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Adverse experiences in childhood and adolescence, defined as subjectively perceived threats to the safety or security of the child's bodily integrity, family, or social structures, are known to be associated with cardiometabolic outcomes over the life course into adulthood. This American Heart Association scientific statement reviews the scientific literature on the influence of childhood adversity on cardiometabolic outcomes that constitute the greatest public health burden in the United States, including obesity, hypertension, type 2 diabetes mellitus, and cardiovascular disease. This statement also conceptually outlines pathways linking adversity to cardiometabolic health, identifies evidence gaps, and provides suggestions for future research to inform practice and policy. We note that, despite a lack of objective agreement on what subjectively qualifies as exposure to childhood adversity and a dearth of prospective studies, substantial evidence documents an association between childhood adversity and cardiometabolic outcomes across the life course. Future studies that focus on mechanisms, resiliency, and vulnerability factors would further strengthen the evidence and provide much-needed information on targets for effective interventions. Given that childhood adversities affect cardiometabolic health and multiple health domains across the life course, interventions that ameliorate these initial upstream exposures may be more appropriate than interventions remediating downstream cardiovascular disease risk factor effects later in life.

This scientific statement presents considerations for clinical management regarding the assessment and risk reduction of select pediatric populations at high risk for premature cardiovascular disease, including acquired arteriosclerosis or atherosclerosis. For each topic, the evidence for accelerated acquired coronary artery disease and stroke in childhood and adolescence and the evidence for benefit of interventions in youth will be reviewed. Children and adolescents may be at higher risk for cardiovascular disease because of significant atherosclerotic or arteriosclerotic risk factors, high-risk conditions that promote atherosclerosis, or coronary artery or other cardiac or vascular abnormalities that make the individual more vulnerable to the adverse effects of traditional cardiovascular risk factors. Existing scientific statements and guidelines will be referenced when applicable, and suggestions for risk identification and reduction specific to each setting will be described. This statement is directed toward pediatric cardiologists, primary care providers, and subspecialists who provide clinical care for these young patients. The focus will be on management and justification for management, minimizing information on pathophysiology and epidemiology.

Use of ambulatory blood pressure monitoring in children and adolescents has markedly increased since publication of the last American Heart Association scientific statement on pediatric ambulatory blood pressure monitoring in 2014. In addition, there has also been significant expansion of the evidence base for use of ambulatory blood pressure monitoring in the pediatric population, including new data linking ambulatory blood pressure levels with the development of blood pressure–related target organ damage. Last, additional data have recently been published that enable simplification of the classification of pediatric ambulatory monitoring studies. This scientific statement presents a succinct review of this new evidence, guidance on optimal application of ambulatory blood pressure monitoring in the clinical setting, and an updated classification scheme for the interpretation of ambulatory blood pressure monitoring in children and adolescents. We also highlight areas of uncertainty where additional research is needed.

This document provides a pediatric-focused companion to the American Heart Association (AHA) Strategic Impact Goal Through 2020 and Beyond, focused on cardiovascular (CV) health promotion and disease reduction in adults and children. The principles detailed in the document reflect the AHA’s new dynamic and proactive goal to promote CV health throughout the lifecourse. The primary focus is on adult CV health and disease prevention, but critical to achievement of this goal is maintenance of ideal CV health from birth through childhood to young adulthood and beyond. Emphasis is placed on the fundamental principles and metrics that define CV health in children for the clinical or research setting and a balanced and critical appraisal of the strengths and weaknesses of the CV health construct in children and adolescents are provided. Specifically, it discusses two important factors: 1) the promotion of ideal CV health in all children, and 2) the improvement of CV health metric scores in children currently classified as having “poor” or “intermediate” CV health. Other topics include the current status of CV health in U.S. children, opportunities for the refinement of health metrics, improvement of health metric scores, and possibilities for promoting ideal CV health. Importantly, concerns about the suitability of using single thresholds to identify elevated CV risk throughout the childhood years and the limits of our current knowledge are noted, while providing suggestions for future directions and research.

Anatomic and functional changes after either a permanent left anterior descending coronary artery occlusion (PO) or 2 h of occlusion followed by reperfusion (OR) in C57BL/6 mice were examined and compared with those in sham-operated mice. Both interventions generated infarcts comprising 30% of the left ventricle (LV) measured at 24 h and equivalent suppression of LV ejection velocity and filling velocity measured by Doppler ultrasound at 1 wk. Serial follow-up revealed that the ventricular ejection velocity and filling velocity returned to the levels of the sham-operated controls in the OR group at 2 wk and remained there; in contrast, PO animals continued to display suppression of both systolic and diastolic function. In contrast, ejection fractions of PO and OR animals were depressed equivalently (50% from sham-operated controls). Anatomic reconstruction of serial cross sections revealed that the percentage of the LV endocardial area overlying the ventricular scar (expansion ratio) was significantly larger in the PO group vs. the OR group (18 ± 1.7% vs. 12 ± 0.9%, P < 0.05). The septum that was never involved in the infarction had a significantly ( P < 0.002) increased mass in PO animals (22.5 ± 1.08 mg) vs. OR (17.8 ± 1.10 mg) or sham control (14.8 ± 0.99 mg) animals. Regression analysis demonstrated that the extent of septal hypertrophy correlated with LV expansion ratio. Thus late reperfusion appears to reduce the degree of infarct expansion even under circumstances in which it no longer can alter infarct size. We suggest that reperfusion promoted more effective ventricular repair, less infarct expansion, and significant recovery or preservation of ventricular function.

Background Although public health programs have led to a substantial decrease in the prevalence of tobacco smoking, the adverse health effects of tobacco smoking is by no means a thing of the past. In the U.S, four out of 10 school aged children and 1 out of 3 adolescents are involuntarily exposed to second-hand tobacco smoke (SHS) with children of minority ethnic backgrounds and those living in low socioeconomic status households being disproportionately affected (68% and 43% respectively). Children are particularly vulnerable with little control over home and social environment and lack the understanding, agency, and ability to avoid SHS exposure on their own volition; they also have physiological or behavioral characteristics that render them especially susceptible to effects of SHS. Side stream smoke (the smoke burned directly off the end of the cigarette), a major component of SHS, contains a higher concentration of some toxins than mainstream smoke (inhaled by the smoker directly), making SHS potentially more dangerous than direct smoking. Compelling animal and human evidence shows that SHS exposure during childhood is detrimental to arterial function and structure resulting in premature atherosclerosis and its cardiovascular consequences. Childhood SHS exposure is also related to impaired cardiac autonomic function and changes in heart rate variability. In addition, childhood SHS exposure is associated with clustering of cardiometabolic risk factors such as obesity, dyslipidemia, and insulin resistance. Individualized interventions to reduce childhood exposure to SHS are shown to be at least modestly effective, so are broader based policy initiatives such as community smoking bans and increased taxation. Purpose The purpose of this statement is to summarize the available evidence on the cardiovascular health consequences of childhood SHS exposure which will support ongoing efforts to reduce and eliminate SHS exposure in this vulnerable population. This statement reviews relevant data from epidemiologic studies; laboratory based experiments, and controlled behavioral trials, concerning SHS and cardiovascular disease risk in children. Information regarding the effects of SHS exposure on the cardiovascular system in animal and pediatric studies, including vascular disruption and platelet activation, oxidation and inflammation, endothelial dysfunction, increased vascular stiffness, changes in vascular structure, and autonomic dysfunction are examined. Conclusion The epidemiological, observational and experimental evidence accumulated to date, demonstrates the detrimental long-term cardiovascular consequences of SHS exposure in children. Implications Increased awareness of these adverse effects will facilitate the development of targeted individual, family-centered and community public health interventions to reduce and ideally eliminate SHS exposure in the vulnerable pediatric population. This evidence calls for a robust public health policy that embraces “zero tolerance” to childhood SHS exposure.

Background-Increased left atrial diameter (LAD) is associated with elevated risk of atrial fibrillation (AF) and cardiovascular disease. Information is limited regarding the short-or long-term correlates of LAD. Methods and Results-We evaluated clinical correlates of LAD for a 16-year period in 4403 Framingham Study participants (mean age, 45 years; 52% women; median observations/participantϭ3) using multilevel modeling. We related age, sex, body mass index (BMI), systolic and diastolic blood pressure (BP), diabetes, and antihypertensive treatment to LAD. Sex-specific growth curves for LAD were estimated for individuals with low, intermediate, and high risk factor burden. We also related risk factors to changes in LAD during a 4-year period in 3365 participants. Age, male sex (3.83 mm compared to women), greater BMI, higher systolic BP (0.24 mm per 10 mm Hg increment), and antihypertensive treatment (0.54 mm) were associated positively with LAD (PϽ0.001). Men had a greater increase in LAD with BMI than women (2.02 versus 1.77 mm in women, per 5-unit increment), and individuals receiving antihypertensive treatment experienced a greater increase in LAD with age (0.95 versus 0.63 mm per 10-year age increment) when compared with those not receiving antihypertensive treatment. Overall, greater risk factor burden was positively associated with LAD. These risk factors were also associated positively with 4-year change in LAD (PϽ0.001). Conclusions-Our longitudinal study of a large community-based sample identified higher BP and greater BMI as key modifiable correlates of LAD, suggesting that maintaining optimal levels of these risk factors through the life course may prevent atrial remodeling and AF. (Circulation. 2010;121:667-674.)