Background-The association between passive smoking exposure in childhood and adverse cardiovascular health in adulthood is not well understood. Using a 26-year follow-up study, we examined whether childhood exposure to passive smoking was associated with carotid atherosclerotic plaque in young adults. Methods and Results-Participants were from the Cardiovascular Risk in Young Finns Study (n=2448). Information on childhood exposure to parental smoking was collected in 1980 and 1983. Carotid ultrasound data were collected in adulthood in 2001 or 2007. Childhood serum cotinine levels from 1980 were measured from frozen samples in 2014 (n=1578). The proportion of children with nondetectable cotinine levels was highest among households in which neither parent smoked (84%), was decreased in households in which 1 parent smoked (62%), and was lowest among households in which both parents smoked (43%). Regardless of adjustment for potential confounding and mediating variables, the relative risk of developing carotid plaque in adulthood increased among those children with 1 or both parents who smoked (relative risk, 1.7; 95% confidence interval, 1.0-2.8; P=0.04). Although children whose parents exercised good "smoking hygiene" (smoking parents whose children had nondetectable cotinine levels) had increased risk of carotid plaque compared with children with nonsmoking parents (relative risk, 1.6; 95% confidence interval, 0.6-4.0; P=0.34), children of smoking parents with poor smoking hygiene (smoking parents whose children had detectable serum cotinine levels) had substantially increased risk of plaque as adults (relative risk, 4.0; 95% confidence interval, 1.7-9.8; P=0.002). Conclusions-Children

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Unstable coronary plaques that are prone to erosion and rupture are the major cause of acute coronary syndromes. Our expanding understanding of the biological mechanisms of coronary atherosclerosis and rapid technological advances in the field of medical imaging has established cardiac computed tomography as a first-line diagnostic test in the assessment of suspected coronary artery disease, and as a powerful method of detecting the vulnerable plaque and patient. Cardiac computed tomography can provide a noninvasive, yet comprehensive, qualitative and quantitative assessment of coronary plaque burden, detect distinct high-risk morphological plaque features, assess the hemodynamic significance of coronary lesions and quantify the coronary inflammatory burden by tracking the effects of arterial inflammation on the composition of the adjacent perivascular fat. Furthermore, advances in machine learning, computational fluid dynamic modeling, and the development of targeted contrast agents continue to expand the capabilities of cardiac computed tomography imaging. In our Review, we discuss the current role of cardiac computed tomography in the assessment of coronary atherosclerosis, highlighting its dual function as a clinical and research tool that provides a wealth of structural and functional information, with far-reaching diagnostic and prognostic implications.

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SignificanceCoronary artery disease (CAD) continues to be a leading cause of morbidity and mortality across the world despite significant progress in prevention, diagnosis and treatment of atherosclerotic disease. Recent AdvancesThe focus of the cardiovascular community has shifted towards seeking a better understanding of the inflammatory mechanisms driving residual CAD risk not modulated by current therapies. Significant progress has been achieved in revealing both pro-inflammatory and anti-inflammatory mechanisms, and how shift of the balance in favour of the former, can drive the development of disease. Critical IssuesAdvances in the non-invasive detection of coronary artery inflammation have been forthcoming. These advances include multiple imaging modalities, with novel applications of computed tomography both with and without positron emission tomography, and experimental ultrasound techniques. These advances will enable better selection of patients for anti-inflammatory treatments and assessment of treatment response. The rapid advancement in pharmaceutical design has enabled the production of specific antibodies against inflammatory pathways of atherosclerosis, with modest success to date. The pursuit of demonstrating efficacy and safety of novel anti-inflammatory and/or pro-inflammation resolution therapies for atherosclerotic CAD has become a major focus. Future DirectionsThis review seeks to provide an update of the latest evidence of all three of these highly related but disparate areas of inquiry: Our current understanding of the key mechanisms by which inflammation contributes to coronary artery atherosclerosis, the evidence for non-invasive assessment of coronary artery inflammation, and finally, the evidence for targeted therapies to treat coronary inflammation for the reduction of CAD risk.