Pregnancy-related SCAD (P-SCAD) is probably associated to hormone-induced structural change in arterial walls including the degeneration of collagen in media and the increase of mucopolysaccharide content resulting in wall weakening (57).In the past SCAD was thought to be associated only with pregnancy and actually is still considered to date the most common cause of pregnancy-associated MI (43%) (49).The cause is not clear, but the most reliable hypothesis is related to the hormonal and hemodynamic changes occurring in pregnancy: indeed, they may weaken the artery wall so as to predispose SCAD onset. High progesterone levels modify the tunica media while estrogen induces a hypercoagulable state, in addition to the arterial shear stress due to the increased cardiac output .Pregnancy-related SCAD may occur ante-partum (up to the fifth week of gestation), early post-partum (<6 weeks), late post-partum (from 6 weeks to 12 months) and very late post-partum (from 12 to 24 months) (43,46) but the majority of cases takes place in the third trimester and in the early post-partum period (49).According to recent data, pregnancy related SCAD is uncommon accounting 2-10% of SCAD cases; even gestational hypertension and pre-eclampsia as well as breastfeeding have been recently associated with SCAD (53).Eosinophilic periadventitial inflammation involving vasa-vasorum were frequently observed in histologic section of dissected coronary arteries (Fig. 7) (19)(20)(21) and reported in over 50% of autopsies of peripartum SCAD (19). Currently, it is not clear if this finding is a reactive phenomenon related to organization of haemorrhage (21) or the cause of dissection by cytolytic adventitial damage from the eosinophilic granules (22).Recent studies have shown P-SCAD, as well as peri-partum SCAD, is associated with a worse prognosis than other cases (45,58).Finally, some evidence suggests multiparity could be a risk for the onset of P-SCAD due to the repeated exposure to hormonal changes (59). 