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Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:e15-e16
doi: 10.1161/01.ATV.0000153090.21990.8c
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*Native-American Health
(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:e15.)
© 2005 American Heart Association, Inc.


Letters to the Editor

Adiponectin and Coronary Heart Disease: The Strong Heart Study

Robert S. Lindsay

MedStar Research Institute, Washington, DC and BHF Glasgow Cardiovascular Research Centre, University of Glasgow, Western Infirmary, Scotland

Helaine E. Resnick; Jianhui Zhu; Min L. Tun; Barbara V. Howard

MedStar Research Institute, Washington, DC

Ying Zhang; Jeunliang Yeh

Center for American Indian Health Research, University of Oklahoma Health Sciences Center, Oklahoma City

Lyle G. Best

Missouri Breaks Industries Research Inc., Timber Lake, SD


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

To the Editor:

The adipocyte secreted protein, adiponectin, is of particular interest in metabolic and vascular disease because of its close associations with insulin sensitivity and obesity.1 Lower levels of adiponectin are associated with later development of type 2 diabetes.2 Recent observations from the Health Professionals Follow-Up Study3 suggest that lower adiponectin concentrations might also be associated with incident myocardial infarction, findings in keeping with prior observations in patients with end-stage renal failure.4

We examined prospective relationships of adiponectin to vascular disease in a case–control series selected from the Strong Heart Study (SHS). The SHS is the largest study of cardiovascular disease in American Indians, a group at particular risk of obesity and type 2 diabetes and in whom an increasing incidence of coronary heart disease (CHD) is seen.5

Cases and controls were selected from the SHS cohort.6 The SHS recruited 4549 volunteers of American Indian heritage from 3 geographic areas (Arizona, North and South Dakota, and Oklahoma).6 Volunteers (59% female) were invited to a study examination on three occasions (SH1, 1988 to 1992; SH2, 1993 to 1995; SH3, 1997 to 1999) and remained under continued surveillance for development of vascular disease as described previously.7,8 Because of availability of plasma samples, baseline data for this study were taken from the second examination (SH2), and participants with prevalent cardiovascular disease at SH2 (definite CHD and stroke), or thyroid or glucocorticoid medication were excluded. Of eligible participants at baseline, 295 had incident CHD (69 fatal or 182 nonfatal CHD events) in subsequent . . . [Full Text of this Article]




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