Preeclampsia (PE) is a major obstetrics issue, particularly in underdeveloped nations, where it is a leading cause of maternal mortality (10%–15%)[1]. According to 74 scientific studies on PE across 40 countries, 1.4%–4.6% of pregnancies are affected by pre-eclampsia[2]. PE and eclampsia were the leading causes of maternal death at Dr. Soetomo General Academic Hospital in Surabaya in 2010[3], [4]. In 2014, the incidence of PE at Dr. Soetomo General Academic Hospital in Surabaya, Indonesia increased from 27.88% to 32.48%. A 2016 multicenter retrospective study of seven tertiary care hospitals in Indonesia reported that the prevalence of hypertension during pregnancy was 22.1% in a total of 17,771 deliveries. Among those, 54% were classified as having late-onset preeclampsia and 46% as having early onset preeclampsia. Maternal and perinatal mortality rates were 2% and 12%, respectively. Dr. Soetomo Academic Hospital saw a high incidence of severe complicated preeclampsia as it is the only tertiary referral hospital in East Java [5].

PE causes substantial morbidity and mortality in the mother and fetus or infant owing to multisystem organ dysfunction[6], [7]. PE is divided into two categories based on delivery timing: preterm PE (P-PE) was diagnosed if PE led to delivery before 37 weeks; term PE (T-PE) was diagnosed if PE led to delivery ≥37 weeks[8], [9], [10]. P-PE and T-PE are hypothesized to result from distinct etiology [11], [12], [13]. P-PE occurs during the first trimester of pregnancy and is associated with immunological and inflammatory responses during implantation. This process involves release of several growth factors and cytokines. P-PE is characterized by shallow trophoblast invasion and suboptimal vascular remodeling, resulting in placental hypoperfusion. This results in the release of reactive chemicals that enter the bloodstream and damage the endothelium, which is essential for maintaining the balance between vasodilation and vasoconstriction via nitric oxide synthesis. In contrast, T-PE is primarily caused by maternal vascular and chronic inflammatory maladaptation, ultimately resulting in preeclampsia[11]. This distinction affects clinical presentation, severity, and prognosis of P-PE compared to those of T-PE. Christensen et al. demonstrated that the gestational age at the onset of preeclampsia is negatively associated with markers of subclinical atherosclerosis, including carotid plaque presence, carotid intima-media thickness, aortic pulse wave velocity, and heart rate augmentation index, 12 years after delivery. After delivery, women with P-PE had worse atherosclerotic characteristics than women with T-PE[12]. In an Australian national cohort study, hypertension in pregnancy, especially early onset hypertension, was associated with a higher risk of cardiovascular disease (CVD) than late-onset hypertension, which was enhanced by smoking[13].

PE is an issue because of its association with mortality and short-term morbidity, and its role in long-term morbidities such as chronic hypertension, CVD, cerebrovascular illness, and metabolic syndrome[14], [15], [16]. Indonesia has a much higher incidence of female metabolic syndrome than European countries. Sigit et al. reported that the prevalence of metabolic syndrome was 46% in Indonesian women and 24% in Dutch women[17]. Compared with women without a history of PE in pregnancy, women with a history of PE in pregnancy have a higher incidence of metabolic syndrome. Obesity, hypertension, insulin resistance, high fasting blood sugar levels, dyslipidemia, and microalbuminuria are the risk factors for CVD. PE can increase the likelihood of developing metabolic syndrome, which may be the primary cause of development of CVD. In a meta-analysis encompassing 55,695 patients, PE was found to significantly increase the risk of metabolic syndrome (Crude odds ratios [OR] = 2.93; 95% confidence interval [CI] = 1.92–4.47 and Adjusted OR = 1.62; 95% CI = 1.25–2.08)[18]. PE shares similar risk factors and pathophysiological problems with arterial-coronary illnesses, including insulin resistance. Framingham Risk Score (FRS) can be used to predict the probability of developing CVD 10 years after PE. A previous study found that the risk of developing CVD was 4.52 times higher in women with a history of PE compared with women with no history of PE[19]. Metabolic syndrome refers to a group of disorders that increase the risk of various diseases[20]. Most studies have indicated that women with preeclampsia have an increased risk of developing metabolic syndrome after birthing, indicating its role in the pathophysiology of diseases, ranging from preeclampsia to long-term CVD. Metabolic syndrome was diagnosed using the National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III)[21].

To date, no Indonesian studies have linked the onset of PE to the risk of chronic hypertension, CVD, or metabolic syndrome. This study was conducted to determine the risk of maternal hypertension, CVD disorders, and metabolic syndrome five years after delivery in women with severe preeclampsia (P-PE and T-PE) compared with normal pregnancy using clinical and laboratory measurements, FRS[21], and NCEP-ATP III criteria[22].