Impact of Lipids and Vascular Damage on Early Atherosclerosis in Adolescents with Parental Premature Coronary Artery Disease

• Published in: High blood pressure & cardiovascular prevention Vol. 31; no. 1; pp. 31 - 41
• Main Authors: Martínez-Alvarado, María Del Rocío, Torres-Tamayo, Margarita, Juárez-Rojas, Juan Gabriel, Medina-Urrutia, Aida X, Cardoso-Saldaña, Guillermo C, López-Uribe, Ángel Rene, Reyes-Barrera, Juan, Jorge-Galarza, Esteban
• Format: Journal Article
• Language: English
• Published: New Zealand Springer Nature B.V 01.01.2024
• Subjects: Apolipoproteins; Atherosclerosis; Body mass index; Cardiovascular disease; Cholesterol; Coronary vessels; Family medical history; Health risks; High density lipoprotein; Insulin; Lipids; Lipoproteins; Mortality; Oxidation; Plasma; Questionnaires; Reproducibility; Risk factors; Teenagers; Triglycerides; Tumor necrosis factor-TNF; United Kingdom > UK; United States > US; Germany; Carotid intima media thickness; Adolescents; Cardiovascular risk factors; Parental history of premature coronary artery disease
• ISSN: 1120-9879; 1179-1985
• DOI: 10.1007/s40292-023-00617-x

To assess the relationship of cardiovascular risk factors (CRFs) with carotid intima media thickness (IMT) in adolescents with a parental history of premature coronary artery disease (PCAD). This cross-sectional study included 50 healthy adolescents, aged 14-18 years, both sexes, with a parental history of PCAD, that were compared to 50 controls without this history. Questionnaires regarding information of CRFs were applied. Blood chemistry analyses, included lipid profile, lipoprotein (a), low density lipoprotein (LDL) susceptibility to oxidation, and inflammatory cytokine levels. The IMT was evaluated by ultrasound. The mean age of all participants was 15.9 years. Anthropometric measurements, blood pressure, and lipid profile were similar in both groups. However, the parental history of PCAD group exhibited lower high density lipoprotein cholesterol concentrations, shorter LDL particle oxidation time, and higher lipoprotein (a) levels compared to the control group. IMT was significantly higher in adolescents with a parental history of PCAD compared to controls, (0.53 ± 0.04 mm vs 0.47 ± 0.02 mm, p = 0.001). Among adolescents with a parental history of PCAD, those with ≥ 3 CRFs had significantly higher IMT values (0.56 mm) than those with < 3 CRFs (0.52 mm) and controls (0.48 mm). Multivariable analyses identified that systolic blood pressure and parental history of PCAD explained 26.8% and 16.1% of the variation in IMT. Furthermore, body mass index, LDL-C, ApoB-100, triglycerides and lipoprotein (a) interact with blood pressure levels to explain the IMT values. Adolescents with a parental history of PCAD had higher IMT values than the control group, primary explained by systolic blood pressure and the parental inheritance. Adolescents with parental history of PCAD and ≥ 3 CRFs exhibited the highest IMT values. Notably, lipids and systolic blood pressure jointly contribute to explain IMT in these adolescents.