence of atherosclerotic disease was present in 22 (13%). Coronary artery dissection was verified in 24%, spasms and embolus in 2% and 1% respectively. Normal coronary arteries were found in 20% [16, 22]
Published studies on ET pregnancies report live birth rates of 50-70% and spontaneous abortion rates of 25-50% [23, 24]. In a recent report of 103 pregnancies that occurred in 62 women with ET, about 50% of first pregnancies experienced complications, although no case of acute coronary syndrome (ACS) or myocardial infarction was reported during pregnancy or postpartum .
Despite the fact that a decrease in platelet count during pregnancies is well documented, pregnancies in ET patients frequently end in early spontaneous abortions, during the first trimester . Their occurrence cannot be predicted from the disease course, platelet count, or a specific therapy. The use of aspirin did not improve pregnancy outcome in a study of 34 patients with ET by Tefferi and coworkers [7, 10]. In addition control of the platelet count alone should not be taken as an appropriate surrogate end point to judge the efficacy of a treatment for ET . In a randomized study comparing anagrelide vs. hydroxyurea therapy (plus low-dose aspirin in both groups) in ET , an excess of vascular events was found in the anagrelide group despite a reduction in the platelet count similar to that in the hydroxyurea group. If the platelet count decreases insufficiently in patients with ET despite pregnancy, interferon is considered the agent of choice, omitting the teratogenicity of cytoreductive agents [7, 27].
Our patient's history of previous early spontaneous abortion, IUGR and the presence of anticardiolipin antibodies suggest the possibility of an incomplete antiphospholipid antibody syndrome, which represent the most common acquired thrombophilia of pregnancy and has been associated with myocardial infarction [28, 29].
Antiphospholipid antibody syndromes may also be associated with autoimmune diseases such as systemic lupus erythematosus, which can cause pericarditis and myocarditis . In the present case, autoantibody screening for ANA was borderline and anti-dsDNA and anti-Histone antibody testing were negative. A nuclear magnetic resonance examination of the heart demonstrated a normal myocardium with no signs of inflammation.
Our patient had experienced a severe migraine attack which has also been found to be a risk factor for myocardial infarction during pregnancy . The possible underlying mechanism may be a generalized vasospasm that makes coronary arteries susceptible to spasms .
Despite the fact that ET-pregnancies carried to term are rarely complicated by thrombohemorrhagic events our patient had experienced recurrent postpartal ACS in the presence of essential thrombocytosis and elevated antio-cardiolipin IgM antibodies. Since patients with ET seems to have an increased prevalence of antiphospholipid antibodies which may be associated with thrombosis  it is not surprising that both episodes of ACS occurred after aspirin discontinuation. We can only speculate that the conjunction of primary etiological factors such as ET and the transiently elevated antiphospholipid antibody titer in the presence of several cardiovascular risk factors (advanced maternal age, hypertension, postpartal vascular changes, coronary plaque) and the lack of antiplatelet therapy finally contributed to recurrent myocardial ischemia.
There are several recommendations  that women whose pregnancies are characterized by fetal complications, such as unexplained fetal growth retardation and stillbirth, should be tested for genetic or acquired markers of thrombophilia as well as antiphospholipid antibodies and autoimmune disease. We propose that, with the continuing trend of childbearing at older ages, maternal complications like the ones described here should be added to the conditions requiring a similar work-up to allow for closer monitoring, or even prophylactic therapy during further pregnancies and beyond.