Over the past two decades, the rising prevalence of maternal obesity has paralleled an increase in metabolic and hypertensive complications during pregnancy. The World Health Organization estimates that more than 650 million adults globally are obese, and among women of reproductive age, this trend is particularly concerning [1]. Obesity before or during pregnancy is a well-established independent risk factor for the development of GDM and preeclampsia, both of which are associated with cardiovascular abnormalities. The mechanistic underpinnings of these associations involve a complex interplay of inflammation, oxidative stress, insulin resistance, and endothelial dysfunction—each exacerbated by excess adiposity [2]. In the context of gestational diabetes, obesity contributes to an exaggerated insulin-resistant state. Normally, pregnancy induces a physiological insulin resistance to ensure glucose availability for the growing fetus. However, in obese pregnant women, this state is intensified, often overwhelming pancreatic beta-cell compensation, leading to hyperglycemia [3]. Chronic hyperglycemia not only affects fetal development—through mechanisms such as fetal hyperinsulinemia and increased adiposity—but also induces maternal vascular injury and disrupts normal cardiac adaptation to pregnancy. Preeclampsia, a multisystem disorder characterized by hypertension and proteinuria after 20 weeks of gestation, also has significant cardiovascular implications. Obesity substantially increases the risk of preeclampsia, not only by promoting systemic inflammation but also by impairing placental development [4]. Obese women often exhibit higher levels of antiangiogenic factors such as soluble fms-like tyrosine kinase-1 (sFlt-1), which disrupt vascular endothelial growth factor (VEGF) signaling critical for normal placental vasculature. This vascular dysregulation contributes to maternal hypertension and can lead to cardiac remodeling, including left ventricular hypertrophy and diastolic dysfunction [5]. The cardiovascular strain imposed by obesity, GDM, and preeclampsia is not confined to the maternal side. The intrauterine environment plays a crucial role in shaping the offspring's long-term health, a concept known as fetal programming [6]. Fetuses exposed to these metabolic and hypertensive disturbances are at greater risk for congenital heart defects, impaired myocardial development, and altered vascular structure. Moreover, epidemiological studies have linked maternal obesity and gestational complications with an increased risk of cardiovascular and metabolic disease in offspring, including early-onset obesity, insulin resistance, and hypertension [7]. These intergenerational effects reinforce the notion that cardiovascular health is not solely determined by genetics or postnatal lifestyle, but is profoundly influenced by maternal health during gestation [8]. Clinically, these findings highlight a critical opportunity for early intervention. Weight optimization before conception, lifestyle modification during pregnancy, and stringent monitoring of blood glucose and blood pressure levels can mitigate some of the cardiovascular risks associated with maternal obesity [9]. Furthermore, postpartum follow-up is essential, as many of these women remain at elevated risk for chronic hypertension, type 2 diabetes, and cardiovascular disease in later life. Offspring born to such pregnancies may also benefit from early lifestyle counseling and cardiovascular risk assessment [10].

Objective

To evaluate the impact of maternal obesity on cardiovascular outcomes in pregnancies complicated by GDM, preeclampsia, or both, with a focus on maternal cardiac function, fetal development, and postpartum outcomes.

This prospective observational cohort study was conducted at Tertiary Care Hospital of Lahore during January 2025 and October 2025. A total of 301 pregnant women were recruited during their second trimester (between 20 and 28 weeks of gestation) following routine prenatal screening.

Inclusion Criteria:

• Singleton pregnancy
• Diagnosed with GDM based on a 75g oral glucose tolerance test (OGTT) using IADPSG criteria
• Diagnosed with preeclampsia as per ACOG guidelines (blood pressure ≥140/90 mmHg on two occasions, with proteinuria or evidence of end-organ damage)
• Obesity defined as a pre-pregnancy body mass index (BMI) ≥30 kg/m²

Exclusion Criteria:

• Pre-existing type 1 or type 2 diabetes
• Chronic hypertension diagnosed before pregnancy
• Known congenital or structural heart disease
• Multiple pregnancies (e.g., twins, triplets)
• Patients lost to follow-up or who delivered outside the institution

Data Collection

All participants had a pre-pregnancy body mass index (BMI) equal to or greater than 30 kg/m², categorizing them as obese. Women with pre-existing type 1 or type 2 diabetes, chronic hypertension diagnosed prior to pregnancy, congenital or structural heart disease, or multiple pregnancies were excluded to maintain cohort homogeneity. Based on diagnosis, participants were grouped into three cohorts: Group A included 107 women with obesity and GDM only; Group B comprised 96 women with obesity and preeclampsia only; and Group C included 98 women with obesity and both GDM and preeclampsia. Data collection occurred at several points during the pregnancy and postpartum period. At baseline (20–28 weeks), participants underwent clinical assessments including medical history, BMI measurement, and blood pressure recording. Laboratory investigations were also conducted, including fasting glucose, HbA1c, lipid profiles, and inflammatory markers such as C-reactive protein (CRP) and interleukin-6 (IL-6). Cardiovascular assessment was a critical component of the study. Maternal cardiac function was evaluated using transthoracic echocardiography between 28- and 32-weeks gestation and repeated at 6 weeks postpartum. Parameters such as left ventricular (LV) mass index, ejection fraction, E/A ratio (a measure of diastolic function), and pulse wave velocity (for arterial stiffness) were recorded. Fetal cardiovascular health was monitored using Doppler ultrasound to assess placental and fetal circulation, along with targeted fetal echocardiography at 32 weeks to evaluate myocardial structure and function. Delivery outcomes were also documented, including gestational age at delivery, mode of delivery, neonatal birth weight, Apgar scores, NICU admission, and any observed congenital or cardiac anomalies. Postpartum follow-up was conducted at 6 weeks, during which maternal blood pressure, echocardiographic parameters, and glucose tolerance were reassessed.

Statistical Analysis

Data were analyzed using SPSS v26. Descriptive statistics were employed to summarize baseline demographics and clinical characteristics of the participants. Continuous variables such as BMI, blood pressure, and echocardiographic indices were reported as means with standard deviations and compared across the three study groups using one-way ANOVA or independent t-tests where applicable. A p-value of less than 0.05 was considered statistically significant throughout the analysis.

Data were collected from 301 patients, divided into three groups: 107 with GDM only, 96 with preeclampsia only, and 98 with both conditions. The mean maternal age was comparable across groups, ranging from 31.5 ± 4.5 to 32.0 ± 4.2 years. Pre-pregnancy BMI was highest in the group with both GDM and preeclampsia (35.7 ± 3.2 kg/m²), followed by the preeclampsia-only group (35.0 ± 2.9 kg/m²), and was lowest in the GDM-only group (34.2 ± 3.1 kg/m²). The proportion of smokers was relatively similar across groups, ranging from 12% to 14%. Multiparity was slightly more common in the combined condition group (60%) compared to GDM only (55%) and preeclampsia only (58%).

Table 1: Baseline Characteristics of Participants

Women with both GDM and preeclampsia demonstrated the most significant cardiovascular changes during and after pregnancy. Their left ventricular mass index was highest (122.3 ± 12.4 g/m²), indicating greater cardiac workload, compared to 117.8 ± 11.3 g/m² in the preeclampsia group and 110.5 ± 10.2 g/m² in the GDM-only group. Diastolic function, assessed by the E/A ratio, was most impaired in the combined group (0.85 ± 0.09), suggesting early signs of cardiac dysfunction. Additionally, arterial stiffness measured by pulse wave velocity was elevated in the combined group (10.2 ± 1.1 m/s), higher than in preeclampsia alone (9.5 ± 0.9 m/s) and GDM alone (9.0 ± 1.0 m/s). Postpartum hypertension was most prevalent in the combined group (41%), compared to 28% in preeclampsia-only and 15% in GDM-only women.

Table 2: Maternal Cardiovascular Outcomes

Abnormal umbilical artery resistance index was noted in 32% of this group, compared to 28% in preeclampsia-only and just 12% in GDM-only pregnancies. Similarly, fetal myocardial hypertrophy was more prevalent in the combined group (17%) than in the preeclampsia (11%) and GDM-only (6%) groups. Mean birth weight was lowest in the group with both conditions (2880 ± 420 g), indicating intrauterine growth restriction, versus 3030 ± 390 g in the preeclampsia group and 3150 ± 410 g in the GDM group. Preterm delivery occurred in 36% of the combined group, significantly higher than in preeclampsia (28%) and GDM-only (15%) groups. NICU admission and low Apgar scores followed the same trend, with 29% and 11% respectively in the combined group, reflecting more severe neonatal compromise.

Table 3: Fetal and Neonatal Outcomes

Women with both GDM and preeclampsia had the highest fasting blood glucose levels (106 ± 14 mg/dL) and HbA1c values (6.1 ± 0.5%), indicating poor glycemic control, compared to lower values in the GDM-only (98 ± 12 mg/dL; 5.6 ± 0.4%) and preeclampsia-only groups (90 ± 10 mg/dL; 5.3 ± 0.3%). Inflammatory markers were also markedly elevated in the combined group. C-reactive protein (CRP) averaged 11.0 ± 2.3 mg/L and serum IL-6 reached 5.1 ± 1.3 pg/mL, higher than in preeclampsia-only (CRP: 9.5 ± 2.1 mg/L; IL-6: 4.2 ± 1.1 pg/mL) and GDM-only (CRP: 7.2 ± 1.8 mg/L; IL-6: 3.1 ± 0.9 pg/mL) groups. LDL cholesterol was also highest in the combined group (135 ± 20 mg/dL), suggesting a more atherogenic lipid profile.

Table 4: Laboratory Markers During Pregnancy

The mean placental weight was lowest in this group (545 ± 55 g), compared to 580 ± 50 g in the preeclampsia-only group and 610 ± 45 g in the GDM-only group, suggesting impaired placental development. Signs of placental dysfunction were also more prevalent in the combined group, including calcification (35%), delayed villous maturity (27%), and vascular malperfusion (41%). These were significantly higher than in the preeclampsia group (28%, 19%, and 34%, respectively) and the GDM group (18%, 14%, and 22%). Placental infarctions were also notably higher in the combined group (24%) compared to preeclampsia (16%) and GDM-only (10%), indicating more extensive placental ischemia and damage in pregnancies complicated by both metabolic and hypertensive disorders.

Table 5: Placental Findings at Delivery

This study provides critical insight into the cardiovascular implications of maternal obesity in the context of gestational diabetes mellitus (GDM) and preeclampsia. By evaluating 301 women stratified into three clinical groups GDM only, preeclampsia only, and both conditions our findings highlight the compounded physiological burden of coexisting metabolic and hypertensive disorders during pregnancy. The results emphasize not only the immediate risks to maternal and fetal cardiovascular health but also the potential for long-term complications extending beyond delivery. One of the most striking observations was the additive adverse effect on maternal cardiovascular function in women with both GDM and preeclampsia [11]. This group exhibited significantly elevated left ventricular (LV) mass index and greater arterial stiffness, as measured by pulse wave velocity, compared to women with either condition alone. These findings are consistent with previous research indicating that both GDM and preeclampsia independently contribute to subclinical cardiac remodeling and endothelial dysfunction. However, our study is among the few to document the synergistic impact of both conditions in obese pregnancies, suggesting that obesity intensifies hemodynamic stress and myocardial workload [12]. The diastolic dysfunction seen in the combined group, as reflected by a lower E/A ratio, further supports the presence of early-stage cardiac compromise. These subclinical cardiac changes may persist postpartum, and they have been associated with increased risk for future heart failure with preserved ejection fraction (HFpEF), particularly in women who remain hypertensive or develop type 2 diabetes after delivery [13]. Fetal and neonatal outcomes mirrored maternal cardiovascular stress. Fetuses exposed to maternal obesity with both GDM and preeclampsia demonstrated higher rates of abnormal Doppler findings, myocardial hypertrophy, and lower average birth weight. These changes suggest altered placental perfusion and intrauterine cardiovascular programming [14]. The rate of preterm deliveries and NICU admissions was also significantly elevated in this group, corroborating previous studies linking preeclampsia and metabolic disease with compromised fetal development and neonatal adaptation [15]. From a biochemical standpoint, inflammatory and metabolic markers were consistently elevated in the combined group. Higher levels of C-reactive protein (CRP), interleukin-6 (IL-6), and HbA1c reflect a systemic pro-inflammatory and insulin-resistant state, which may drive both endothelial damage and placental insufficiency. These findings are clinically relevant, as inflammation has been implicated in the pathogenesis of both maternal cardiovascular disease and impaired fetal vascular development [16]. The placental findings further substantiated these physiological disturbances. Increased rates of vascular malperfusion, infarction, and villous maturity delays were observed in the group with both GDM and preeclampsia. These placental abnormalities are associated with reduced nutrient and oxygen delivery, contributing to fetal growth restriction and adverse neonatal outcomes [17]. Importantly, the long-term postpartum data indicate that a significant proportion of women with both conditions had persistent hypertension, impaired fasting glucose, and signs of subclinical cardiac dysfunction. These findings stress the importance of structured postpartum surveillance and intervention to mitigate the risk of chronic cardiovascular and metabolic disease [18-20],

It is concluded that maternal obesity significantly amplifies the adverse cardiovascular outcomes associated with gestational diabetes mellitus (GDM) and preeclampsia, both for the mother and the fetus. The combination of these conditions results in a synergistic increase in maternal cardiac workload, endothelial dysfunction, and vascular stiffness, as evidenced by elevated left ventricular mass index, diastolic dysfunction, and arterial stiffness. These changes not only pose risks during pregnancy but also predispose women to long-term cardiovascular and metabolic disease

1. Leddy MA, Power ML, Schulkin J. The impact of maternal obesity on maternal and fetal health. Rev Obstet Gynecol. 2008 Fall;1(4):170-8. PMID: 19173021; PMCID: PMC2621047.
2. Bajaj G, Davu G. Effect of obesity in pregnancy: implications for maternal and fetal health. Int J Reprod Contracept Obstet Gynecol 2024;13:2215-9
3. Navaee M, Kashanian M, Kabir A, Zamaninour N, Chamari M, Pazouki A. Maternal and fetal/neonatal outcomes in pregnancy, delivery and postpartum following bariatric surgery and comparison with pregnant women with obesity: a study protocol for a prospective cohort. Reprod Health. 2024 Jan 17;21(1):8. doi: 10.1186/s12978-023-01736-3. PMID: 38233940; PMCID: PMC10795358.
4. Chopra M, Kaur N, Singh KD, Jacob CM, Divakar H, Babu GR, et al. Population estimates, consequences, and risk factors of obesity among pregnant and postpartum women in India: results from a national survey and policy recommendations. Int J Gynecol Obstet. 2020;151(1):57–67.
5. John J, Mahendran M. Maternal and fetal outcomes of obese pregnant women: a prospective cohort study. Int J Reprod Contracept Obstet Gynecol. 2017;6(2):725.
6. Melchor I, Burgos J, del Campo A. Effect of maternal obesity on pregnancy outcomes in women delivering singleton babies: a historical cohort study. J Perinat Med. 2019;47(6):625–30.
7. Jahan F, Bagchi AK, Bagchi RA. Maternal obesity: impacts on the cardiovascular health of mother and offspring. Biochem Cardiovasc Dysfunct Obes. 2020:55–75.
8. O’Brien CM, Louise J, Deussen A. The effect of maternal obesity on fetal biometry, body composition, and growth velocity. J Matern Fetal Neonatal Med. 2020;33(13):2216–26.
9. Creanga AA, Catalano PM, Bateman BT. Obesity in pregnancy. N Engl J Med. 2022;387(3):248–59.
10. Mohammed ZM, Alsakkal GS. Adverse outcomes of obesity on pregnancy. Australas Med J. 2019;5(2):89–93.
11. Barbour LA. Metabolic culprits in obese pregnancies and gestational diabetes mellitus: big babies, big twists, big picture: the 2018 Norbert Freinkel Award Lecture. Diabetes Care. 2019;42(5):718–26.
12. Slack E, Best KE, Rankin J, Heslehurst N. Maternal obesity classes, preterm and post-term birth: a retrospective analysis of 479,864 births in England. BMC Pregnancy Childbirth. 2019;19(1):434.
13. Stubert J, Reister F, Hartmann S. The risks associated with obesity in pregnancy. Dtsch Arztebl Int. 2018;115(16):276–83.
14. Hitrova-Nikolova S, Karamisheva V. The newborn infant by caesarean section. Akush Ginekol (Sofiia). 2020;59(1):32–7.
15. Reichetzeder C. Overweight and obesity in pregnancy: their impact on epigenetics. Eur J Clin Nutr. 2021;75(12):1710–22.
16. Patel R, Jain A, Patel Z, Kavani H, Patel M, Gadhiya DK, et al. Artificial intelligence and machine learning in hepatocellular carcinoma screening, diagnosis and treatment—a comprehensive systematic review. Glob Acad J Med Sci. 2024;6(2):83–97.
17. Mabhout Moghadam T, Mosaferi Ziaaldini M, Fathi M, Attarzadeh Hoseini SR. Review the effect of high intensity interval training on obesity-related hormones. Res Sport Sci Med Plants. 2020;1(1):1–18.
18. World Health Organization (2018) Obesity and Overweight Fact Sheet, World Health Organization. https://www.who.int/news-room/fact-sheets/detail/obesity-and-overweight.
19. Senobari M, Azmoude E, Mousavi M. The relationship between body mass index, body image, and sexual function: a survey on Iranian pregnant women. Int J Reprod Biomed. 2019;17(7):503.

Gilmore LA, Redman LM. Weight gain in pregnancy and application of the 2009 IOM guidelines: toward a uniform approach. Obesity. 2015;23(3):507–511. doi: 10.1002/oby.20951