Abstract Body (Do not enter title and authors here): Background: Tobacco smoking in adolescence has been associated with increased risk of premature death in mid-forties. However, due to the scarcity of repeated measures of cardiac structure and function in a large cohort of children and adolescents, there is limited knowledge regarding the independent associations of initiating and progressive tobacco smoking with premature cardiac damage in apparently healthy youth. The earliest manifestation of the cardiovascular consequence of tobacco smoking is critical for public health intervention and preventive cardiology.
Purpose: To investigate the incidence of tobacco smoking during growth from childhood through young adulthood and the longitudinal association of tobacco smoking with structural and functional cardiac damage.
Methods: From the Avon Longitudinal Study of Parents and Children (ALSPAC), UK birth cohort, 1931 children had questionnaire-based smoking status assessed at ages 10, 13, 15, 17 and 24 years clinic visits were included. Repeated echocardiography measured left ventricular mass indexed for height^2.7 (LVMI^2.7), relative wall thickness (RWT), LV diastolic function from mitral E/A ratio (LVDF), and LV filling pressure from E/e ratio (LVFP) were available at ages 17 and 24 years. LVMI^2.7 ≥51g/m^2.7, RWT ≥0.44, LVDF<1.5, and LVFP ≥8 were categorised as LV hypertrophy, high RWT, LVD dysfunction, and high LVFP, respectively.
Results: Among 1931 children (mean [SD] age at baseline was 10.6 [0.26] years; 1211 [62.7%] females]) the prevalence of smoking was 0.3%, 1.6%, 13.6%, 24%, and 26.4% at ages 10, 13, 15, 17, and 24 years, respectively. The prevalence of LV hypertrophy increased from 2.8% to 7.5% at age 24 years while LVD dysfunction prevalence increased from 10.4% to 16.9%. In a fully adjusted model, persistent smoking from childhood through young adulthood was significantly associated with higher odds of LV hypertrophy (odds ratio 1.52; [95% CI, 1.39 – 1.66], p<0.001), high RWT (1.38; [1.26 – 1.51], p<0.001), LVD dysfunction (1.33; [1.22 – 1.46], p<0.001), and high LVFP (1.35; [1.25 – 1.45], p<0.001) at age 24 years. Persistent smoking from childhood contributed 0.46g/m^2.7 (0.17 – 0.75) of 2.84g/m^2.7 increase in LVMI from ages 17 – 24 years.
Conclusion: Tobacco smoking from childhood through young adulthood was prospectively associated with structural and functional cardiac damage and contributed 16% to cardiac mass increase between ages 17 to 24 years.