TY - JOUR
T1 - Relation of subclinical coronary artery atherosclerosis to cerebral white matter disease in healthy subjects from families with early-onset coronary artery disease
AU - Kral, Brian G.
AU - Nyquist, Paul
AU - Vaidya, Dhananjay
AU - Yousem, David
AU - Yanek, Lisa R.
AU - Fishman, Elliot K.
AU - Becker, Lewis C.
AU - Becker, Diane M.
N1 - Funding Information:
This work was supported by grants RC1HL099747 and K23HL094747 from the National Heart, Lung, and Blood Institute (National Institutes of Health, Rockville, Maryland), grant R01NS062059 from the National Institute of Neurological Disorders and Stroke (National Institutes of Health, Rockville, Maryland), and grant TR000424 from the Institute for Clinical and Translational Research (Johns Hopkins, Baltimore, Maryland).
PY - 2013/9/15
Y1 - 2013/9/15
N2 - White matter disease (WMD) of the brain is associated with incident stroke. Similarly, subclinical calcified coronary artery plaque has been associated with incident coronary artery disease (CAD) events. Although atherogenesis in both vascular beds may share some common mechanisms, the extent to which subclinical CAD is associated with WMD across age ranges in subjects with a family history of early-onset CAD remains unknown. We screened 405 apparently healthy participants in the Genetic Study of Atherosclerotic Risk for CAD risk factors and for the presence of noncalcified and calcified coronary plaque using dual-source multidetector cardiac computed tomographic angiography. The presence and volumes of WMD were assessed by 3-Tesla brain magnetic resonance imaging. Participants were 60% women, 36% African-American, mean age 51.6 ± 10.6 years. The overall prevalence of coronary plaque was 43.0%. Subjects with coronary plaque had significantly greater WMD volumes (median 1,222 mm3, interquartile range 448 to 3,871) compared with those without coronary plaque (median 551 mm3, interquartile range 105 to 1,523, p <0.001). In multivariate regression analysis, adjusting for age, gender, race, traditional risk factors, total brain volume, and intrafamilial correlations, the presence of coronary plaque was independently associated with WMD volume (p = 0.05). This study shows a significant association betweenWMDand noncalcified and calcified coronary plaque in healthy subjects, independent of age and risk factors. In conclusion, these findings support the premise of possible shared causal pathways in 2 vascular beds in families at increased risk for early-onset vascular disease.
AB - White matter disease (WMD) of the brain is associated with incident stroke. Similarly, subclinical calcified coronary artery plaque has been associated with incident coronary artery disease (CAD) events. Although atherogenesis in both vascular beds may share some common mechanisms, the extent to which subclinical CAD is associated with WMD across age ranges in subjects with a family history of early-onset CAD remains unknown. We screened 405 apparently healthy participants in the Genetic Study of Atherosclerotic Risk for CAD risk factors and for the presence of noncalcified and calcified coronary plaque using dual-source multidetector cardiac computed tomographic angiography. The presence and volumes of WMD were assessed by 3-Tesla brain magnetic resonance imaging. Participants were 60% women, 36% African-American, mean age 51.6 ± 10.6 years. The overall prevalence of coronary plaque was 43.0%. Subjects with coronary plaque had significantly greater WMD volumes (median 1,222 mm3, interquartile range 448 to 3,871) compared with those without coronary plaque (median 551 mm3, interquartile range 105 to 1,523, p <0.001). In multivariate regression analysis, adjusting for age, gender, race, traditional risk factors, total brain volume, and intrafamilial correlations, the presence of coronary plaque was independently associated with WMD volume (p = 0.05). This study shows a significant association betweenWMDand noncalcified and calcified coronary plaque in healthy subjects, independent of age and risk factors. In conclusion, these findings support the premise of possible shared causal pathways in 2 vascular beds in families at increased risk for early-onset vascular disease.
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U2 - 10.1016/j.amjcard.2013.05.002
DO - 10.1016/j.amjcard.2013.05.002
M3 - Article
C2 - 23742943
AN - SCOPUS:84886700218
SN - 0002-9149
VL - 112
SP - 747
EP - 752
JO - American Journal of Cardiology
JF - American Journal of Cardiology
IS - 6
ER -