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JAMA will present new research from its theme issue on Pain Management at the Millennium Broadway Hotel, 145 W. 44th St., New York from 9:45 a.m. to noon on Tuesday, November 11. A program and registration are available online.

JAMA news releases are made available to the public after 3 pm US Central time on the first 4 Tuesdays of each month. The Archives Journals news releases are made available to the public after 3 pm Central time on Mondays. We also provide a list of previous news releases.

JAMA NEWS RELEASES
(Embargoed for Release: 3 p.m. CT, Tuesday, November 4, 2003)

JAMA NEW RELEASES

   CHOLESTEROL LEVELS IN CHILDHOOD MAY PREDICT RISK OF CARDIOVASCULAR DISEASE IN ADULTHOOD

   CERTAIN GENETIC VARIATION IN ESTROGEN RECEPTOR ASSOCIATED WITH SUBSTANTIAL INCREASE IN RISK OF HEART ATTACK

   SMALL STUDY SUGGESTS POSSIBLE NEW APPROACH FOR TREATING CORONARY DISEASE

JAMA REPORT (VIDEO NEWS RELEASE SCRIPT)

   SPECIFIC RISK FACTORS IN CHILDREN PREDICT HIGHER HEART DISEASE RISK FACTORS IN YOUNG ADULTS

INFORMATION CONTAINED IN THESE NEWS RELEASES IS PROTECTED BY COPYRIGHT. JOURNAL ATTRIBUTION IS REQUIRED.

TV Note: This week's JAMA video news release is on childhood cholesterol levels being able to predict risk of cardiovascular disease in adulthood. The release will be fed Tuesday, November 4, from 9:00 - 9:30 a.m. ET on Telstar 6, Transponder 11 (C-Band) and from 2:00 - 2:30 p.m. ET on Telstar 6, Transponder 11 (C-Band). For more information, call 312/464-JAMA (5262).

Please Note: Our e-mail has changed to mediarelations{at}jama-archives.org

EMBARGOED FOR RELEASE: 3 P.M. (CT) TUESDAY, NOVEMBER 4, 2003
Media Advisory: To contact the corresponding author for the first study, Gerald S. Berenson, M.D., call Fran Simon at 504/588-5221.
To contact Olli T. Raitakari, M.D., Ph.D., email: olli.raitakari{at}utu.fi
To contact editorialist Henry C. McGill, Jr., M.D., call Will Sansom at 210/567-2570.

"The fact that body fatness, as measured by BMI, is also a significant childhood predictor in this regard points to the potential usefulness of LDL-C level along with BMI, both modifiable and interrelated risk factors, in CAD risk assessment and intervention in childhood," the researchers add.
(JAMA. 2003; 290:2271-2276. Available post-embargo at jama.com)

Editor's Note: This study was supported by grants from the National Heart, Lung, and Blood Institute; from the National Institute on Aging; from the National Institute of Child Health and Human Development; and from the American Heart Association.

In a related article, Olli T. Raitakari, M.D., Ph.D., of the University of Turku, Finland, and colleagues studied the relationship between cardiovascular risk factors measured in childhood and adolescence and common carotid artery IMT, a marker of preclinical atherosclerosis, measured in adulthood. Atherosclerosis is a disease characterized by the deposition of fatty substances called plaques in the walls of medium and large arteries.

The study was conducted at five centers in Finland among 2,229 white adults aged 24 to 39 years who were examined in childhood and adolescence at ages 3 to 18 years in 1980 and reexamined 21 years later, between September 2001 and January 2002.

The researchers found that the number of risk factors measured at ages 12 to 18 years, including high levels of LDL-C, systolic blood pressure, body mass index, and cigarette smoking, were directly related to carotid IMT measured at ages 33 to 39 years, and remained significant after adjustment for other risk variables. IMT in adulthood was significantly associated with childhood LDL-C levels, systolic blood pressure, body mass index, and smoking, and with adult systolic blood pressure, body mass index, and smoking.

"Our findings indicate that children and adolescents with several risk factors are at increased risk of developing atherosclerosis in adulthood. Risk factors such as obesity, dyslipidemia [disorders of lipoprotein metabolism, including lipoprotein overproduction or deficiency], and elevated blood pressure are metabolically linked, and reductions in these factors could be potentially achieved in children with lifestyle modifications such as inducing changes in the diet, increasing levels of physical activity, and controlling obesity," the authors conclude.
(JAMA. 2003; 290:2277-2283. Available post-embargo at jama.com)

Editor's Note: This study was supported by the Academy of Finland, Helsinki; the Social Insurance Institution of Finland, Helsinki; Turku University Foundation, Turku, Finland; Juho Vainio Foundation, Helsinki; Finnish Foundation of Cardiovascular Research, Helsinki; and the Finnish Cultural Foundation, Helsinki.

EDITORIAL: STARTING EARLIER TO PREVENT HEART DISEASE

In an accompanying editorial, Henry C. McGill, Jr., M.D., and C. Alex McMahan, Ph.D., of the University of Texas Health Science Center at San Antonio, write that assessing cardiovascular risk factors in youth is easy and inexpensive.

"There is little cost and much benefit in assessing obesity, smoking, and blood pressure at all ages. The guidelines of the Adult Treatment Panel III recommend measuring lipids and lipoproteins beginning at age 20 years. Screening for dyslipidemia in younger persons is not widely recommended unless there is a family history of precocious coronary heart disease (CHD). With the evidence now emerging that shows that cholesterol and other risk factors do matter during adolescence, it may now be time to reconsider the age at which measurement of cholesterol levels should begin."

"The available evidence indicates that it is time to move forward to start earlier to prevent CHD. From a public health perspective, it is essential to promote a culture in which young persons are encouraged to maintain safe and healthy lifestyles. The difficulty of modifying lifestyles of teenagers in the current environment of the industrialized societies should not be underestimated, and success may require decades, perhaps even generations. Meanwhile, in clinical medicine, physicians and other health professionals caring for adolescents should be sure their patients and their parents know it is a good (and safe) bet that promoting and maintaining a healthy lifestyle in youth will reduce the risk of precocious cardiovascular disease in adulthood," they conclude.
(JAMA. 2003; 290:2320-2321). Available post-embargo at jama.com.

For More Information: Contact the JAMA/Archives Media Relations Department at 312/464-JAMA (5262) or email: mediarelations{at}jama-archives.org (please note new email address).

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EMBARGOED FOR RELEASE: 3 P.M. (CT) TUESDAY, NOVEMBER 4, 2003
Media Advisory: To contact Amanda M. Shearman, Ph.D., call Deborah Halber at 617/258-9276.
To contact editorialist Paul N. Hopkins, M.D., M.S.P.H., call Phil Sahm at 801/581-7387.

"These findings support the importance of estrogen receptors in CVD susceptibility, especially in men. Estrogen receptor variation also has potential to explain recent conflicting data regarding the effects of hormone therapy on CVD susceptibility in women," the authors conclude.
(JAMA. 2003; 290:2263-2270. Available post-embargo at jama.com)

Editor's Note: This work was supported by a National Heart, Lung, and Blood Institute (NHLBI) Specialized Center of Research in Ischemic Heart Disease grant and in part by grants from the NHLBI to co-author David E. Housman, Ph.D. This work is also supported by the NHLBI's Framingham Heart Study.

EDITORIAL: ESTROGEN RECEPTOR 1 VARIANTS AND CORONARY ARTERY DISEASE - SHEDDING LIGHT INTO A MURKY POOL

In an accompanying editorial, Paul N. Hopkins, M.D., M.S.P.H., and Eliot A. Brinton, M.D., of the University of Utah, Salt Lake City, write that "the article by Shearman et al in this issue of THE JOURNAL brings intriguing genetic data to bear on several issues of considerable current controversy-the relationship between coronary artery disease (CAD) and estrogen action, the general utility of CAD associations with variants in candidate genes, and the challenges of identifying causative gene variants for common disease."

"Curiously, MI was the only end point associated with the [homozygous ESR1 c.454-397T>C] genotype; non-MI end points, if anything, showed an opposite trend. This raises the question of whether the CC genotype marks risk for precipitation to MI rather than promotion of underlying atherosclerosis," they add.

"That the study by Shearman et al confirms prior observations is of paramount importance in light of current thinking about genetic association studies, which are often considered untrustworthy because of the frequent inability to confirm initially reported positive associations," the editorialists write.
(JAMA. 2003; 290:2317-2319). Available post-embargo at jama.com.

Editor's Note: Dr. Brinton has received honoraria from Wyeth, Pfizer, and Lilly.

For More Information: Contact the JAMA/Archives Media Relations Department at 312/464-JAMA (5262) or email: mediarelations{at}jama-archives.org (please note new email address).

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EMBARGOED FOR RELEASE: 3 P.M. (CT) TUESDAY, NOVEMBER 4, 2003
Media Advisory: To contact Steven E. Nissen, M.D., call Alicia Sokol at 216/445-9661. To contact editorial author Daniel J. Rader, M.D., call Susan Winston at 215/349-8368.

In conclusion the authors write: "This initial trial of an exogenously (synthetic) produced HDL mimetic demonstrated significant evidence of rapid regression of atherosclerosis. The potential utility of the new approach must be fully explored in a larger patient population with longer follow-up, assessing a variety of clinical end points, including morbidity and mortality."
(JAMA. 2003; 290:2292-2300. Available post-embargo at jama.com)

Editor's Note: The study was funded by Esperion Therapeutics, Ann Arbor, Mich. Please see the JAMA article for author's financial disclosures.

EDITORIAL: HIGH-DENSITY LIPOPROTEINS AS AN EMERGING THERAPEUTIC TARGET FOR ATHEROSCLEROSIS

In an accompanying editorial, Daniel J. Rader, M.D., from the University of Pennsylvania School of Medicine, Philadelphia writes: "The results of this study are surprising to even the most optimistic supporters of the concept of targeting HDL as a therapy for atherosclerosis. Patients who received the 5 infusions of apoA-I Milano experienced statistically significant regression in coronary atheroma volume in the target segment compared with baseline measurements. A smaller placebo group that received only saline infusions had no significant change in atheroma volume."

Rader notes several important limitations of the study, including small sample size, short duration of treatment, and the fact that intravascular ultrasound has not been established to be a reliable surrogate for clinical benefit. In addition, he states that it is possible that if normal ApoA-I were infused instead of ApoA-I Milano, it may have given the same or better results, but that study has not been performed. Nevertheless, Rader states that this concept has important implications for future atherosclerosis research.

"If this concept is confirmed in future studies, some day patients with acute coronary syndromes may receive 'acute induction therapy' with HDL-based therapies for rapid regression and stabilization of lesions, followed by long-term therapy to prevent the regrowth of these lesions. In this model, long-term HDL-based therapies will still be needed as a vital component of the preventive phase. ... If the pace of these discoveries continues, the next two decades may be to HDL what the last two decades were to LDL: an era in which the development of new therapies may permit the unequivocal demonstration of the clinical benefit of targeting HDL to reduce the burden of atherosclerotic cardiovascular disease."
(JAMA. 2003; 290:2322-2324). Available post-embargo at jama.com.

Editor's Note: DFor the financial disclosures of Dr. Rader, please see the JAMA editorial.

For More Information: Contact the JAMA/Archives Media Relations Department at 312/464-JAMA (5262) or email: mediarelations{at}jama-archives.org (please note new email address).

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JAMA REPORTS