Coronary Artery Risk Development in Young

Hozawa, A, Jacobs, DR, Jr., Steffes, MW, Gross, MD, Steffen, LM, and Lee, DH, 2007. Relationships of circulating carotenoid concentrations with several markers of inflammation, oxidative stress, and endothelial dysfunction The Coronary Artery Risk Development in Young Adults (CARDIA)/Young Adult Longitudinal Trends in Antioxidants (YALTA) study. Clin Chem 53,447 455. 

Hughes, G.H. and Jacobs, D.R. Racial differences in serum cotinine levels among smokers in the coronary artery risk development in (young) adults study. Am J Public Health 80 1053-1056, 1990. 

Stemfeld, B., Sidney, S., Jacobs, D.R., Jr., Sadler, M.C., Haskell, W.L., and Schreiner, PJ. Seven-year changes in physical fitness, physical activity, and hpid profile in the CARDIA study. Coronary Artery Risk Development in Young Adults. Anno Is of Evidemioloev 1999 9 25-33. 

Surprisingly, no clinical trials have specifically addressed the contribution of hypertension to the development of peripheral arterial disease. Most of the data comes from multiple regression analysis of many parameters looking for correlations, or subgroup analysis of trials designed primarily to look at coronary artery disease. However, Kannel cidA.. (6) has shown that epidemiological data analyzed in this way accurately predicts disease risk in a variety of American population samples, and in elderly as well as young coronary candidates. 

An analysis has been reported of relationship of lipids and lipoproteins to development of coronary heart disease (CHD) over 14 years in 5127 men and women in the Framingham Study. Serum cholesterol, LDL and VLDL showed strong statistical discriminatory power for development of CHD, VLDL somewhat less than the other two. In men of all ages and in young women VLDL did not predict CHD when its cholesterol risk factor was statistically removed. In women of 54-69 years, however, VLDL appeared to be the important risk factor, rather than cholesterol. With the exception of these older women, the data seem to indicate that cholesterol, presented to the artery either as LDL or VLDL, is the pathogenic agent. 

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