attenuated in normal pregnancy, but augmented in preeclampsia. There are consistent results demonstrating that preeclampsia leads to a state of increased arterial stiffness, generalised vasoconstriction and higher TVR. In contrast, there are contradictory results on hemodynamic, myocardial and cardiac chamber function in preeclampsia. There are numerous possible methodological, technical and analytic reasons for the conflicting conclusions of these studies. Studies using afterload-corrected indices, tissue Doppler derived deformation indices and validated algorithms for analysis have provided more reliable evaluation of the cardiovascular system in this disease state. These studies have demonstrated that both preterm and term preeclampsia exhibit global biventricular diastolic dysfunction, LV altered geometry and widespread myocardial impairment. However, only preterm preeclampsia is characterized by global biventricular systolic dysfunction and severe LV hypertrophy. The cardiovascular implications of preeclampsia also do not end with the birth of the baby and placenta. At one year postpartum, LV moderate-severe dysfunction, hypertrophy and stage B asymptomatic heart failure was present in the majority of women who had previously had preterm preeclampsia. The risk of developing essential hypertension within 2 years was 40% in these women. The cardiac assessment of women with preterm PE may be of relevance in identifying women at higher risk of developing cardiovascular morbidity and mortality in later life. Conventional risk factors for cardiovascular morbidity are linked to aging and only become apparent at advanced stages when intervention is less efficacious. A strategy of echocardiographic assessment to screen and treat those women at highest risk of subsequent cardiovascular morbidity needs to be evaluated in larger prospective interventional studies. Such targeted cardiac assessment may serve to reduce the gender discrepancy in outcomes of cardiovascular disease.