This study aimed to evaluate the independent effect of parental smoking on early markers of atherosclerosis in children, specifically carotid intima-media thickness and epicardial adipose tissue thickness.

A total of 106 healthy children aged 6–16 years were enrolled, including 53 with parental smoking exposure and 53 unexposed controls. Participants underwent clinical evaluation, laboratory assessment, transthoracic echocardiography, and carotid ultrasonography. Data on parental smoking habits, sociodemographic characteristics, and children’s daily sleep duration were collected. Multivariable analyses were performed to assess the independent association between parental smoking and subclinical atherosclerotic markers.

Children exposed to parental smoking demonstrated significantly greater epicardial adipose tissue thickness and carotid intima-media thickness compared with controls (p = 0.014 and p = 0.001, respectively). Lipid parameters did not differ significantly between groups. Daily sleep duration was negatively correlated with epicardial adipose tissue thickness (r = –0.325, p = 0.018) and carotid intima-media thickness (r = –0.484, p < 0.001). Parental smoking remained independently associated with both markers after adjustment for relevant covariates.

Parental smoking is associated with early atherosclerotic changes in children, demonstrated by increased carotid intima-media thickness and epicardial adipose tissue thickness, independent of traditional cardiovascular risk factors.

Patients diagnosed with hypertension (HT) are at high risk for end-organ damage. With changing living conditions and access to healthcare facilities worldwide, the rate of diagnosis in childhood is increasing. In this study, healthy children were compared with a group of pediatric patients diagnosed with hypertension. Cardiac findings in the hypertensive group were compared at presentation and at six months. We aimed to determine the discriminatory value of epicardial adipose tissue (EAT) measurements as an early imaging marker for cardiac involvement in children with HT compared to healthy children and to determine its prognostic feature for HT treatment response.

Fifty-nine primary hypertension patients and 76 control patients aged 0-18 years were compared. EAT values measured between the healthy group and the patient group and at the beginning of treatment and subsequent follow-ups in the patient group were evaluated with M-mode measurements.

There was no difference between the groups in terms of sex, and age. EAT was found to be significantly higher in the patient group than in the healthy group. There was a statistically significant difference between the EAT measurements evaluated before and after treatment in the patient group.

Hypertension is an important cause of morbidity and mortality. Using EAT measurements as a noninvasive parameter may provide information about early cardiac involvement due to HT. EAT is promising as an imaging marker that can be used in diagnosis and follow-up.

Obesity is usually related to insulin resistance and glucose metabolism disorders. The relationship between insulin resistance and epicardial adipose tissue and atrial electromechanical delay has been described in previous studies.

This study aims to demonstrate the effects of metformin on epicardial adipose tissue and electromechanical delay in patients using metformin for insulin resistance.

A total of 30 patients using metformin for insulin resistance were included in the study. Pre-treatment and post-treatment epicardial adipose tissue and electromechanical delay were evaluated.

There was a statistically significant decrease in epicardial adipose tissue thickness after 3 months of metformin therapy (6.4 ± 2.1 versus 4.7 ± 2.0; p = 0.008). Furthermore, the inter-atrial and intra-atrial electromechanical delay also significantly decreased after 3 months of metformin monotherapy (23.6 ± 8.2 versus 18.1 ± 5.8; p < 0.001, 9.1 ± 2.9 versus 6.3 ± 3.6; p = 0.003, respectively).

In this study, we show that metformin monotherapy significantly decreases epicardial adipose tissue thickness and electromechanical delay in obese children.